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The Protective Role of Antioxidants in the Defence against ROS/RNS-Mediated Environmental Pollution

Borut Poljšak, Rok Fink

Oxidative Medicine and Cellular Longevity · 2014 · Review

doi:10.1155/2014/671539

Abstract

Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants, such as ionising and nonionising radiation, ultraviolet radiation, elevated concentrations of ozone, nitrogen oxides, sulphur dioxide, cigarette smoke, asbestos, particulate matter, pesticides, dioxins and furans, polycyclic aromatic hydrocarbons, and many other compounds present in the environment. It appears that increased oxidative/nitrosative stress is often neglected mechanism by which environmental pollutants affect human health. Oxidation of and oxidative damage to cellular components and biomolecules have been suggested to be involved in the aetiology of several chronic diseases, including cancer, cardiovascular disease, cataracts, age-related macular degeneration, and aging. Several studies have demonstrated that the human body can alleviate oxidative stress using exogenous antioxidants. However, not all dietary antioxidant supplements display protective effects, for example, β -carotene for lung cancer prevention in smokers or tocopherols for photooxidative stress. In this review, we explore the increases in oxidative stress caused by exposure to environmental pollutants and the protective effects of antioxidants.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 24, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Many environmental pollutants are sources of several reactive species (RS). RS is a collective term that includes both oxygen radicals and other reactive oxygen and nitrogen species (ROS/RNS). Free radicals, important for living organisms, include hydroxyl (OH•), superoxide (O2 •−), nitric oxide (NO•), thyl (RS•), and peroxyl (RO2 •) radical. Peroxynitrite (ONOO−), hypochlorous acid (HOCl), hydrogen peroxide (H2O2), singlet oxygen (1O2), and ozone (O3) are not free radicals but can easily lead to free radical reactions in living organisms. The term reactive oxygen species (ROS) is often used to include not only free radicals but also the nonradicals (e.g., 1O2, ONOO−, H2O2, O3).

There is strong evidence that RS is involved in oxidative/nitrosative stress (O/NS) as a common mechanism by which several environmental pollutants induce damage. Oxidative stress can be defined as an excessive amount of RS, which is the net result of an imbalance between production and destruction of RS (the latter is regulated by antioxidant defences). Oxidative stress is a consequence of an increased generation of RS and/or reduced physiological activity of antioxidant defences against RS. Environmental pollutants stimulate a variety of mechanisms of toxicity on molecular level and oxidative stress seems to be the common denominator leading to the damage to cellular membrane lipids, DNA, and proteins, as well as modulation of antioxidant enzymes. RS are, due to their high reactivity (e.g., hydroxyl radical formation), prone to cause damage to any type of molecule within the cell, for example, polyunsaturated fatty acids, glutathione, certain amino acids, and so forth.

When the antioxidant defence in the human body becomes overwhelmed, oxidative stress to the cellular components often occurs, inducing inflammatory, adaptive, injurious, and reparative processes. On other hand, lifestyle and nutrition might play an important role against environmental oxidant exposure and damage. Protection against O/NS-mediated environmental pollutants can generally occur at two levels: (i) physiochemical protection to lower the dose of exposure, which typically cannot be accomplished by individuals living in polluted areas, or (ii) physiological protection to increase the antioxidative defence of the organism. There is growing scientific evidence that low molecular-weight antioxidants are involved in the prevention of or the decrease in the damage caused by certain environmental pollutants. Because we have little influence on the increasing levels of endogenous antioxidants, it would be reasonable to increase the amount of exogenous antioxidants (mainly through ingestion) to strengthen the defensive properties of organisms against environmental oxidative stress. The current evidence suggests that increased consumption of fruits and vegetables or certain dietary supplements can substantially enhance the protection against many common types of environmentally induced O/NS.

2. Purpose

This review aims to determine whether antioxidants can modulate the toxicity of environmental pollutants, thereby influencing health and disease outcome associated with oxidative stress-induced insults. Evidence will be presented that environmental pollution increases oxidative stress and that dietary supplementation with antioxidants may play a role on the neutralization or buffering of the effects of pollutants with oxidizing properties. The recommendation for the use of dietary antioxidants in areas of increased environmental pollution will be discussed.

This review summarises the most common and health-relevant sources of oxidative stress like air pollution, radiation, pesticides, noise, and household chemicals. Due to space constrains and a broad scientific data, not all the studies could be covered in this review. The reader is thus referred to search through provided references (and references therein) for further details on selected environmental pollutant or selected antioxidant.

2.1. Air Pollution-Induced Oxidative Stress and Protection against It

The health effects of air pollution result from minor irritation of the eyes and the upper respiratory system to chronic respiratory disease, heart and vascular disease, lung cancer, and death. Different studies presented in Table 1 are demonstrating increased oxidative stress/damage due to air pollutant exposure and that antioxidants could offer certain level of protection.

Oxygen could be presented as the leading air pollutant in regard to oxidative stress formation. Molecular O2 itself qualifies as a free radical because it has two unpaired electrons with parallel spin in different π-antibonding orbitals. This spin restriction accounts for its relative stability and paramagnetic properties. O2 is capable of accepting electrons to its antibonding orbitals, becoming “reduced” in the process, and, therefore, functioning as a strong oxidizing agent. The diatomic molecule of oxygen contains two uncoupled electrons and can therefore undergo reduction, yielding several different oxygen metabolites, which are collectively called ROS. Mitochondria are the main site of intracellular oxygen consumption and the main source of ROS formation. Once ROS are produced, they are removed by cellular defenses which include the enzymes superoxide dismutase (Mn-SOD, Cu/Zn-SOD, and extracellular (EC)-SOD), catalase, glutathione peroxidase, peroxiredoxins, and the nonenzymatic antioxidants, like glutathione (GSH), thioredoxin, ascorbate, α-tocopherol, and uric acid. Since oxidative damage of cells increases with age, the increased intake of exogenous antioxidants may support the endogenous antioxidative defense. Clinical studies imply that eating a diet rich in fruits, vegetables, whole grains, legumes, and omega-3 fatty acids can help humans in decreasing oxidative stress and postponing the incidence of degenerative diseases.

Ozone is formed from dioxygen by the action of ultraviolet light and atmospheric electrical discharges. Ozone is a very reactive gas whose uptake depends on the availability of antioxidants in the lining fluids. The surface of the lung is covered with a thin layer of fluid that contains a range of antioxidants that appear to provide the first line of defence against air pollutants. Mudway et al. studied the interaction of ozone with antioxidants and found that the hierarchy toward ozone in human epithelial lining fluid was ascorbic acid followed by uric acid and then glutathione. Wu and Meng analysed the effects of sea buckthorn seed oil on the protection against sulphur dioxide inhalation. They found that buckthorn seed oil contributed antioxidant effects. Furthermore, study by Zhao et al. revealed the protective effect of salicylic acid and vitamin C on sulphur dioxide-induced lipid peroxidation in mice.

Tobacco smoke is one of the most common air pollutants and generates high amounts of various ROS/RNS. Cigarette-induced oxidative stress was found to be affected by the protective effects of vitamin C, glutathione, and other antioxidants, mainly as quenchers of ROS/RNS (Table 1).

Kienast et al. demonstrated that alveolar macrophages and peripheral blood mononuclear cells become activated following exposure to nitrogen dioxide. Several studies have demonstrated that certain antioxidants might play a beneficial role in NOx-induced toxicity. Guth and Mavis and Sevanian et al. examined the effect of vitamin E content on the lungs. Furthermore, a study by Böhm et al. revealed that dietary uptake of tomato lycopene protects human cells against nitrogen dioxide-mediated damage. The possible influence of dietary antioxidants, especially vitamin C, on the increasing prevalence of asthma was explored by Hatch.

Particulate matter can also cause oxidative stress via direct generation of ROS from the surfaces of soluble compounds, altering the function of mitochondria or reducing the activity of nicotinamide adenine dinucleotide phosphate-oxidase, inducing the activation of inflammatory cells to generate ROS and RNS and mediating oxidative DNA damage. Antioxidants could also provide protection against particulate matter-induced toxicity. Indeed, lung lining fluid antioxidants (urate, glutathione, and ascorbate) were demonstrated to be effective in a study by Greenwell et al.. Luo et al. detected an inhibitory effect of green tea extract on the carcinogenesis induced by the combination of asbestos and benzo(a)pyrene in rats drinking 2% green tea extract throughout their lives.

As the diet is the main source of antioxidant micronutrients, a plausible link now exists between the exposure to air pollution and the quality of food consumed.

2.2. Radiation-Induced Oxidative Stress and Protection against It

Ionising radiation consists of highly energetic particles which can generate ROS. These ROS can either be generated primarily via radiolysis of water or they may be formed by secondary reactions. Extensive doses of ionizing radiation have been shown to have a mutating effect; for example, Sperati et al. concluded that indoor radioactivity appears to affect the urinary excretion of 8-OHdG among females, who are estimated to exhibit a higher occupancy in the dwellings measured than males (Table 2). Many compounds have been demonstrated to protect against cell injury caused by radiation-induced ROS formation. One of these compounds is ebselen, a selenoorganic compound. Another compound is N-acetylcysteine, which reduces nitrosative damage during radiotherapy as well as oxidative damage. The radioprotective effects of quercetin and the ethanolic extract of propolis in gamma-irradiated mice were also detected. The radioprotective and radiosensitising activities of curcumin were demonstrated in a study by Jagetia.

Aside from ionising radiation, nonionising radiation also causes oxidative stress. Magnetic fields can affect biological systems by increasing the release of free radicals. There are several studies that indicate a relationship between electromagnetic fields, ROS levels, and OS to exert toxic effects on living organisms. Because it is unlikely that electromagnetic fields can induce DNA damage directly due to their low energy levels, most studies have examined their effects on the cell membrane, general and specific gene expression levels, and signal transduction pathways. Musaev et al. indicated that decimetric microwaves exert oxidant effects at a high intensity of irradiation (specific absorption rate of 15 mW/kg) and antioxidant effects at a low intensity (specific absorption rate of 5 mW/kg) (Table 2). The protective effects of melatonin and caffeic acid phenethyl ester against retinal oxidative stress during the long-term use of mobile phones were reported. Jajte et al. concluded that melatonin provides protection against DNA damage to rat lymphocytes. Another investigation revealed that Ginkgo biloba prevents mobile phone-induced oxidative stress. Guney et al. found that vitamins E and C reduce phone-induced endometrial damage.

Visible and UV light are insufficient to ionize most biomolecules. Nevertheless, human exposure to ultraviolet radiation has important public health implications. Although the skin possesses extremely efficient antioxidant activities, during aging, the ROS levels rise and the antioxidant activities decline. In addition, UV exposure to the skin results in the generation of ROS, such as singlet oxygen, peroxy radicals, the superoxide anion, and hydroxyl radicals, which damage DNA and non-DNA cellular targets and accelerate the skin aging process. UV-radiation alters endogenous antioxidant protection; for example, in a study by Shindo et al., after UV-irradiation, the epidermal and dermal catalase and superoxide dismutase activities were greatly decreased. With respect to the protective role of antioxidants, many studies (Table 2) investigated the effect of vitamin C on ultraviolet-radiation- (UVR-) induced damage. Oral vitamin C supplements resulted in significant increases in plasma and skin vitamin C content. In the study by Aust et al., the photoprotective effects of synthetic lycopene after 12 weeks of supplementation were examined, and significant increases in the lycopene serum and total skin carotenoid levels were detected. Studies of animals and humans suggested that green tea polyphenols are photoprotective and can be administered to prevent solar UVB light-induced skin disorders. A review of the research reveals that polyphenols or other phytochemicals, such as green tea polyphenols, grape seed proanthocyanidins, resveratrol, silymarin, genistein, and others, exert substantial photoprotective effects against UV-induced skin inflammation, oxidative stress, DNA damage, and so forth.

