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The Role of Oxidative Stress and Antioxidant Balance in Pregnancy

Tarique Hussain, Ghulam Murtaza, Elsayed Metwally and 8 more

Mediators of Inflammation · 2021 · Review · CC BY

doi:10.1155/2021/9962860

Abstract

It has been widely known that oxidative stress disrupts the balance between reactive oxygen species (ROS) and the antioxidant system in the body. During pregnancy, the physiological generation of ROS is involved in a variety of developmental processes ranging from oocyte maturation to luteolysis and embryo implantation. While abnormal overproduction of ROS disrupts these processes resulting in reproductive failure. In addition, excessive oxidative stress impairs maternal and placental functions and eventually results in fetal loss, IUGR, and gestational diabetes mellitus. Although some oxidative stress is inevitable during pregnancy, a balancing act between oxidant and antioxidant production is necessary at different stages of the pregnancy. The review aims to highlight the importance of maintaining oxidative and antioxidant balance throughout pregnancy. Furthermore, we highlight the role of oxidative stress in pregnancy‐related diseases.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 21, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Several reproductive problems have been linked to oxidative stress. Oxidative stress occurs when the body's antioxidant system is depleted owing to an excess of reactive oxygen species (ROS). ROS are highly reactive molecules that are unstable and short-lived. These molecules contribute to the control of signaling pathways, as well as cellular and physiological processes. However, excess ROS may cause cellular toxicity. Animals have an enzymatic antioxidant defense mechanism that suppresses the formation of reactive oxygen species (ROS). It is worth noting that cellular integrity is maintained by a balance of enzymatic and non-enzymatic antioxidant systems. When oxidative stress increases, both antioxidant systems are depleted resulting in reproductive problems. Enzymatic antioxidants like glutathione peroxidase (GPx) and superoxide dismutase (SOD) are antioxidants to neutralize free radicals. On other hand, the non-enzymatic antioxidants such as vitamin C, vitamin E, plant polyphenol, carotenoids, and glutathione interrupt free radical chain reactions. Importantly, antioxidants may have therapeutic promise in the treatment of reproductive-related problems.

ROS has a biological effect on various reproductive processes, such as oocyte maturation, fertilization, embryo development, pregnancy, as well as oocyte maturation and fertility. A number of research studies, including animals and humans, showed that ROS has been implicated with female reproduction, particularly ovaries, fallopian tubes and embryos.

The primary function of the placenta is to exchange nutrients and oxygen between mother and fetus. Therefore, interference in these functions leads to hypoxia due to oxidative stress. The disruption in placental function is due to many factors resulting in pregnancy complications. A large number of studies reported that pregnancy problems have been associated with overwhelming oxidative stress from the placenta and or maternal tissues. Other mechanisms are also implicated in the etiology of these complications; oxidative stress has evolved to regulate the cellular and molecular pathways such as altered angiogenesis and inflammation to mediate disease outcomes. The oxidative scenario develops due to increased ROS and depletion of the antioxidant system. Though the development of abnormal oxidative stress leads to spontaneous abortion, idiopathic recurrent pregnancy loss and embryogenesis defect.

Oxidative stress has been linked to a number of metabolic processes that affect animal health and performance. The study of oxidative stress has increased as a result of its role in adverse pregnancy outcomes. Oxidative stress exhibits dual functions, it aids in the maintenance of redox balance and it plays a part in female reproductive processes. As a result, oxidative stress may aggravate IUGR, endometriosis, and other reproductive issues. Oxidative stress also regulates signaling networks including Kelch-like ECH-associated protein 1, Nuclear factor erythroid 2-related factor 2 (Keap1-Nrf2), nuclear factor kappa-B (NF-κB), forkhead transcription factors of the O class (FOXO) and Mitogen-activated protein kinase (MAPK). Lastly, targeting these pathways appears attractive as a potential therapeutic strategy against pregnancy-related anomalies.