Presently, we are exposed to various sources of radiation, both ionising and nonionising. The results of many studies indicate that the human body can cope with radiation-induced oxidative stress to a certain degree by consuming an appropriate antioxidant diet.

2.3. Pesticide-Induced Oxidative Stress and Protection against It

Pesticides have become an integral constituent of the ecosystem due to their widespread use, distribution, and the stability of some of the pesticides in the environment. Pesticide exposure may play a major role in increased oxidative stress of the organisms and may result in altered disease susceptibility. Bagchi et al. demonstrated that pesticides induce the production of ROS and oxidative damage to tissues. de Liz Oliveira Cavalli found that exposure to glyphosate causes oxidative stress and activates multiple stress-response pathways leading to Sertoli cell death in prepubertal rat testis. The role of oxidative stress in immune cell toxicity induced by the pesticides lindane, malathion, and permethrin was examined by Olgun and Misra. Hassoun et al. reported that chlordane produces oxidative tissue damage based on the levels of hepatic lipid peroxidation and DNA damage (Table 3). Bus et al. reported that paraquat pulmonary toxicity results from the cyclic reduction and oxidation of paraquat. The results of a study performed by Pérez-Maldonado et al. demonstrated the induction of apoptosis by DDT. Hassoun et al. reported that lindane, DDT, chlordane, and endrin exposure resulted in significant increases in hepatic lipid peroxidation and DNA damage. Another study by Senft et al. found out that dioxin increases mitochondrial respiration-dependent ROS production. On the other hand, Ciftci et al. reported a protective effect of curcumin on the immune system of rats intoxicated with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Additionally, Hung et al. suggested that tea melanin might be a potential agent against the development of tetrachlorodibenzodioxin-induced oxidative stress. Gultekin et al. examined the effects of melatonin and vitamins E and C on the reduction of chlorpyrifos-ethyl.

Another group of pesticides are polychlorinated biphenyls (PCBs), which also induce increased intracellular ROS production. Zhu et al. indicated that different PCB compounds (Aroclor 1254, PCB153, and the 2-(4-chlorophenyl)-1,4-benzoquinone metabolite of PCB3) increase the steady-state levels of intracellular O2 •− and H2O2 in breast and prostate epithelial cells. Many antioxidants showed protection also against PCB-induced oxidative stress and damage. Ramadass et al. tested the hypothesis that flavonoids modify PCB-mediated cytotoxicity and found that flavonoids inhibit PCB-induced oxidative stress. Zhu et al. demonstrated that treatment with N-acetylcysteine significantly protected cells against PCB-mediated toxicity. Red ginseng, which displays a variety of biological and pharmacological activities, including antioxidant, anti-inflammatory, antimutagenic, and anticarcinogenic effects, was found to protect the body against oxidative stress/damage induced by PCB exposure. Sridevi et al. also reported that the effect of alpha-tocopherol against PCB-induced neurotoxicity resulted in decreased oxidative stress. Another study reported the synergistic effects of vitamins C and E against PCB- (Aroclor 1254) induced oxidative damage.

Dioxins and furans are byproducts of chemicals production. Dioxins may be released into the environment through the production of pesticides and other chlorinated substances. Both dioxins and furans are related to a variety of incineration reactions and the use of a variety of chemical products. Ciftci and coworkers reported that dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD) causes an oxidative stress response in the rats liver. The subcellular sources and underlying mechanisms of dioxin-induced reactive oxygen species, however, are not well understood. TCDD increases the formation of thiobarbituric acid-reactive substances. It also causes a significant decline in the levels of glutathione, catalase, GSH-Px, and Cu-Zn superoxide dismutase in rats. The impact of 2-furan-2-yl-1H-benzimidazole on vitamins A, E, C, and Se, malondialdehyde, and glutathione peroxidase levels on rats was analysed in a study by Karatas et al.. The results showed that vitamins A, E, C, and Se levels were lower than the control groups, while serum MDA level and GSH-Px activity flexibly increased, depending on the injection days. The observed decreases in vitamins A, E, C, and Se levels in the blood might be causally related to the increased amount of ROS. The potential protective effect of quercetin on TCDD induced testicular damage in rats was studied by Ciftci et al.. The results showed that exposure to TCDD induces testicular damage, and quercetin prevents TCDD-induced testicular damage in rats. Resveratrol's antioxidative effects were also investigated against in a study by Ishida et al.. The results suggested that oral resveratrol is an attractive candidate for combating dioxin toxicity. Türkez et al. analysed effects of propolis against TCDD induced hepatotoxicity in rats and found that propolis alleviate pathological effects and prevents the suppression of antioxidant enzymes in the livers.

It can be concluded that the stimulation of ROS production, the induction of lipid peroxidation and oxidative DNA and protein damage, and the disturbance of the total antioxidant capacity of the body are mechanisms of the toxicity induced by most pesticides, including organophosphates, bipyridyl herbicides, and organochlorines. Antioxidant nutrients and related bioactive compounds common in fruits and vegetables as well as food additives can protect against environmental exposure to pesticides-induced oxidative stress/damage (Table 3).

2.4. Household Chemical-Induced Oxidative Stress and Protection against It

The predominant use of industrial resins, such as urea-formaldehyde, phenol-formaldehyde, polyacetal, and melamine-formaldehyde resins, can be found in domestic environments in adhesives and binders for wood products, pulp products, paper products, plastics, synthetic fibres, and in textile finishing. Formaldehyde was demonstrated to exert increased oxidative stress formation (Table 4), primarily as lipid peroxidation, as found in a study performed by Chang and Xu. Also in the case of household chemical-induced oxidative stress certain antioxidants showed protection. In a recent study, Köse et al. reported that rose oil inhalation protects against formaldehyde-induced testicular damage in rats. Zararsiz et al. demonstrated that exposure to formaldehyde increased the free radical levels in rats and that omega-3 fatty acids prevented this oxidative stress. The protective effect of melatonin against formaldehyde-induced renal oxidative damage in rats has also been reported.

Many studies have been performed on carbon tetrachloride because it is a well-known model of inducing chemical hepatic injury in mice. Also carbon tetrachloride exposure increases oxidative stress/damage in tested model organisms and carbon tetrachloride-induced damage has been reversed by many antioxidants examined. Thus, the antioxidant and hepatoprotective effects of many antioxidants and plant extracts against oxidative stress induced by carbon tetrachloride have been reported. For example, chlorella-mediated protection against carbon tetrachloride-induced oxidative damage in rats was demonstrated in a study by Peng et al.. Ozturk et al. found that apricot (Prunus armeniaca L) feeding exerted beneficial effects. The potency of vitamin E to enhance the recovery from carbon tetrachloride-induced renal oxidative damage in mice was revealed in a study by Adaramoye. The protective effects of Curcuma longa Linnwere reported by Lee et al.. The protective effect of blackberry extract against oxidative stress in carbon tetrachloride-treated rats was reported by Cho et al..

Chemicals found in common household and personal care goods are major sources of oxidant exposure that can lead to oxidative stress. Many antioxidants, such as melatonin, vitamin E, ascorbate, and extracts from various plants, for example, rose, green tea, and blackberry, were reported to decrease oxidative stress and/or damage in vivo and in vitro.

2.5. Disinfection Byproducts (DBP) and Other Water Born Pollutants

The beneficial role of water ingestion can be minimised due to the formation of disinfection byproducts. Chlorination and ozonation in the water treatment process are believed to produce various active oxygen species, which seem to participate in the reaction with fumic acid, pollutants, and bacteria (Table 4). Hypochlorous acid (HOCl) is formed when Cl2 is added to the water for disinfection purposes. This acid is highly reactive and is capable of oxidising many biological molecules. HOCl reacts with O2 − to give OH• and with H2O2 to form singlet O2. HOCl affects endogenous enzymatic antioxidants and increases oxidative stress. For example, Hassoun and Ray demonstrated the induction of oxidative stress and cellular death of drinking water disinfection byproducts. Similar observations were reported by Leustik et al.. Studies suggest that Cl2 inhalation damages both airway and alveolar epithelial tissues and that these damaging effects were ameliorated by the prophylactic administration of low molecular-weight antioxidants. Trolox was reported to be protective against oxidative injury induced by HOCl to Ca-ATPase in the sarcoplasmic reticulum of skeletal muscle. Ascorbic acid might also play a protective role (Table 4), especially in individuals consuming supplements containing this vitamin. Also thioallyl and S-allylcysteine (both are garlic-derived compounds), melatonine, glutathione, glutathione disulfide, S-methylglutathione, lipoic acid, and dihydrolipoic acid were reported to protect against hypochlorous acid and peroxynitrite-induced damage).

Additionally, the following plant extracts display a protective effect against HOCl-induced oxidative damage: Agaricus campestris, Cynara cardunculus, Thymus pulegioides, and Vicia faba. When resolving the problem of DBP, first the cause of their formation should be assessed with different engineering approaches DBP, for example, by moving the point of chlorination downstream in the treatment train, reducing the natural organic matter precursor concentration, replacing prechlorination by peroxidation, and so forth.

The use of antioxidants as compounds which ameliorate DBP-induced toxicity should be just the last alternative when all other approaches deal with the DBP formation in the drinking water fail.

Researches in the past two decades have pointed out that redox active metals like iron (Fe), copper (Cu), chromium (Cr), cobalt (Co), and other metals present in water possess the ability to produce ROS such as superoxide anion radical and nitric oxide. Disruption of metal ion homeostasis may lead to oxidative stress, a state where increased formation of reactive oxygen species overwhelms body antioxidant protection and subsequently induces DNA damage, lipid peroxidation, protein modification, and other effects. Pollutants in water like heavy metals As, Cd, Cu, Fe, Pb, and Zn can cause oxidative stress in fish. On other hand Yang and coworkers reports that water spinach containing chlorophyll and lycopene have potential to reduce cytotoxicity and oxidative stress in liver induced by heavy metals. Besides heavy metals also pesticides in water can represent sources of oxidative stress. Atrazine and chlorpyrifos are the most common pesticides found in freshwater ecosystems throughout the world. Xing et al. investigated the oxidative stress responses in the liver of common carp after exposure to atrazine and chlorpyrifos and found that exposure or their mixture could induce decrease in antioxidant enzyme activities and increase in MDA content in a dose-dependent manner. Eroğlu et al. reported organophosphate pesticides produce oxidative stress due to the generation of free radicals, which alter the antioxidant defence system in erythrocytes and that vitamins C and E can act as protective role.

2.6. The Role of Oxidative Stress in Noise-Induced Hearing Damage

Noise is a disturbing and unwanted sound. Exposure to noise causes many health problems such as hearing loss, sleep disturbance, and impairs performance as well as effecting cognitive performance. It also increases aggression and reduces the processing of social cues seen as irrelevant to task performance, as well as leading to coronary heart disease, hypertension, higher blood pressure, increased mortality risk, serious psychological effects, headache, anxiety, and nausea ( and references within). Prolonged exposure to noise can also cause oxidative stress in the cochlea which results in the loss (via apoptotic pathways) of the outer hair cells of the organ of Corti. Increased noise exposure results in increased levels of reactive oxygen species formation that play a significant role in noise-induced hair cell death. Acute as well as long-term exposure to noise can produce excessive free radicals alter endogenous antioxidative enzymes as superoxide dismutase, catalase, and glutathione peroxidase.

In a study by Demirel et al. the effect of noise on oxidative stress parameters in rats was analyzed by measuring malondialdehyde, nitric oxide levels, and glutathione peroxidase activity. The results showed an elevation in MDA level, an indicator of lipid peroxidation, as well as NO level and GSH-Px activity through noise exposure, suggesting that the presence of oxidative stress may have led to various degrees of damages in the cells. Additionally, increases in oxidative stress parameters, such as MDA level, and decreases in CAT and SOD activities in textile workers exposed to elevated levels of noise supports the hypothesis that noise causes oxidative stress. It seems that noise might cause damage not only in the ears but also across the entire body, leading to oxidative stress. In a study by van Campen et al., the time course of ROS damage following exposure was assessed. Based upon oxidative DNA damage present in the cochlea following intense noise, the researchers postulate that the first 8 h following exposure might be a critical period for antioxidant treatment. Thus, the ROS quenching properties of antioxidants and medicinal plants are attracting more and more research to counteract noise-induced oxidative stress. Manikandan and Devi investigated the antioxidant property of alpha-asarone against noise stress induced changes in different regions of the rat brain and their data proved that the antioxidant property of alpha-asarone acts against noise stress induced damage. The aim of a study performed by Manikandan et al. was to evaluate the protective effect of both ethyl acetate and methanolic extract of Acorus calamus against noise stress induced changes in the rat brain. Both the ethyl acetate and methanolic extract of Acorus calamus protected most of the changes in the rat brain induced by noise stress. N-acetyl-cysteine also offered protection against noise-induced hearing loss in the Sprague Dawley rat. The study by Ewert et al. determined if administration of a combination of antioxidants 2,4-disulfonyl α-phenyl tertiary butyl nitrone (HPN-07) and N-acetylcysteine could reduce both temporary and permanent hearing loss. The results showed that a combination of antioxidants HPN-07 and NAC can both enhance the temporary threshold shift recovery and prevent permanent threshold shift by reducing damage to the mechanical and neural components of the auditory system when administered shortly after blast exposure. Additionally, arboxy alkyl esters (esters of quinic acid found in fruits and vegetables) have been shown to improve DNA repair capacity of spiral ganglion neurons in response to noise stress.

The problem of oxidative stress in the production of hearing loss is even worse when the synergistic effects takes place since a broad range of environmental and occupational contaminants can interact with noise to enhance noise-induced hearing loss, for example, through carbon monoxide and by acrylonitrile.

2.7. Adverse or Insignificant Effects of Antioxidant Treatment after Exposure to Environmental Pollutants

Administration of antioxidants in cases of environmentally induced oxidative stress does not always demonstrate protection (Table 5). Hackney et al. analysed whether vitamin E supplementation protected against O3 exposure and found no significant differences between the vitamin E- and placebo-treated groups. Another study demonstrated that in a high-risk group, such as smokers, high doses of beta-carotene increased the rate of lung cancer. Additionally, the results of large, controlled trials of an intervention of beta-carotene supplementation did not support the detected beneficial associations or a role for supplemental beta-carotene in lung cancer prevention; instead, they provided striking evidence for its adverse effects among smokers. McArdle et al. investigated the effects of oral vitamin E and beta-carotene supplementation on ultraviolet radiation-induced oxidative stress to the human skin. The results revealed that vitamin E or beta-carotene supplementation displayed no effect on the sensitivity of the skin to UVR. A study by Stahl et al. was performed in which the antioxidant effect of carotenoids and tocopherols was investigated based on their ability to scavenge ROS generated during photooxidative stress. The antioxidants used in this study provided protection against erythema in humans and may be useful for diminishing the sensitivity to ultraviolet light (Table 5).

Iron and copper have been reported to aggravate the toxicity of paraquat in E. coli. Treatment with ferrous iron in a study by Korbashi et al. led to an enhancement of bacterial killing by paraquat, whereas treatment with chelating agents, such as nitrilotriacetate and desferrioxamine, markedly reduced, up to complete abolishment, the toxic effects. Some compounds contribute to the antioxidant defence by chelating transition metals and preventing them from catalysing the production of free radicals in the cell. Metal-chelating antioxidants, such as transferrin, albumin, and ceruloplasmin, ameliorate radical production by inhibiting the Fenton reaction, which is catalysed by copper or iron. Latchoumycandane and Mathur investigated whether treatment with vitamin E protects the rat testis against oxidative stress induced by tetrachlorodibenzodioxin and revealed that the activities of antioxidant enzymes and the levels of hydrogen peroxide and lipid peroxidation did not change in the animals coadministered tetrachlorodibenzodioxin and vitamin E. Although several studies have demonstrated the protective effect of antioxidant administration against oxidative stress, it is important to note that not all antioxidants exert health benefits.

2.8. What Could Be the Reason?

The inappropriate use of dietary supplements may lead to “antioxidative stress.” Detailed description of the negative effects of antioxidants can be found in publications by Poljsak et al.,, Poljsak and Milisav, and references therein. Briefly, the intake of only one antioxidant may alter the complex system of endogenous antioxidative defence of cells or alter the cell apoptosis pathways. The beneficial physiological cellular use of ROS is being demonstrated in different fields, including intracellular signalling and redox regulation and synthetic antioxidants cannot distinguish among the radicals that have a beneficial role and those that cause oxidative damage to biomolecules. If administration of antioxidant supplements decreases total ROS/RNS formation, it may also interfere with the immune system to fight bacteria and essential defensive mechanisms for removal of damaged cells, including those that are precancerous and cancerous. When large amounts of antioxidant nutrients are taken, they can also act as prooxidants by increasing oxidative stress. None of the major clinical studies using mortality or morbidity as an end point has found positive effects of antioxidant, such as vitamin C, vitamin E, or β-carotene, supplementation. Some recent studies demonstrated that antioxidant therapy displays no effect and can even increase mortality (The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group, 1994;, Heart Protection Study Collaborative Group, 2002; Age-Related Eye Disease Study Research Group, 2001). On the other hand, antioxidant supplements do appear to be effective in lowering an individual's oxidative stress if his/her initial oxidative stress is above normal or above his/her set point of regulation. Thus, the antioxidant supplements may help the organism to correct the elevated levels of oxidative stress when it cannot be controlled by the endogenous antioxidants.

3. Conclusions

There is substantial evidence that environmental pollution increases oxidative stress and that dietary antioxidant supplementation and/or increased ingestion of fruit and vegetable may play a role in neutralising or buffering the effects of pollutants that display oxidising properties. In vitro and in vivo studies suggest that antioxidant nutrients and related bioactive compounds common in fruits and vegetables can protect against environmental toxic insults. It is important to emphasise that antioxidants as dietary supplements can provide protection against ROS-induced damage under conditions of elevated oxidative stress to the organism. It could be postulated that antioxidants would be therapeutically effective under circumstances of elevated oxidative stress or in aged mammals exposed to a stressor that generates exacerbated oxidative injury. Evidence is presented demonstrating that synthetic antioxidant supplements cannot provide appropriate or complete protection against oxidative stress and damage under “normal” conditions and that the administration of antioxidants to prevent disease or the aging process is controversial under conditions of “normal” oxidative stress. Many clinical trials in which individuals received one or more synthetic antioxidants failed to detect beneficial effects (reviewed in). Thus, the results of clinical trials of exogenous antioxidant intake are conflicting and contradictory. These findings indicate that other compounds in fruits and vegetables (possibly flavonoids) or a complex combination of compounds may contribute to the improvement in cardiovascular health and the decrease in cancer incidence detected among individuals who consume more of these foods.

It must be understood that the use of synthetic vitamin supplements is not an alternative to regular consumption of fruits and vegetables. Cutler explains that most humans maintain stable levels of oxidative stress, and no matter how much additional antioxidant that individuals consume in their diet, no further decrease in oxidative stress occurs. However, antioxidant supplements do appear to be effective in lowering an individual's oxidative stress if his/her initial oxidative stress level is above normal or above his/her stably regulated level. Thus, antioxidant supplements may only provide a benefit to an organism if it was necessary to correct a high level of oxidative stress that could not be controlled by endogenous antioxidants. All of this evidence indicates the need to determine an individual's oxidative stress level prior to the initiation of antioxidant supplement therapy. Both, the ROS/RNS formation and the antioxidative defense potential should be measured in a person in order to determine his/her oxidative stress status. Multiple methods of oxidative stress measurement are available today, each with their own advantages and disadvantages (reviewed in).

In the end it should be stressed that more research should be performed to strengthen the evidence for dietary supplements as modulators of the adverse effects caused by increased exposure to environmental pollution.

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    Not in our library10.1016/s0891-5849(01)00724-9

  10. 10.

    Forman HJ, Boveris A, Pryor E. Superoxide radical and hydrogen peroxide in mitochondria. Free Radicals in Biology. 1982;65-90.

    Not in our library

  11. 11.
    Superoxide accelerates DNA damage by elevating free-iron levels · 1996
    Not checked
  12. 12.

    Hutchinson F. Chemical changes induced in DNA by ionizing radiation. Progress in Nucleic Acid Research and Molecular Biology. 1985;32:115-154.

    Not in our library10.1016/s0079-6603(08)60347-5

  13. 13.

    Ames BN. Dietary carcinogens and anticarcinogens. Science. 1983;221(4617):1256-1263.

    Not in our library10.1126/science.6351251

  14. 14.

    Friedberg EC, McDaniel LD, Schultz RA. DNA Repair and Mutagenesis. 1995.

    Not in our library

  15. 15.

    Speakman JR, van Acker A, Herper EJ. Age-related changes in the metabolism and body composition of three dog breeds and their relationship to life expectancy. Aging Cell. 2003;2(5):265-275.

    Not in our library10.1046/j.1474-9728.2003.00061.x

  16. 16.

    Shackelford RE, Kaufmann WK, Paules RS. Cell cycle control, checkpoint mechanisms, and genotoxic stress. Environmental Health Perspectives. 1999;107(1):5-24.

    Not in our library10.1289/ehp.99107s15

  17. 17.

    Mudway IS, Housley D, Eccles R, et al. Differential depletion of human respiratory tract antioxidants in response to ozone challenge. Free Radical Research. 1996;25(6):499-513.

    Not in our library10.3109/10715769609149072

  18. 18.

    Pryor WA. How far does ozone penetrate into the pulmonary air/tissue boundary before it reacts? Free Radical Biology and Medicine. 1992;12(1):83-88.

    Not in our library10.1016/0891-5849(92)90060-t

  19. 19.

    Grievink L, Zijlstra AG, Ke X. Double-blind intervention trial on modulation of ozone effects on pulmonary function by antioxidant supplements. American Journal of Epidemiology. 1999;149(4):306-314.

    Not in our library10.1093/oxfordjournals.aje.a009814

  20. 20.