2. Oxidative Stress and Its Regulatory Mechanism

ROS are oxidative metabolic byproducts that play an important part in cellular activity. They are also implicated in a number of pathological diseases, including in-vitro and in-vivo pregnancy difficulties. The factors responsible for overproduction of ROS are ultraviolet radiation, cigarette smoking, alcohol, non-steroidal anti-inflammatory medication, ischemia-reperfusion injury, chronic infections, and inflammatory diseases. The enzyme superoxide dismutase converts the superoxide anion radical to hydrogen peroxide and oxygen, and catalase eliminates hydrogen peroxide when its quantities in the cell are higher. Glutathione reductase is found throughout the body tissues and operates similarly to GPx. Using several systems; the GSR enzyme reduced oxidized glutathione by utilizing NADPH.

The secondary defense is based on the GPx enzyme, which possesses peroxidase activity and may eliminate lipid hydroperoxides irrespective phospholipase A2. There are also a number of oxido-reductases that catalyse thiol and other protein reduction processes. Protective enzymes against free radicals are produced once the cellular components have been oxidatively damaged. For example, DNA nuclear enzymes are known to protect DNA from oxidative damage induced by free radicals. Vitamin E functions as a cofactor for glutathione peroxidase enzymes, and its presence in all cellular membranes suggests that it can protect lipids from oxidation. The ascorbic acid-GSH redox couple directly reduces the tocopherol radical. While β-carotene functions in concert with vitamin E, which is a strong scavenger of free radicals, but β -carotene only works at low oxygen pressure. Vitamin E, on the other hand, protects β-carotene against oxidative damage. In addition, some antioxidants work as free radical quenchers. Early pregnancy deficiency in antioxidants has been associated with the development of maternal-related disorders such as gestational hypertension, gestational diabetes, and other complications. Therefore, the generation of ROS molecules controls several signaling pathways that govern a variety of cellular functions. The activation of these signals causes a change in cellular function, which has a pathogenic effect on the cell.

3. Oxidative Stress Scenarios in Pregnancy

In normal pregnancy, the developing tissues and organs of the fetus require enough nutrition and oxygen. These processes generate ROS in both maternal and fetal tissues that influence fetal growth development. To provide a suitable environment for the fetus and maternal body, the balance between ROS and antioxidants could be maintained. During pregnancy, the body undergoes numerous physiological changes. The evidence of ROS formation in the second trimester of pregnancy was assumed by the researchers. Increased production of ROS occurs due to the enhanced metabolism, high consumption of oxygen and utilization of fatty acids. During third trimester of pregnancy, increase insulin resistance, fat catabolism, and release of free fatty acids resulting in enhanced production of hydrogen peroxide. Placental cells have a lot of mitochondria, which are the main source of pro-oxygenates. The superoxide anion radical produces more radical species and their generation rises as the pregnancy continues.

Several studies have found that oxidative stress is linked to pregnancy complications that may influence fetal development. The major causes are a lack of nutrition and oxygen for developing fetuses, which causes hypoplasia and disrupts placental function. The difference in total plasma antioxidants status between pregnant and non-pregnant individuals has been observed, implying a low level in the first phase of pregnancy. The total antioxidant capacity of a pregnant woman increases during the second and third trimesters, and by the last week of pregnancy, it has reached the level of a non-pregnant woman. TAC activity increases after the 8th week of pregnancy, and these changes are linked to differences in plasma uric acid levels. Furthermore, reduced TAC levels in pregnancy have been linked to low levels of serum albumin, bilirubin, and vitamin E. As result, it appears that plasma SOD activity is reduced during pregnancy. The SOD reduction promoted triglycerides, total cholesterol, and low-density lipoprotein (LDL) cholesterol levels in blood plasma. Therefore, SOD refers as indicator of oxidative stress and lipid peroxide activity followed by 25 weeks of pregnancy. As a result, lipid peroxidation levels in the blood are higher in pregnant women, serving as a marker of oxidative stress. Previous studies have found that supplementing pregnant individuals with the dietary vitamins, antioxidants, and minerals enhanced TAC activity.