    Grievink L, Zijlstra AG, Ke X, Brunekreef B. Acute effects of ozone on pulmonary function in antioxidant supplemented cyclists. European Respiratory Journal. 1997;10(supplement 25, article 229S).

    Not in our library

  21. 21.

    Samet JM, Hatch GE, Horstman D, et al. Effect of antioxidant supplementation on ozone-induced lung injury in human subjects. American Journal of Respiratory and Critical Care Medicine. 2001;164(5):819-825.

    Not in our library10.1164/ajrccm.164.5.2008003

  22. 22.

    Menzel DB. The toxicity of air pollution in experimental animals and humans: the role of oxidative stress. Toxicology Letters. 1994;72(1–3):269-277.

    Not in our library10.1016/0378-4274(94)90038-8

  23. 23.

    Romieu I, Sienra-Monge JJ, Ramírez-Aguilar M, et al. Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants. The American Journal of Respiratory and Critical Care Medicine. 2002;166(5):703-709.

    Not in our library10.1164/rccm.2112074

  24. 24.

    Romieu I, Meneses F, Ramirez M, et al. Antioxidant supplementation and respiratory functions among workers exposed to high levels of ozone. American Journal of Respiratory and Critical Care Medicine. 1998;158(1):226-232.

    Not in our library10.1164/ajrccm.158.1.9712053

  25. 25.

    Grievink L, Smit HA, Brunekreef B. Anti-oxidants and air pollution in relation to indicators of asthma and COPD: a review of the current evidence. Clinical & Experimental Allergy. 2000;30(10):1344-1354.

    Not in our library10.1046/j.1365-2222.2000.00835.x

  26. 26.

    Ballinger CA, Cueto R, Squadrito G, et al. Antioxidant-mediated augmentation of ozone-induced membrane oxidation. Free Radical Biology and Medicine. 2005;38(4):515-526.

    Not in our library10.1016/j.freeradbiomed.2004.11.009

  27. 27.

    Meng Z, Qin G, Zhang B, et al. Oxidative damage of sulfur dioxide inhalation on lungs and hearts of mice. Environmental Research. 2003;93(3):285-292.

    Not in our library10.1016/s0013-9351(03)00045-8

  28. 28.

    Meng Z, Bai W. Oxidation damage of sulfur dioxide on testicles of mice. Environmental Research. 2004;96(3):298-304.

    Not in our library10.1016/j.envres.2004.04.008

  29. 29.

    Ergonul Z, Erdem A, Balkanci ZD, Kilinc K. Vitamin E protects against lipid peroxidation due to cold-SO2 coexposure in mouse lung. Inhalation Toxicology. 2007;19(2):161-168.

    Not in our library10.1080/08958370601051883

  30. 30.

    Etlik Ö, Tomur A, Tuncer M, Yalçin Ridvanağaoğlu A, Andaç O. Protective effect on antioxidant vitamins on red blood cell lipoperoxidation induced by SO2 inhalation. Journal of Basic and Clinical Physiology and Pharmacology. 1997;8(1-2):31-43.

    Not in our library10.1515/jbcpp.1997.8.1-2.31

  31. 31.

    Zhao JQ, Wen YF, Bhadauria M, et al. Protective effects of propolis on inorganic mercury induced oxidative stress in mice. Indian Journal of Experimental Biology. 2009;47(4):264-269.

    Not in our library

  32. 32.

    Etlik O, Tomur A, Kutman MN, Yorukan S, Duman O. The effects of sulfur dioxide inhalation and antioxidant vitamins on red blood cell lipoperoxidation. Environmental Research. 1995;71(1):25-28.

    Not in our library10.1006/enrs.1995.1063

  33. 33.

    Zhao H, Xu X, Na J, et al. Protective effects of salicylic acid and vitamin C on sulfur dioxide-induced lipid peroxidation in mice. Inhalation Toxicology. 2008;20(9):865-871.

    Not in our library10.1080/08958370701861512

  34. 34.

    Wu D, Meng Z. Effect of sulfur dioxide inhalation on the glutathione redox system in mice and protective role of sea buckthorn seed oil. Archives of Environmental Contamination and Toxicology. 2003;45(3):423-428.

    Not in our library10.1007/s00244-003-2157-z

  35. 35.

    Langley-Evans SC, Phillips GJ, Jackson AA. Sulphur dioxide: a potent glutathione depleting agent. Comparative Biochemistry and Physiology C: Pharmacology Toxicology and Endocrinology. 1996;114(2):89-98.

    Not in our library10.1016/0742-8413(96)00012-6

  36. 36.

    Midgette AS, Baron JA, Rohan TE. Do cigarette smokers have diets that increase their risks of coronary heart disease and cancer? American Journal of Epidemiology. 1993;137(5):521-529.

    Not in our library10.1093/oxfordjournals.aje.a116705

  37. 37.

    Banerjee KK, Marimuthu P, Sarkar A, Chaudhuri RN. Influence of cigarette smoking on Vitamin C, glutathione and lipid peroxidation status. Indian Journal of Public Health. 1998;42(1):20-23.

    Not in our library

  38. 38.

    Bloomer RJ. Decreased blood antioxidant capacity and increased lipid peroxidation in young cigarette smokers compared to nonsmokers: impact of dietary intake. Nutrition Journal. 2007;6, article 39.

    Not in our library10.1186/1475-2891-6-39

  39. 39.

    Aycicek A, Erel O, Kocyigit A. Decreased total antioxidant capacity and increased oxidative stress in passive smoker infants and their mothers. Pediatrics International. 2005;47(6):635-639.

    Not in our library10.1111/j.1442-200x.2005.02137.x

  40. 40.

    Tsuchiya M, Asada A, Kasahara E, Sato EF, Shindo M, Inoue M. Smoking a single cigarette rapidly reduces combined concentrations of nitrate and nitrite and concentrations of antioxidants in plasma. Circulation. 2002;105(10):1155-1157.

    Not in our library10.1161/hc1002.105935

  41. 41.

    Zhou JF, Yan XF, Guo FZ, Sun NY, Qian ZJ, Ding DY. Effects of cigarette smoking and smoking cessation on plasma constituents and enzyme activities related to oxidative stress. Biomedical and Environmental Sciences. 2000;13(1):44-55.

    Not in our library

  42. 42.
    Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C · 2008
    Not checked
  43. 43.

    Mayne ST, Cartmel B. Antioxidant vitamin supplementation and lipid peroxidation in smokers. American Journal of Clinical Nutrition. 1999;69(6).

    Not in our library10.1093/ajcn/69.6.1292

  44. 44.

    Chung FL, Morse MA, Eklind KI, Xu Y, Rylander R, Krinsky N. Inhibition of the tobacco-specific nitrosamine-induced lung tumorigenesis by compounds derived from cruciferous vegetables and green tea. Annals of the New York Academy of Sciences. 1993;686:186-201.

    Not in our library10.1111/j.1749-6632.1993.tb39174.x

  45. 45.

    Xu Y, Ho CT, Amin SG, Han C, Chung FL. Inhibition of tobacco-specific nitrosamine-induced lung tumorigenesis in A/J mice by green tea and its major polyphenol as antioxidants. Cancer Research. 1992;52(14):3875-3879.

    Not in our library

  46. 46.

    Jha JC, Maharjan BR, Adhikari D, et al. Cigarette smoke induced oxidative insult in local population of Pokhara. Kathmandu University Medical Journal. 2007;5(4):511-517.

    Not in our library

  47. 47.

    Chung FL. The prevention of lung cancer induced by a tobacco-specific carcinogen in rodents by green and black tea. Proceedings of the Society for Experimental Biology and Medicine. 1999;220(4):244-248.

    Not in our library10.1046/j.1525-1373.1999.d01-42.x

  48. 48.

    Zhou J, Guo F, Qian Z. Effects of cigarette smoking on antioxidant vitamin and activities of antioxidases. Zhonghua Yu Fang Yi Xue Za Zhi. 1997;31(2):67-70.

    Not in our library

  49. 49.

    Dietrich M, Block G, Norkus EP, et al. Smoking and exposure to environmental tobacco smoke decrease some plasma antioxidants and increase γ-tocopherol in vivo after adjustment for dietary antioxidant intakes. American Journal of Clinical Nutrition. 2003;77(1):160-166.

    Not in our library10.1093/ajcn/77.1.160

  50. 50.

    Chávez J, Cano C, Souki A, et al. Effect of cigarette smoking on the oxidant/antioxidant balance in healthy subjects. The American Journal of Therapeutics. 2007;14(2):189-193.

    Not in our library10.1097/01.psp.0000249918.19016.f6

  51. 51.

    Polidori MC, Mecocci P, Stahl W, Sies H. Cigarette smoking cessation increases plasma levels of several antioxidant micronutrients and improves resistance towards oxidative challenge. British Journal of Nutrition. 2003;90(1):147-150.

    Not in our library10.1079/bjn2003890

  52. 52.

    Pryor WA, Church DF. Aldehydes, hydrogen peroxide, and organic radicals as mediators of ozone toxicity. Free Radical Biology and Medicine. 1991;11(1):41-46.

    Not in our library10.1016/0891-5849(91)90186-7

  53. 53.

    Last JA, Sun WM, Witschi H. Ozone, NO, and NO2: oxidant air pollutants and more. Environmental Health Perspectives. 1994;102, supplement 10:179-184.

    Not in our library10.1289/ehp.94102s10179

  54. 54.

    Kienast K, Knorst M, Lubjuhn S, Muller-Quernheim J, Ferlinz R. Nitrogen dioxide-induced reactive oxygen intermediates production by human alveolar macrophages and peripheral blood mononuclear cells. Archives of Environmental Health. 1994;49(4):246-250.

    Not in our library10.1080/00039896.1994.9937474

  55. 55.

    Guth DJ, Mavis RD. The effect of lung α-tocopherol content on the acute toxicity of nitrogen dioxide. Toxicology and Applied Pharmacology. 1986;84(2):304-314.

    Not in our library10.1016/0041-008x(86)90138-9

  56. 56.

    Sevanian A, Elsayed N, Hacker AD. Effects of vitamin E deficiency and nitrogen dioxide exposure on lung lipid peroxidation: use of lipid epoxides and malonaldehyde as measures of peroxidation. Journal of Toxicology and Environmental Health. 1982;10(4-5):743-756.

    Not in our library10.1080/15287398209530292

  57. 57.

    Kelly FJ, Tetley TD. Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid. Biochemical Journal. 1997;325(part 1):95-99.

    Not in our library10.1042/bj3250095

  58. 58.

    Kelly FJ, Blomberg A, Frew A, Holgate ST, Sandstrom T. Antioxidant kinetics in lung lavage fluid following exposure of humans to nitrogen dioxide. American Journal of Respiratory and Critical Care Medicine. 1996;154(6, part 1):1700-1705.

    Not in our library10.1164/ajrccm.154.6.8970358

  59. 59.

    Rietjens IMCM, Poelen MCM, Hempenius RA, Gijbels MJ, Alink GM. Toxicity of ozone and nitrogen dioxide to alveolar macrophages: comparative study revealing differences in their mechanism of toxic action. Journal of Toxicology and Environmental Health. 1986;19(4):555-568.

    Not in our library10.1080/15287398609530952

  60. 60.

    Mohsenin V. Effect of vitamin C on NO2-induced airway hyperresponsiveness in normal subjects: a randomized double-blind experiment. American Review of Respiratory Disease. 1987;136(6):1408-1411.

    Not in our library10.1164/ajrccm/136.6.1408

  61. 61.

    Khopde SM, Priyadarsini KI, Mukherjee T, Kulkarni PB, Satav JG, Bhattacharya RK. Does β-carotene protect membrane lipids from nitrogen dioxide? Free Radical Biology and Medicine. 1998;25(1):66-71.

    Not in our library10.1016/s0891-5849(98)00046-x

  62. 62.

    Böhm F, Edge R, Burke M, Truscott TG. Dietary uptake of lycopene protects human cells from singlet oxygen and nitrogen dioxide—ROS components from cigarette smoke. Journal of Photochemistry and Photobiology B: Biology. 2001;64(2-3):176-178.

    Not in our library10.1016/s1011-1344(01)00221-4

  63. 63.

    González-Flecha B. Oxidant mechanisms in response to ambient air particles. Molecular Aspects of Medicine. 2004;25((1-2)):169-182.

    Not in our library10.1016/j.mam.2004.02.017

  64. 64.

    Pinho RA, Silveira PCL, Silva LA, Luiz Streck E, Dal-Pizzol F, F. Moreira JC. N-Acetylcysteine and deferoxamine reduce pulmonary oxidative stress and inflammation in rats after coal dust exposure. Environmental Research. 2005;99(3):355-360.

    Not in our library10.1016/j.envres.2005.03.005

  65. 65.

    Aganasur K, Jeff Inmon P, Dailey LA, Madden MC, Ghio AJ, Gallagher JE. Air pollution particles mediated oxidative DNA base damage in a cell free system and in human airway epithelial cells in relation to particulate metal content and bioreactivity. Chemical Research in Toxicology. 2001;14:879-887.

    Not in our library10.1021/tx010022e

  66. 66.

    Hatzis C, Godleski JJ, González-Flecha B, Wolfson JM, Koutrakis P. Ambient particulate matter exhibits direct inhibitory effects on oxidative stress enzymes. Environmental Science and Technology. 2006;40(8):2805-2811.

    Not in our library10.1021/es0518732

  67. 67.

    Possamai FP, Júnior SÁ, Parisotto EB, et al. Antioxidant intervention compensates oxidative stress in blood of subjects exposed to emissions from a coal electric-power plant in South Brazil. Environmental Toxicology and Pharmacology. 2010;30(2):175-180.

    Not in our library10.1016/j.etap.2010.05.006

  68. 68.

    Kamp DW, Graceffa P, Pryor WA, Weitzman SA. The role of free radicals in asbestos-induced diseases. Free Radical Biology and Medicine. 1992;12(4):293-315.

    Not in our library10.1016/0891-5849(92)90117-y

  69. 69.

    Walker C, Everitt J, Barrett JC. Possible cellular and molecular mechanisms for asbestos carcinogenicity. The American Journal of Industrial Medicine. 1992;21(2):253-273.

    Not in our library10.1002/ajim.4700210214

  70. 70.

    Luo SQ, Liu XZ, Wang CJ. Inhibitory effect of green tea extract on the carcinogenesis induced by asbestos plus benzo(a)pyrene in rat. Biomedical and Environmental Sciences. 1995;8(1):54-58.

    Not in our library

  71. 71.

    Lewczuk E, Owczarek H. The role of oxygen free radicals in asbestos cytotoxicity. Medycyna pracy. 1992;43(4):335-342.

    Not in our library

  72. 72.

    Fattman CL, Tan RJ, Tobolewski JM, Oury TD. Increased sensitivity to asbestos-induced lung injury in mice lacking extracellular superoxide dismutase. Free Radical Biology and Medicine. 2006;40(4):601-607.

    Not in our library10.1016/j.freeradbiomed.2005.09.030

  73. 73.

    Hei TK, Xu A, Huang SX, Zhao Y. Mechanism of fiber carcinogenesis: from reactive radical species to silencing of the βigH3 gene. Inhalation Toxicology. 2006;18(12):985-990.

    Not in our library10.1080/08958370600835310

  74. 74.

    Pelclová D, Fenclová Z, Kacer P, Kuzma M, Navrátil T, Lebedová J. Increased 8-isoprostane, a marker of oxidative stress in exhaled breath condensate in subjects with asbestos exposure. Industrial Health. 2008;46(5):484-489.

    Not in our library10.2486/indhealth.46.484

  75. 75.

    Marczynski B, Rozynek P, Kraus T, Schlösser S, Raithel HJ, Baur X. Levels of 8-hydroxy-2'-deoxyguanosine in DNA of white blood cells from workers highly exposed to asbestos in Germany. Mutation Research: Genetic Toxicology and Environmental Mutagenesis. 2000;468(2):195-202.

    Not in our library10.1016/s1383-5718(00)00053-x

  76. 76.

    Thannickal VJ, Fanburg BL. Reactive oxygen species in cell signaling. American Journal of Physiology: Lung Cellular and Molecular Physiology. 2000;279(6):L1005-L1028.

    Not in our library10.1152/ajplung.2000.279.6.l1005

  77. 77.

    Ames BN. Delaying the mitochondrial decay of aging. Annals of the New York Academy of Sciences. 2004;1019:406-411.

    Not in our library10.1196/annals.1297.073

  78. 78.

    Radi R, Peluffo G, Alvarez MN, Naviliat M, Cayota A. Unraveling peroxynitrite formation in biological systems. Free Radical Biology and Medicine. 2001;30(5):463-488.

    Not in our library10.1016/s0891-5849(00)00373-7

  79. 79.

    Willett WC. The Mediterranean diet: science and practice. Public Health Nutrition. 2006;9(1):105-110.

    Not in our library10.1079/phn2005931

  80. 80.

    Sevanian A, Hacker AD, Elsayed N. Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes. Lipids. 1982;17(4):269-277.

    Not in our library10.1007/bf02534941

  81. 81.

    Hatch GE. Asthma, inhaled oxidants, and dietary antioxidants. American Journal of Clinical Nutrition. 1995;61(supplement 3):625S-630S.

    Not in our library10.1093/ajcn/61.3.625s

  82. 82.

    Risom L, Møller P, Loft S. Oxidative stress-induced DNA damage by particulate air pollution. Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis. 2005;592(1-2):119-137.

    Not in our library10.1016/j.mrfmmm.2005.06.012

  83. 83.

    Greenwell LL, Moreno T, Richards RJ. Pulmonary antioxidants exert differential protective effects against urban and industrial particulate matter. Journal of Biosciences. 2003;28(1):101-107.

    Not in our library10.1007/bf02970139

  84. 84.

    Sperati A, Abeni DD, Tagesson C, Forastiere F, Miceli M, Axelson O. Exposure to indoor background radiation and urinary concentrations of 8-hydroxydeoxyguanosine, a marker of oxidative DNA damage. Environmental Health Perspectives. 1999;107(3):213-215.

    Not in our library10.1289/ehp.99107213

  85. 85.

    Tak JK, Park JW. The use of ebselen for radioprotection in cultured cells and mice. Free Radical Biology and Medicine. 2009;46(8):1177-1185.

    Not in our library10.1016/j.freeradbiomed.2009.01.023

  86. 86.

    Kilciksiz S, Demirel C, Ayhan SE, et al. N-acetylcysteine ameliorates nitrosative stress on radiation-inducible damage in rat liver. Journal of B.U.ON. 2011;16(1):154-159.

    Not in our library

  87. 87.

    Kilciksiz S, Demirel C, Erdal N, et al. The effect of N-acetylcysteine on biomarkers for radiation-induced oxidative damage in a rat model. Acta Medica Okayama. 2008;62(6):403-409.

    Not in our library10.18926/amo/30946

  88. 88.

    Benković V, Knezević AH, Dikić D, et al. Radioprotective effects of quercetin and ethanolic extract of propolis in gamma-irradiated mice. Archives of Industrial Hygiene and Toxicology. 2009;60(2):129-138.

    Not in our library10.2478/10004-1254-60-2009-1908

  89. 89.

    Jagetia GC. Radioprotection and radiosensitization by curcumin. Advances in Experimental Medicine and Biology. 2007;595:301-320.

    Not in our library10.1007/978-0-387-46401-5_13

  90. 90.

    Kovacic P, Somanathan R. Electromagnetic fields: mechanism, cell signaling, other bioprocesses, toxicity, radicals, antioxidants and beneficial effects. Journal of Receptors and Signal Transduction. 2010;30(4):214-226.

    Not in our library10.3109/10799893.2010.488650

  91. 91.

    Simkó M, Mattsson M. Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: possible immune cell activation. Journal of Cellular Biochemistry. 2004;93(1):83-92.

    Not in our library10.1002/jcb.20198

  92. 92.

    Musaev AV, Ismailova LF, Shabanova AB, Magerramov AA, Iusifov EI, Gadzhiev AM. Pro- and antioxidant effect of electromagnetic fields of extremely high frequency (460 MHz) on brain tissues in experiment. Voprosy Kurortologii, Fizioterapii, i Lechebnoi Fizicheskoi Kultury. 2004;(2):19-23.

    Not in our library

  93. 93.

    Ozguner F, Bardak Y, Comlekci S. Protective effects of melatonin and caffeic acid phenethyl ester against retinal oxidative stress in long-term use of mobile phone: a comparative study. Molecular and Cellular Biochemistry. 2006;282(1-2):83-88.

    Not in our library10.1007/s11010-006-1267-0

  94. 94.

    Jajte J, Zmyślony M, Palus J, Dziubaltowska E, Rajkowska E. Protective effect of melatonin against in vitro iron ions and 7 mT 50 Hz magnetic field-induced DNA damage in rat lymphocytes. Mutation Research. 2001;483((1-2)):57-64.

    Not in our library10.1016/s0027-5107(01)00230-5

  95. 95.

    Ilhan A, Gurel A, Armutcu F, et al. Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain. Clinica Chimica Acta. 2004;340(1-2):153-162.

    Not in our library10.1016/j.cccn.2003.10.012

  96. 96.

    Guney M, Ozguner F, Oral B, Karahan N, Mungan T. 900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat endometrium: protection by vitamins E and C. Toxicology and Industrial Health. 2007;23(7):411-420.

    Not in our library10.1177/0748233707080906

  97. 97.

    Wambi CO, Sanzari JK, Sayers CM, et al. Protective effects of dietary antioxidants on proton total-body irradiation-mediated hematopoietic cell and animal survival. Radiation Research. 2009;172(2):175-186.

    Not in our library10.1667/rr1708.1

  98. 98.

    Andrade ER, Cruz IBM, Andrade VVR, et al. Evaluation of the potential protective effects of ad libitum black grape juice against liver oxidative damage in whole-body acute X-irradiated rats. Food and Chemical Toxicology. 2011;49(4):1026-1032.

    Not in our library10.1016/j.fct.2011.01.011

  99. 99.

    Nair GG, Nair CKK. Protection of cellular DNA and membrane from γ-radiation-induced damages and enhancement in DNA repair by sesamol. Cancer Biotherapy and Radiopharmaceuticals. 2010;25(6):629-635.

    Not in our library10.1089/cbr.2010.0803

  100. 100.

    El-Missiry MA, Fayed TA, El-Sawy MR, El-Sayed AA. Ameliorative effect of melatonin against gamma-irradiation-induced oxidative stress and tissue injury. Ecotoxicology and Environmental Safety. 2007;66(2):278-286.