4. Oxidative Stress in Ovary, Uterus and Placenta

Almost every stage of pregnancy is affected by ROS. ROS is known to be the important regulator of ovarian cellular activity. The ROS positive impact has been already mentioned. Previous studies showed that the presence of SOD in ovary, copper-zinc SOD (Cu-Zn SOD) in granulosa cells of follicles and manganese superoxide dismutase (MnSOD) in luteal cells of the corpus luteum in rats. The sources of ROS in the follicles are macrophages, leukocytes and cytokines. Ovulation is dependent on concentration of ROS. ROS suppressors have been demonstrated to interfere with the ovulatory process. Follicles development is associated with an increased metabolic function of granulosa cells, particularly excess amount of cytochrome P450 and steroidogenesis. The presence of ROS in pre-ovulatory follicles alters blood flow and finally leads to follicle rupture. Furthermore, FSH stimulates the synthesis of estrogen, while the overexpression of CAT in developing follicles protects them from apoptosis, ensuring that ovarian function is preserved. Depletion of oxygen is required for follicular angiogenesis. The corpus luteum contributes to functional luteolysis by producing ROS. During the luteal phase, both the ROS and antioxidants are linked to progesterone production. The beneficial effects of ROS and antioxidants in female reproductive and pregnancy outcomes are depicted in Table 1.

The developing fetus has a high energy requirement due to the placental hyperactive metabolic rate, resulting in oxidative stress. Of note, that superoxide anions produced by placental mitochondria appear to be the essential source of ROS and lipid peroxidation in the placenta. As the pregnancy progresses, mitochondrial synthesis of lipid peroxides, free radicals, and vitamin E may also increase. The placenta and large blood arteries mature slowly in the second phase of the pregnancy. After that, maternal blood pumps via interstitial space into the mother's spiral artery. Free radicals are abundant in placental tissues, and oxidation occurs throughout the process. With the help of antioxidant activity, the placenta can slowly adapt to the environment after recovering from stress.

SOD activity decreases during the late luteal phase due to increased amounts of lipid peroxide. Importantly, ROS are known to have a role in numerous phases of the endometrial cycle, and may also produce PGF2 through NF-κB activation. Estrogen and progesterone levels dropped significantly as a result of lower SOD expression. In a consequence, ROS accumulates in the uterus, leading to implantation failure. The basal level of ROS controls angiogenic activity in the endometrium and results in endometrial regeneration during each cycle. Thus, appropriate ROS concentration is critical for normal homeostasis. However, an increased level of ROS from the placenta has been associated with pregnancy-related disorders. The TNF-α cytokine that influences endothelial cell dysfunction and the antioxidant Mn-SOD are both disrupted and have protective effects. The production of cytokines and prostaglandins is increased by ROS-related poor placental function, producing endothelial cell injury and contributing to preeclampsia.

5. Regulation of Multiple Signaling Pathways by Oxidative Stress

Oxidative stress has been linked to influence signaling pathways, particularly in reproductive diseases ranging from egg production to ovulation. It alters immune system of the uterus resulting in embryonic failure. Oxidative stress has also been involved in regulating molecular pathways in reproductive disorders such as p38 MAPK, Keap1-Nrf2, the Jun N-terminal kinase (JNK), the FOXO family, and apoptotic pathways. Therefore, the research on this aspect may yield new insights that might influence female reproductive system.