    Not in our library10.1016/j.ecoenv.2006.03.008

  101. 101.

    Karbownik M, Reiter RJ. Antioxidative effects of melatonin in protection against cellular damage caused by ionizing radiation. Experimental Biology and Medicine. 2000;225(1):9-22.

    Not in our library10.1177/153537020022500102

  102. 102.

    Nair CKK, Devi PU, Shimanskaya R, et al. Water soluble vitamin E (TMG) as a radioprotector. Indian Journal of Experimental Biology. 2003;41(12):1365-1371.

    Not in our library

  103. 103.

    Noaman E, Zahran AM, Kamal AM, Omran MF. Vitamin E and selenium administration as a modulator of antioxidant defense system: biochemical assessment and modification. Biological Trace Element Research. 2002;86(1):55-64.

    Not in our library10.1385/bter:86:1:55

  104. 104.

    Berbée M, Fu Q, Boerma M, Wang J, Kumar KS, Hauer-Jensen M. γ-Tocotrienol ameliorates intestinal radiation injury and reduces vascular oxidative stress after total-body irradiation by an HMG-CoA Reductase-dependent mechanism. Radiation Research. 2009;171(5):596-605.

    Not in our library10.1667/rr1632.1

  105. 105.

    Srinivasan M, Devipriya N, Kalpana KB, Menon VP. Lycopene: an antioxidant and radioprotector against γ-radiation-induced cellular damages in cultured human lymphocytes. Toxicology. 2009;262(1):43-49.

    Not in our library10.1016/j.tox.2009.05.004

  106. 106.

    Hu Y, Guo D, Liu P, et al. Bioactive components from the tea polyphenols influence on endogenous antioxidant defense system and modulate inflammatory cytokines after total-body irradiation in mice. Phytomedicine. 2011;18(11):970-975.

    Not in our library10.1016/j.phymed.2011.02.012

  107. 107.

    Wolf FI, Fasanella S, Tedesco B, et al. Peripheral lymphocyte 8-OHdG levels correlate with age-associated increase of tissue oxidative DNA damage in Sprague-Dawley rats. Protective effects of caloric restriction. Experimental Gerontology. 2005;40(3):181-188.

    Not in our library10.1016/j.exger.2004.11.002

  108. 108.

    Güler G, Turkozer Z, Tomruk A, Seyhan N. The protective effects of N-acetyl-L-cysteine and Epigallocatechin-3- gallate on electric field-induced hepatic oxidative stress. International Journal of Radiation Biology. 2008;84(8):669-680.

    Not in our library10.1080/09553000802241747

  109. 109.

    Ozgur E, Güler G, Seyhan N. Mobile phone radiation-induced free radical damage in the liver is inhibited by the antioxidants N-acetyl cysteine and epigallocatechin-gallate. International Journal of Radiation Biology. 2010;86(11):935-945.

    Not in our library10.3109/09553002.2010.496029

  110. 110.

    Simkó M. Cell type specific redox status is responsible for diverse electromagnetic field effects. Current Medicinal Chemistry. 2007;14(10):1141-1152.

    Not in our library10.2174/092986707780362835

  111. 111.

    Reiter RJ. Melatonin suppression by static and extremely low frequency electromagnetic fields: relationship to the reported increased incidence of cancer. Reviews on Environmental Health. 1994;10(3-4):171-186.

    Not in our library10.1515/reveh.1994.10.3-4.171

  112. 112.

    Naziroğlu M, Gümral N. Modulator effects of L-carnitine and selenium on wireless devices (2.45 GHz)-induced oxidative stress and electroencephalography records in brain of rat. International Journal of Radiation Biology. 2009;85(8):680-689.

    Not in our library10.1080/09553000903009530

  113. 113.

    Peak JG, Peak MJ, Sikorski RA, Jones RA. Induction of DNA-protein cross-links in human cells by ultraviolet and visible radiations: action spectrum. Photochemistry and Photobiology. 1988;41(3):295-302.

    Not in our library10.1111/j.1751-1097.1985.tb03488.x

  114. 114.

    Beehler BC, Przybyszewski J, Box HB, Kulesz-Martin MF. Formation of 8-hydroxydeoxyguanosine within DNA of mouse keratinocytes exposed in culture to UVB and H2O2. Carcinogenesis. 1992;13(11):2003-2007.

    Not in our library10.1093/carcin/13.11.2003

  115. 115.

    Berton TR, Mitchell DL, Fischer SM, Locniskar MF. Epidermal proliferation but not the quantity of DNA photodamage is correlated with UV-induced mouse skin carcinogenesis. Journal of Investigative Dermatology. 1997;109(3):340-347.

    Not in our library10.1111/1523-1747.ep12335984

  116. 116.

    Li G, Mitchell DL, Ho VC, Reed JC, Tron VA. Decreased DNA repair but normal apoptosis in ultraviolet-irradiated skin of p53-transgenic mice. American Journal of Pathology. 1996;148(4):1113-1123.

    Not in our library

  117. 117.

    Masaki H. Role of antioxidants in the skin: anti-aging effects. Journal of Dermatological Science. 2010;58(2):85-90.

    Not in our library10.1016/j.jdermsci.2010.03.003

  118. 118.

    McArdle F, Rhodes LE, Parslew R, Jack CIA, Friedmann PS, Jackson MJ. UVR-induced oxidative stress in human skin in vivo: effects of oral vitamin C supplementation. Free Radical Biology and Medicine. 2002;33(10):1355-1362.

    Not in our library10.1016/s0891-5849(02)01042-0

  119. 119.

    Humbert PG, Haftek M, Creidi P, et al. Topical ascorbic acid on photoaged skin. Clinical, topographical and ultrastructural evaluation: double-blind study vs. placebo. Experimental Dermatology. 2003;12(3):237-244.

    Not in our library10.1034/j.1600-0625.2003.00008.x

  120. 120.

    Ritter EF, Axelrod M, Minn KW, et al. Modulation of ultraviolet light-induced epidermal damage: beneficial effects of tocopherol. Plastic and Reconstructive Surgery. 1997;100(4):973-980.

    Not in our library10.1097/00006534-199709001-00021

  121. 121.

    Packer L, Weber SU, Rimbach G. Molecular aspects of α-tocotrienol antioxidant action and cell signalling. Journal of Nutrition. 2001;131(2):369S-373S.

    Not in our library10.1093/jn/131.2.369s

  122. 122.

    Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. American Journal of Clinical Nutrition. 2000;71(3):795-798.

    Not in our library10.1093/ajcn/71.3.795

  123. 123.

    Kligman LH, Kligman AM. The nature of photoaging: its prevention and repair. Photodermatology. 1986;3(4):215-227.

    Not in our library

  124. 124.

    Stahl W, Mukhtar H, Afaq F, Sies H, Gilchrest B, Krutmann J. Vitamins and polyphenols XE polyphenols in systemic photoprotection. Skin Aging. 2006.

    Not in our library

  125. 125.

    Sies H, Stahl W. Carotenoids and UV protection. Photochemical and Photobiological Sciences. 2004;3(8):749-752.

    Not in our library10.1039/b316082c

  126. 126.

    Cho S, Lee DH, Won CH, et al. Differential effects of low-dose and high-dose beta-carotene supplementation on the signs of photoaging and type I procollagen gene expression in human skin in vivo. Dermatology. 2010;221(2):160-171.

    Not in our library10.1159/000305548

  127. 127.

    Shindo Y, Witt E, Packer L. Antioxidant defense mechanisms in murine epidermis and dermis and their responses to ultraviolet light. Journal of Investigative Dermatology. 1993;100(3):260-265.

    Not in our library10.1111/1523-1747.ep12469048

  128. 128.

    Packer L, Valacchi G. Antioxidants and the response of skin to oxidative stress: vitamin E as a key indicator. Skin Pharmacology and Applied Skin Physiology. 2002;15(5):282-290.

    Not in our library10.1159/000064531

  129. 129.

    Thiele JJ. Oxidative targets in the stratum corneum: a new basis for antioxidative strategies. Skin Pharmacology and Applied Skin Physiology. 2001;14(1):87-91.

    Not in our library10.1159/000056395

  130. 130.

    Ribaya-Mercado JD, Garmyn M, Gilchrest BA, Russell RM. Skin lycopene is destroyed preferentially over β-carotene during ultraviolet irradiation in humans. Journal of Nutrition. 1995;125(7):1854-1859.

    Not in our library10.1093/jn/125.7.1854

  131. 131.

    Heinrich U, Gärtner C, Wiebusch M, et al. Supplementation with β-carotene or a similar amount of mixed carotenoids protects humans from UV-induced erythema. Journal of Nutrition. 2003;133(1):98-101.

    Not in our library10.1093/jn/133.1.98

  132. 132.

    Lee J, Jiang S, Levine N, Watson RR. Carotenoid supplementation reduces erythema in human skin after simulated solar radiation exposure. Proceedings of the Society for Experimental Biology and Medicine. 2000;223(2):170-174.

    Not in our library10.1046/j.1525-1373.2000.22323.x

  133. 133.

    Stahl W, Junghans A, de Boer B, Driomina ES, Briviba K, Sies H. Carotenoid mixtures protect multilamellar liposomes against oxidative damage: synergistic effects of lycopene and lutein. FEBS Letters. 1998;427(2):305-308.

    Not in our library10.1016/s0014-5793(98)00434-7

  134. 134.

    Aust O, Stahl W, Sies H, Tronnier H, Heinrich U. Supplementation with tomato-based products increases lycopene, phytofluene, and phytoene levels in human serum and protects against UV-light-induced erythema. International Journal for Vitamin and Nutrition Research. 2005;75(1):54-60.

    Not in our library10.1024/0300-9831.75.1.54

  135. 135.

    Yeh SL, Huang CS, Hu ML. Lycopene enhances UVA-induced DNA damage and expression of heme oxygenase-1 in cultured mouse embryo fibroblasts. European Journal of Nutrition. 2005;44(6):365-370.

    Not in our library10.1007/s00394-004-0536-5

  136. 136.

    Afaq F, Mukhtar H. Photochemoprevention by botanical antioxidants. Skin Pharmacology and Physiology. 2002;15:297-306.

    Not in our library10.1159/000064533

  137. 137.

    Katiyar SK, Ahmad N, Mukhtar H. Green tea and skin. Archives of Dermatology. 2000;136(8):989-994.

    Not in our library10.1001/archderm.136.8.989

  138. 138.

    Katiyar SK. Skin photoprotection by green tea: antioxidant and immunomodulatory effects. Current Drug Targets: Immune, Endocrine and Metabolic Disorders. 2003;3(3):234-242.

    Not in our library10.2174/1568008033340171

  139. 139.

    Katiyar SK, Vaid M, van Steeg H, Meeran SM. Green tea polyphenols prevent uv-induced immunosuppression by rapid repair of DNA damage and enhancement of nucleotide excision repair genes. Cancer Prevention Research. 2010;3(2):179-189.

    Not in our library10.1158/1940-6207.capr-09-0044

  140. 140.

    Lu YP, Lou YR, Peng QY, Xie JG, Nghiem P, Conney AH. Effect of caffeine on the ATR/Chk1 pathway in the epidermis of UVB-irradiated mice. Cancer Research. 2008;68(7):2523-2529.

    Not in our library10.1158/0008-5472.can-07-5955

  141. 141.

    Singh RP, Agarwal R. Flavonoid antioxidant silymarin and skin cancer. Antioxidants and Redox Signaling. 2002;4(4):655-663.

    Not in our library10.1089/15230860260220166

  142. 142.

    Bonina F, Lanza M, Montenegro L, et al. Flavonoids as potential protective agents against photo-oxidative skin damage. International Journal of Pharmaceutics. 1996;145(1-2):87-94.

    Not in our library

  143. 143.

    Wei H, Bowen R, Cai Q, Barnes S, Wang Y. Antioxidant and antipromotional effects of the soybean isoflavone genistein. Proceedings of the Society for Experimental Biology and Medicine. 1995;208(1):124-130.

    Not in our library10.3181/00379727-208-43844

  144. 144.

    Saliou C, Rimbach G, Moini H, et al. Solar ultraviolet-induced erythema in human skin and nuclear factor-kappa-B-dependent gene expression in keratinocytes are modulated by a French maritime pine bark extract. Free Radical Biology and Medicine. 2001;30(2):154-160.

    Not in our library10.1016/s0891-5849(00)00445-7

  145. 145.

    Bagchi D, Bagchi M, Hassoun EA, Stohs SJ. In vitro and in vivo generation of reactive oxygen species, DNA damage and lactate dehydrogenase leakage by selected pesticides. Toxicology. 1995;104(1–3):129-140.

    Not in our library10.1016/0300-483x(95)03156-a

  146. 146.

    de Liz Oliveira Cavalli VL, Cattani D, Heinz Rieg CE, et al. Roundup disrupts male reproductive functions by triggering calcium-mediated cell death in rat testis and Sertoli cells. Free Radical Biology and Medicine. 2013;65:335-346.

    Not in our library10.1016/j.freeradbiomed.2013.06.043

  147. 147.

    Olgun S, Misra HP. Pesticides induced oxidative stress in thymocytes. Molecular and Cellular Biochemistry. 2006;290(1-2):137-144.

    Not in our library10.1007/s11010-006-9178-7

  148. 148.

    Hassoun E, Bagchi M, Bagchi D, Stohs SJ. Comparative studies on lipid peroxidation and DNA-single strand breaks induced by lindane, DDT, chlordane and endrin in rats. Comparative Biochemistry and Physiology C. 1993;104(3):427-431.

    Not in our library10.1016/0742-8413(93)90013-b

  149. 149.

    Bus JS, Aust SD, Gibson JE. Paraquat toxicity: proposed mechanism of action involving lipid peroxidation. Environmental Health Perspectives. 1976;16:139-146.

    Not in our library10.1289/ehp.7616139

  150. 150.

    Pérez-Maldonado IN, Herrera C, Batres LE, González-Amaro R, Díaz-Barriga F, Yáñez L. DDT-induced oxidative damage in human blood mononuclear cells. Environmental Research. 2005;98(2):177-184.

    Not in our library10.1016/j.envres.2004.11.001

  151. 151.

    Senft AP, Dalton TP, Nebert DW, Genter MB, Hutchinson RJ, Shertzer HG. Dioxin increases reactive oxygen production in mouse liver mitochondria. Toxicology and Applied Pharmacology. 2002;178(1):15-21.

    Not in our library10.1006/taap.2001.9314

  152. 152.

    Ciftci O, Tanyildizi S, Godekmerdan A. Protective effect of curcumin on immune system and body weight gain on rats intoxicated with 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). Immunopharmacology and Immunotoxicology. 2010;32(1):99-104.

    Not in our library10.3109/08923970903164318

  153. 153.

    Hung Y, Huang GS, Sava VM, Blagodarsky VA, Hong M. Protective effects of tea melanin against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxicity: antioxidant activity and aryl hydrocarbon receptor suppressive effect. Biological and Pharmaceutical Bulletin. 2006;29(11):2284-2291.

    Not in our library10.1248/bpb.29.2284

  154. 154.

    Gultekin F, Delibas N, Yasar S, Kilinc I. In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats. Archives of Toxicology. 2001;75(2):88-96.

    Not in our library10.1007/s002040100219

  155. 155.

    Zhu Y, Kalen AL, Li L, et al. Polychlorinated-biphenyl-induced oxidative stress and cytotoxicity can be mitigated by antioxidants after exposure. Free Radical Biology and Medicine. 2009;47(12):1762-1771.

    Not in our library10.1016/j.freeradbiomed.2009.09.024

  156. 156.

    Ramadass P, Meerarani P, Toborek M, Robertson LW, Hennig B. Dietary flavonoids modulate PCB-induced oxidative stress, CYP1A1 induction, and AhR-DNA binding activity in vascular endothelial cells. Toxicological Sciences. 2003;76(1):212-219.

    Not in our library10.1093/toxsci/kfg227

  157. 157.

    Park S, Jang J, Chen C, Na H, Surh Y. A formulated red ginseng extract rescues PC12 cells from PCB-induced oxidative cell death through Nrf2-mediated upregulation of heme oxygenase-1 and glutamate cysteine ligase. Toxicology. 2010;278(1):131-139.

    Not in our library10.1016/j.tox.2010.04.003

  158. 158.

    Sridevi N, Venkataraman P, Senthilkumar K, Krishnamoorthy G, Arunakaran J. Oxidative stress modulates membrane bound ATPases in brain regions of PCB (Aroclor 1254) exposed rats: protective role of α-tocopherol. Biomedicine and Pharmacotherapy. 2007;61(7):435-440.

    Not in our library10.1016/j.biopha.2007.03.003

  159. 159.

    Murugesan P, Muthusamy T, Balasubramanian K, Arunakaran J. Studies on the protective role of vitamin C and E against polychlorinated biphenyl (Aroclor 1254)—induced oxidative damage in Leydig cells. Free Radical Research. 2005;39(11):1259-1272.

    Not in our library10.1080/10715760500308154

  160. 160.

    Ciftci O, Ozdemir I, Tanyildizi S, Yildiz S, Oguzturk H. Antioxidative effects of curcumin, β-myrcene and 1,8-cineole against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in rats liver. Toxicology and Industrial Health. 2011;27(5):447-453.

    Not in our library10.1177/0748233710388452

  161. 161.

    Karatas F, Servi S, Kara H, Kiran TR, Saydam S. Investigation of oxidative status of the 2-furan-2-yl-1H-benzimidazole in rats. Biological Trace Element Research. 2008;126(1–3):214-221.

    Not in our library10.1007/s12011-008-8202-z

  162. 162.

    Ishida T, Takeda T, Koga T, et al. Attenuation of 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity by resveratrol: a comparative study with different routes of administration. Biological and Pharmaceutical Bulletin. 2009;32(5):876-881.

    Not in our library10.1248/bpb.32.876

  163. 163.

    Türkez H, Geyikoğlu F, Yousef MI, Toğar B, Vançelik S. Propolis alleviates 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced histological changes, oxidative stress and DNA damage in rat liver. Toxicology and Industrial Health. 2012;29(8):677-685.

    Not in our library10.1177/0748233712440139

  164. 164.

    Song NH, Yin XL, Chen GF, Yang H. Biological responses of wheat (Triticum aestivum) plants to the herbicide chlorotoluron in soils. Chemosphere. 2007;68(9):1779-1787.

    Not in our library10.1016/j.chemosphere.2007.03.023

  165. 165.

    Bagchi D, Bhattacharya G, Stohs SJ. In vitro and in vivo induction of heat shock (stress) protein (Hsp) gene expression by selected pesticides. Toxicology. 1996;112(1):57-68.

    Not in our library10.1016/0300-483x(96)03350-1

  166. 166.

    Kisby GE, Muniz JF, Scherer J, et al. Oxidative stress and DNA damage in agricultural workers. Journal of Agromedicine. 2009;14(2):206-214.

    Not in our library10.1080/10599240902824042

  167. 167.

    Yi X, Ding H, Lu Y, Liu H, Zhang M, Jiang W. Effects of long-term alachlor exposure on hepatic antioxidant defense and detoxifying enzyme activities in crucian carp (Carassius auratus). Chemosphere. 2007;68(8):1576-1581.

    Not in our library10.1016/j.chemosphere.2007.02.035

  168. 168.

    Kesavachandran C, Singh VK, Mathur N, et al. Possible mechanism of pesticide toxicity-related oxidative stress leading to airway narrowing. Redox Report. 2006;11(4):159-162.

    Not in our library10.1179/135100006x116673

  169. 169.

    Combs GF, Peterson FJ. Protection against acute paraquat toxicity by dietary selenium in the chick. Journal of Nutrition. 1983;113(3):538-545.

    Not in our library10.1093/jn/113.3.538

  170. 170.

    Glass M, Sutherland MW, Forman HJ, Fisher AB. Selenium deficiency potentiates paraquat-induced lipid peroxidation in isolated perfused rat lung. Journal of Applied Physiology. 1985;59(2):619-622.

    Not in our library10.1152/jappl.1985.59.2.619

  171. 171.

    Cheng WH, Ho YS, Valentine BA, Ross DA, Combs GF, Lei XG. Cellular glutathione peroxidase is the mediator of body selenium to protect against paraquat lethality in transgenic mice. Journal of Nutrition. 1998;128(7):1070-1076.

    Not in our library10.1093/jn/128.7.1070

  172. 172.

    Takizawa M, Komori K, Tampo Y, Yonaha M. Paraquat-induced oxidative stress and dysfunction of cellular redox systems including antioxidative defense enzymes glutathione peroxidase and thioredoxin reductase. Toxicology in Vitro. 2007;21(3):355-363.

    Not in our library10.1016/j.tiv.2006.09.003

  173. 173.

    Aono M, Saji H, Fujiyama K, Sugita M, Kondo N, Tanaka K. Decrease in activity of glutathione reductase enhances paraquat sensitivity in transgenic Nicotiana tabacum. Plant Physiology. 1995;107(2):645-648.

    Not in our library10.1104/pp.107.2.645

  174. 174.

    Akturk O, Demirin H, Sutcu R, Yilmaz N, Koylu H, Altuntas I. The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat heart and ameliorating role of vitamin E and vitamin C. Cell Biology and Toxicology. 2006;22(6):455-461.

    Not in our library10.1007/s10565-006-0138-5

  175. 175.

    Verma RS, Mehta A, Srivastava N. In vivo chlorpyrifos induced oxidative stress: attenuation by antioxidant vitamins. Pesticide Biochemistry and Physiology. 2007;88(2):191-196.

    Not in our library

  176. 176.

    Altuntas I, Delibas N, Sutcu R. The effects of organophosphate insecticide methidathion on lipid peroxidation and anti-oxidant enzymes in rat erythrocytes: role of vitamins E and C. Human and Experimental Toxicology. 2002;21(12):681-685.

    Not in our library10.1191/0960327102ht304oa

  177. 177.

    Goel A, Dani V, Dhawan DK. Protective effects of zinc on lipid peroxidation, antioxidant enzymes and hepatic histoarchitecture in chlorpyrifos-induced toxicity. Chemico-Biological Interactions. 2005;156(2-3):131-140.

    Not in our library10.1016/j.cbi.2005.08.004

  178. 178.

    Stevenson DE, Walborg EF, North DW, et al. Monograph: reassessment of human cancer risk of aldrin/dieldrin. Toxicology Letters. 1999;109(3):123-186.