Nrf2 is a signaling molecule that protects cellular function by acting as an antioxidant in response to oxidative stress. Physiologically, Nrf2 binds with Keap1 in the cytoplasm before being degraded by the proteasome. Once the Nrf2 is activated, it translocate into nucleus, where it activates several antioxidant genes. In contrast, activation of antioxidant genes and restoration of vascular redox homeostasis are required when OS is evident suggesting the crucial function of Nrf2. The deficiency of Nrf2 induced fetal DNA damage and neurological discrepancies and inactivation of Nrf2 were also exhibited inflammation triggered trophoblastic apoptosis. Previous evidence showed that Nrf2 plays an important role in pregnancy and protects the fetus from OS in-utero. The maternal immune system is susceptible to Nrf2. Nrf2 is only decreased once the full-term foetus is delivered in a normal pregnancy. When a fetus is infected in utero, the Nrf2 expression is favorably reduced. In the case of OS-induced metritis, it is expected that Nrf2 would be considerably decreased, and Keap1 would bind to Nrf2. Similarly, FOXO3 is essential in the interaction between Keap1 and Nrf2. In the absence of FOXO3, Nrf2 is activated by AKT and protects cells against OS. Lastly, we hypothesized that OS causes inflammation in the reproductive system, with FOXO3 playing a role in the interaction between Keap1 and Nrf2, which may be used as a marker for OS insults.

NF-κB is an inert molecule, its family comprises five transcription factors c-Rel, p50, p52, RelB and RelA (p65). NF-B is a redox-sensitive transcription factor that is the primary regulator of the inflammatory response. Therefore, the beneficial effects of NF-κB are evident in embryonic stress that activates NF-κB and other diverse inflammatory cytokines which persuades apoptosis within placenta. Hence, it was concluded that NF-κB plays an important role in the cell survival by releasing anti-apoptotic genes. In normal conditions, NF-κB is bound to inhibitory IκB proteins and remains inactive in the cytoplasm. The breakdown of IκB proteins activates NF-B, which subsequently translocate into the nucleus and generates desirable genes, whereas IκB proteins are mediated by the IκB kinase (IKK) complex (IKKα and IKKβ). Increased expression of NF-κB in cultured endometrial stromal cells has been found in reproductive diseases such as endometriosis. Altered production of NF-κB production has been associated with inflammation. Endometriosis is a condition induced by OS which increases the concentration of TNF-α, resulting in inflammation thereby; NF-κB is activated. Moreover, IL-1β activates NF-κB, which in turn produces inflammatory cytokines, comprising macrophage migration inhibitory factor (MIF) in endometrial stromal cells and TNF-α in immortalized epithelial (12Z) cell line. In summary, OS-mediated reproductive disorders are caused by NF-κB activation.

FOXO1 and FOXO3 have been contributed to OS and pregnancy. The FOXO subfamily of Forkhead transcription factors is a direct downstream target of the PI3K/Akt pathway. The family of FOXO proteins is involved in different biological processes such as proliferation, apoptosis, autophagy, metabolism, inflammation, differentiation and stress tolerance. The FOXC1 displays a pivotal role in reproduction and also mediates cyclic differentiation and apoptosis in normal endometrium. Recent studies have shown that FOXO1 knockdown disrupts the expression of over 500 genes in decidualized human endometrial stromal cells. Previous research has shown that FOXO transcription factors can control multiple gene responses to change hormone levels. Besides, that FOXO1 is also responsible for the induction of decidual marker genes, including WNT4, prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP1).

Three signaling molecules are triggered by the extracellular milieu, including ERK, which is activated by inflammation and growth factors, and JNK and p38 MAPK, which are mostly activated by stress and inflammation. It has been shown that ERK activation is increased in endometrial tissue, suggesting that ERK may play a role in endometriosis and phosphorylated ERK is increased in primary eutopic epithelial cells. ERK activation can also be influenced by oxidative stress. In response to normal women, hydrogen peroxide causes ERK phosphorylation in endometriotic stromal cells.