    Not in our library10.1016/s0378-4274(99)00132-0

  179. 179.

    Bachowski S, Xu Y, Stevenson DE, Walborg EF, Klaunig JE. Role of oxidative stress in the selective toxicity of dieldrin in the mouse liver. Toxicology and Applied Pharmacology. 1998;150(2):301-309.

    Not in our library10.1006/taap.1998.8372

  180. 180.

    Stevenson DE, Kehrer JP, Kolaja KL, Walborg EF, Klaunig JE. Effect of dietary antioxidants on dieldrin-induced hepatotoxicity in mice. Toxicology Letters. 1995;75(1–3):177-183.

    Not in our library10.1016/0378-4274(94)03178-a

  181. 181.

    Klaunig JE, Xu Y, Bachowski S, et al. Oxidative stress in nongenotoxic carcinogenesis. Toxicology Letters. 1995;82-83:683-691.

    Not in our library10.1016/0378-4274(95)03514-1

  182. 182.

    Stohs SJ. Oxidative stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Free Radical Biology and Medicine. 1990;9(1):79-90.

    Not in our library10.1016/0891-5849(90)90052-k

  183. 183.

    Alsharif NZ, Hassoun EA. Protective effects of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced body wasting, hepatomegaly, thymic atrophy, production of reactive oxygen species and DNA damage in C57BL/6J mice. Basic and Clinical Pharmacology and Toxicology. 2004;95(3):131-138.

    Not in our library10.1111/j.1742-7843.2004.950305.x

  184. 184.

    Wen S, Yang F, Gong Y, et al. Elevated levels of urinary 8-hydroxy-2′-deoxyguanosine in male electrical and electronic equipment dismantling workers exposed to high concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans, polybrominated diphenyl ethers, and polychlorinated biphenyls. Environmental Science and Technology. 2008;42(11):4202-4207.

    Not in our library10.1021/es800044m

  185. 185.

    Song Y, Wagner BA, Lehmler HJ, Buettner GR. Semiquinone radicals from oxygenated polychlorinated biphenyls: electron paramagnetic resonance studies. Chemical Research in Toxicology. 2008;21(7):1359-1367.

    Not in our library10.1021/tx8000175

  186. 186.

    Shimizu K, Ogawa F, Thiele JJ, Bae S, Sato S. Lipid peroxidation is enhanced in Yusho victims 35 years after accidental poisoning with polychlorinated biphenyls in Nagasaki, Japan. Journal of Applied Toxicology. 2007;27(2):195-197.

    Not in our library10.1002/jat.1205

  187. 187.

    Shimizu K, Ogawa F, Sato S. Estimation of total antioxidant power in the serum of Yusho victims. Fukuoka Igaku Zasshi. 2007;98(5):141-142.

    Not in our library

  188. 188.

    Banudevi S, Krishnamoorthy G, Venkataraman P, Vignesh C, Aruldhas MM, Arunakaran J. Role of α-tocopherol on antioxidant status in liver, lung and kidney of PCB exposed male albino rats. Food and Chemical Toxicology. 2006;44(12):2040-2046.

    Not in our library10.1016/j.fct.2006.07.017

  189. 189.

    Krishnamoorthy G, Venkataraman P, Arunkumar A, Vignesh RC, Aruldhas MM, Arunakaran J. Ameliorative effect of vitamins (α-tocopherol and ascorbic acid) on PCB (Aroclor 1254) induced oxidative stress in rat epididymal sperm. Reproductive Toxicology. 2007;23(2):239-245.

    Not in our library10.1016/j.reprotox.2006.12.004

  190. 190.

    Zhou C, Zhang C. Protective effects of antioxidant vitamins on Aroclor 1254-induced toxicity in cultured chicken embryo hepatocytes. Toxicology in Vitro. 2005;19(5):665-673.

    Not in our library10.1016/j.tiv.2005.03.010

  191. 191.

    Venkataraman P, Krishnamoorthy G, Vengatesh G, Srinivasan N, Aruldhas MM, Arunakaran J. Protective role of melatonin on PCB (Aroclor 1254) induced oxidative stress and changes in acetylcholine esterase and membrane bound ATPases in cerebellum, cerebral cortex and hippocampus of adult rat brain. International Journal of Developmental Neuroscience. 2008;26(6):585-591.

    Not in our library10.1016/j.ijdevneu.2008.05.002

  192. 192.

    Elumalai P, Krishnamoorthy G, Selvakumar K, Arunkumar R, Venkataraman P, Arunakaran J. Studies on the protective role of lycopene against polychlorinated biphenyls (Aroclor 1254)-induced changes in StAR protein and cytochrome P450 scc enzyme expression on Leydig cells of adult rats. Reproductive Toxicology. 2009;27(1):41-45.

    Not in our library10.1016/j.reprotox.2008.11.053

  193. 193.

    Chang JR, Xu DQ. Effects of formaldehyde on the activity of superoxide dismutases and glutathione peroxidase and the concentration of malondialdehyde. Wei Sheng Yan Jiu. 2006;35(5):653-655.

    Not in our library

  194. 194.

    Köse E, Sarsılmaz M, Taş U, et al. Rose oil inhalation protects against formaldehyde-induced testicular damage in rats. Andrologia. 2011;44(supplement 1):342-348.

    Not in our library10.1111/j.1439-0272.2011.01187.x

  195. 195.

    Zararsiz I, Meydan S, Sarsilmaz M, Songur A, Ozen OA, Sogut S. Protective effects of omega-3 essential fatty acids against formaldehyde-induced cerebellar damage in rats. Toxicology and Industrial Health. 2011;27(6):489-495.

    Not in our library10.1177/0748233710389852

  196. 196.

    Zararsiz I, Sarsilmaz M, Tas U, Kus I, Meydan S, Ozan E. Protective effect of melatonin against formaldehyde-induced kidney damage in rats. Toxicology and Industrial Health. 2007;23(10):573-579.

    Not in our library10.1177/0748233708089022

  197. 197.

    Brent JA, Rumack BH. Role of free radicals in toxic hepatic injury. II. Are free radicals the cause of toxin-induced liver injury? Journal of Toxicology: Clinical Toxicology. 1993;31(1):173-196.

    Not in our library10.3109/15563659309000384

  198. 198.

    Tsai C, Hsu Y, Chen W, et al. Hepatoprotective effect of electrolyzed reduced water against carbon tetrachloride-induced liver damage in mice. Food and Chemical Toxicology. 2009;47(8):2031-2036.

    Not in our library10.1016/j.fct.2009.05.021

  199. 199.

    Morrow JD, Awad JA, Kato T, et al. Formation of novel non-cyclooxygenase-derived prostanoids (F2-lsoprostanes) in carbon tetrachloride hepatotoxicity: an animal model of lipid peroxidation. Journal of Clinical Investigation. 1992;90(6):2502-2507.

    Not in our library10.1172/jci116143

  200. 200.

    Basu S. Carbon tetrachloride-induced lipid peroxidation: eicosanoid formation and their regulation by antioxidant nutrients. Toxicology. 2003;189(1-2):113-127.

    Not in our library10.1016/s0300-483x(03)00157-4

  201. 201.

    Ozturk F, Gul M, Ates B, et al. Protective effect of apricot (Prunus armeniaca L.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats. British Journal of Nutrition. 2009;102(12):1767-1775.

    Not in our library10.1017/s0007114509991322

  202. 202.

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    Oliva M, Vicente JJ, Gravato C, Guilhermino L, Galindo-Riaño ML. Oxidative stress biomarkers in Senegal sole, Solea senegalensis, to assess the impact of heavy metal pollution in a Huelva estuary (SW Spain): seasonal and spatial variation. Ecotoxicology and Environmental Safety. 2012;75(1):151-162.

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    Yang UJ, Park TS, Shim SM. Protective effect of chlorophyllin and lycopene from water spinach extract on cytotoxicity and oxidative stress induced by heavy metals in human hepatoma cells. Journal of Toxicology and Environmental Health A. 2013;76(23):1307-1315.

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    Xing H, Li S, Wang Z, Gao X, Xu S, Wang X. Oxidative stress response and histopathological changes due to atrazine and chlorpyrifos exposure in common carp. Pesticide Biochemistry and Physiology. 2012;103(1):74-80.

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    Manikandan S, Srikumar R, Parthasarathy NJ, Devi RS. Protective effect of Acorus calamus Linn on free radical scavengers and lipid peroxidation in discrete regions of brain against noise stress exposed rat. Biological & Pharmaceutical Bulletin. 2005;28(12):2327-2330.

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    Ozguner F, Altinbas A, Ozaydin M, et al. Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester. Toxicology and Industrial Health. 2005;21(9):223-230.

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    van Campen LE, Murphy WJ, Franks JR, Mathias PI, Toraason MA. Oxidative DNA damage is associated with intense noise exposure in the rat. Hearing Research. 2002;164(1-2):29-38.

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    Ewert DL, Lu J, Li W, Du X, Floyd R, Kopke R. Antioxidant treatment reduces blast-induced cochlear damage and hearing loss. Hearing Research. 2012;285(1-2):29-39.

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    Neuhouser ML, Patterson RE, Thornquist MD, Omenn GS, King IB, Goodman GE. Fruits and vegetables are associated with lower lung cancer risk only in the placebo arm of the β-Carotene and Retinol Efficacy Trial (CARET). Cancer Epidemiology Biomarkers and Prevention. 2003;12(4):350-358.

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    McArdle F, Rhodes LE, Parslew RAG, et al. Effects of oral vitamin E and β-carotene supplementation on ultraviolet radiation-induced oxidative stress in human skin. American Journal of Clinical Nutrition. 2004;80(5):1270-1275.

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    Wolf C, Steiner A, Honingsmann H. Do oral carotenoids protect human skin against ultraviolet erythema, psoralen phototoxicity, and ultraviolet-induced DNA-damage? Journal of Investigative Dermatology. 1988;90(1):55-57.

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    Garmyn M, Ribaya-Mercado JD, Russel RM, Bhawan J, Gilchrest BA. Effect of beta-carotene supplementation on the human sunburn reaction. Experimental Dermatology. 1995;4(2):104-111.

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    Latchoumycandane C, Mathur PP. Effects of vitamin E on reactive oxygen species-mediated 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity in rats testis. Journal of Applied Toxicology. 2002;22(5):345-351.

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    Sakano K, Oikawa S, Hiraku Y, Kawanishi S. Oxidative DNA damage induced by a melatonin metabolite, 6-hydroxymelatonin, via a unique non-o-quinone type of redox cycle. Biochemical Pharmacology. 2004;68(9):1869-1878.

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    Achieving the Balance between ROS and Antioxidants: When to Use the Synthetic Antioxidants · 2013
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    The Neglected Significance of “Antioxidative Stress” · 2012
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    Salganik RI. The benefits and hazards of antioxidants: controlling apoptosis and other protective mechanisms in cancer patients and the human population. The Journal of the American College of Nutrition. 2001;20(supplement 5):464S-472S.

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    Podmore ID, Griffiths HR, Herbert KE, Mistry N, Mistry P, Lunec J. Vitamin C exhibits pro-oxidant properties. Nature. 1998;392(6676):p. 559.

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    Miller ER, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Annals of Internal Medicine. 2005;142(1):37-46.

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