6.1. Intrauterine Growth Restriction

Intrauterine growth restriction (IUGR) is a pregnancy ailment in which an underweight/incomplete fetus develops in the uterus. The causes are multifactorial such as maternal, fetal, placental, infectious, or genetics. About 76% of intrauterine deaths have been associated with IUGR. The most significant cause of IUGR is utero-placental dysfunction occurs due to the congested maternal utero-placental blood flow. Proper functioning of the placenta requires greater energy demand for cell growth, proliferation and metabolic activity which in turn produce oxidative stress. Oxidative stress plays an essential role against various stimuli which influence placental function. Cellular injury occurs as a result of lipid peroxidation and fatty acid oxidation, and it is mostly utilised to identify oxidative stress indicators. Evidence of IUGR in livestock has been raised through environmental factors and affects goats, sheep, pigs and other animals. Of note, that significant evidence of IUGR exists in multi-fetal animals including pigs. It has been documented those animals with this condition have reduced birth weight, postnatal growth, development and liver dysfunction. A detailed description of IUGR occurrences in clinical and health deviations is well been ascribed in the previous studies. More evidence is required to be revealed the underlying molecular mechanisms.

6.2. Spontaneous Miscarriage and Recurrent Pregnancy Loss

Spontaneous abortion can be classified as loss of pregnancy before 20 weeks of gestation. The incidence may range from 8-20% in pregnancies and is due to chromosomal aberration, which accounts for 50% of all miscarriages. While, the rest are associated with congenital and uterine malfunctions, infections, maternal diseases and unknown causes.

In early pregnancy losses, elevated levels of MDA and lipid peroxides were observed in placental tissues in comparison with controls. Previous studies have shown that overloading of ROS could lead to the premature and sudden formation of maternal placental perfusion. Other evidence reported that oxidative stress damage the trophoblast and ultimately leading to early pregnancy losses. The incidence of oxidative stress occurred due to the depletion of the antioxidants system and thus unable to scavenge free radicals. Although there is diversity in previous studies, it seems to be a relationship between ROS and antioxidants in miscarriage. The abnormal placentation may arise from syncytiotrophoblasts and may be vulnerable to idiopathic recurrent pregnancy loss. Oxidative stress enables the potential to influence pregnancies due to the depletion of antioxidant capacity within the body. The influence of oxidative stress in pregnancy problems is depicted in Figure 1. The issue of recurrent pregnancy losses, research gaps, and their treatment has been thoroughly reviewed.

6.3. Gestational Diabetes Mellitus (GDM)

GDM is a type of diabetes mellitus in which pregnant women develops glucose intolerance to a different degree. It was reported in 2-5% of pregnancies while; data suggested the incidences increased up to 18% in all pregnancies. GDM develops during the second trimester of pregnancy, causing fetal macrosomia, perinatal mortality, and making mother vulnerable for T2DM.

The pregnancy has been linked to an imbalance of pro and anti-inflammatory mediators. The levels of T cells subsets were increased in women with GDM compared to control healthy subjects whereas; T cells expressing CTLA-4, a downregulation of the immune system which lightly expressed in Tregs were suppressed. Changes in the Treg population suggest that the Treg pool in GDM is becoming less active. Thus, it suggests that the lack of immune down-regulation helps maternal-fetal tolerance. Although, the toll-like receptors TLR-2 and TLR-4 stimulate inflammatory cytokines which were enhanced in peripheral blood mononuclear cells of women with GDM. Previous literature revealed the ambiguous results of TNF-α in GDM condition, but more descriptive role of GDM is well-highlighted somewhere else. An evidence of oxidative stress-related problems during pregnancy is well-reviewed by others.

7. Antioxidant Approaches in Pregnancy

The detrimental effects of oxidative stress and ROS on female reproduction system have been well illustrated for since long. It was suggested that the generation of ROS is impaired by cytochrome P450 and corpus luteum, which itself is considered a key source. The initiation of oocyte maturation and others processes are mostly affected by different levels of ROS and antioxidants. Endometriosis and unexplained infertility conditions are also linked to the OS.

Antioxidant supplementation possess positive effects through a variety of pathways, including direct scavenging of reactive oxygen species (ROS) and damage repair. The protective effects on fertility consisting enhanced blood circulation in endometrium, reduced hyperandrogenism, lowered insulin resistance, and positive impact on prostaglandin synthesis and steroidogenesis. A current systematic review indicates the positive impact of antioxidants in female fertility. Antioxidants were also involved in enhancing live birth weight and clinical pregnancy rates. Though, the evidence is poor with a slight increase to high heterogeneity due to the trials on enrolled women offering various kinds of antioxidants. Antioxidants have shown various responses when they are taken alone or in combination exerted a positive effect on pregnancy rate. Moreover, dietary/injectable source of antioxidants during periparturient period provide beneficial effects on pregnancy outcome and growth performance of suckling kids of goats.

There is evidence that increased antioxidant levels confront and scavenge ROS in women who have repeated abortions as a result of ROS overload. Previous research has found that women with recurrent abortion have higher levels of lipoperoxides and lower amounts of vitamin A, E, and beta carotene, suggesting the role of ROS. When compared to healthy subject, glutathione activity was low in women who had recurrent abortions. Moreover, selenium concentration from hair samples was also significantly reduced in recurrent abortion than the healthy pregnancies. Increased glucose levels during pregnancy cause teratogenic consequences due to chemical changes and DNA rearrangements. Increased glucose causes the formation of glycation products, which affect genomic function and negatively regulate embryonic development. In diabetic pregnancy, changes in membrane lipids induce biological prostaglandin events, and an enhanced level of ROS causes dysmorphogenesis in the fetus. A reduced level of lipid peroxidation in women with GDM was reported due to depletion of antioxidants activity. Hydroperoxide production affects prostaglandin synthesis patterns, which may result in morbidity owing to antioxidant depletion. GDM also triggers oxidative stress in fetus, thus the intake of antioxidants during pregnancy is essential factor for improving pregnancy health. Further, a detailed description on the role of antioxidants in pregnancy is well-discussed in the previous studies.

8. Conclusion

Antioxidant defense has been established to regulate the generation of ROS; however the increased amount of ROS cannot be controlled, resulting in oxidative stress. So, the potential strategies of antioxidant to decrease ROS levels are critical. According to a large number of studies, oxidative stress is the primary contributing factor in a variety of pregnancy complications. Overstimulation of ROS can cause hyperglycemia, IUGR, miscarriage, and spontaneous abortion throughout all stages of pregnancy. Placental oxidative stress is caused by a number of variables, including maternal history, genetics, and environmental factors, and can lead to negative pregnancy outcomes. Future research should focus on improving the breakdown of intracellular ROS and enhancing antioxidant bioavailability. Targeting signaling molecules with natural bioactive compounds will be used to minimize the occurrence of reproductive problems.

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    Shkolnik K., Tadmor A., Ben-Dor S., Nevo N., Galiani D., Dekel N. Reactive oxygen species are indispensable in ovulation. Proceeding National Academy of Sciences, U S A. 2011;108(4):1462-1467.

    Not in our library10.1073/pnas.1017213108

  48. 48.

    Richards J. S. Hormonal control of gene expression in the ovary. Endocrine Reviews. 1994;15(6):725-751.

    Not in our library10.1210/edrv-15-6-725

  49. 49.

    du B., Takahashi K., Ishida G. M., Nakahara K., Saito H., Kurachi H. Usefulness of intraovarian artery pulsatility and resistance indices measurement on the day of follicle aspiration for the assessment of oocyte quality. Fertility and Sterility. 2006;85(2):366-370.

    Not in our library10.1016/j.fertnstert.2005.07.1316

  50. 50.

    Sugino N. Roles of reactive oxygen species in the corpus luteum. Animal Sciences Journal. 2006;77(6):556-565.

    Not in our library10.1111/j.1740-0929.2006.00386.x

  51. 51.

    Rizzo A., Roscino M. T., Binetti F., Sciorsci R. L. Roles of reactive oxygen species in female reproduction. Reproduction in Domestic Animals. 2012;47(2):344-352.

    Not in our library10.1111/j.1439-0531.2011.01891.x

  52. 52.

    Myatt L., Cui X. L. Oxidative stress in the placenta. Histochemistry and Cell Biology. 2004;122(4):369-382.

    Not in our library10.1007/s00418-004-0677-x

  53. 53.

    Wang Y., Walsh S. W. Placental mitochondria as a source of oxidative stress in pre-eclampsia. Placenta. 1998;19(8):581-586.

    Not in our library10.1016/s0143-4004(98)90018-2

  54. 54.

    Jauniaux E., Gulbis B., Burton G. J. The human first trimester gestational sac limits rather than facilitates oxygen transfer to the foetus--a review. Placenta. 2003;24(Suppl A):S86-S93.

    Not in our library10.1053/plac.2002.0932

  55. 55.

    Lim K. H., Zhou Y., Janatpour M., et al. Human cytotrophoblast differentiation/invasion is abnormal in pre-eclampsia. American Journal of Pathology. 1997;151:1809-1818.

    Not in our library

  56. 56.

    Preutthipan S., Chen S. H., Tilly J. L., Kugu K., Lareu R. R., Dharmarajan A. M. Inhibition of nitric oxide synthesis potentiates apoptosis in the rabbit corpus luteum. Reproductive Biomedicine Online. 2004;9(3):264-270.

    Not in our library10.1016/s1472-6483(10)62140-2

  57. 57.

    Ghafourifar P., Richter C. Nitric oxide synthase activity in mitochondria. Federation of European Biochemical Societies Letters. 1997;418(3):291-296.

    Not in our library10.1016/s0014-5793(97)01397-5

  58. 58.

    Menon R., Fortunato S. J., Yu J., et al. Cigarette smoke induces oxidative stress and apoptosis in normal term fetal membranes. Placenta. 2011;32(4):317-322.

    Not in our library10.1016/j.placenta.2011.01.015

  59. 59.

    Smith R., Maiti K., Aitken R. J. Unexplained antepartum stillbirth: a consequence of placental aging? Placenta. 2013;34(4):310-313.

    Not in our library10.1016/j.placenta.2013.01.015

  60. 60.

    Oner-Iyidogan Y., Kocak H., Gurdol F., Korkmaz D., Buyru F. Indices of oxidative stress in eutopic and ectopic endometria of women with endometriosis. Gynecologic and Obstetric Investigation. 2004;57(4):214-217.

    Not in our library10.1159/000076691

  61. 61.

    Perucci L. O., Corrêa M. D., Dusse L. M., Gomes K. B., Sousa L. P. Resolution of inflammation pathways in preeclampsia—a narrative review. Immunologic Research. 2017;65(4):774-789.

    Not in our library10.1007/s12026-017-8921-3

  62. 62.
    Oxidative Stress in Placenta: Health and Diseases · 2015
    No notice
  63. 63.

    Itoh K., Chiba T., Takahashi S., et al. An Nrf2/Small Maf Heterodimer Mediates the Induction of Phase II Detoxifying Enzyme Genes through Antioxidant Response Elements. Biochemical and Biophysical Research Communications. 1997;236(2):313-322.

    Not in our library10.1006/bbrc.1997.6943

  64. 64.

    Itoh K., Wakabayashi N., Katoh Y., et al. Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain. Genes & Development. 1999;13(1):76-86.

    Not in our library10.1101/gad.13.1.76

  65. 65.

    Cho H.-Y., Reddy S. P., DeBiase A., Yamamoto M., Kleeberger S. R. Gene expression profiling of NRF2-mediated protection against oxidative injury. Free Radical Biology and Medicine. 2005;38(3):325-343.

    Not in our library10.1016/j.freeradbiomed.2004.10.013

  66. 66.

    Ishii T., Itoh K., Takahashi S., et al. Transcription Factor Nrf2 Coordinately Regulates a Group of Oxidative Stress- inducible Genes in Macrophages∗. Journal of Biological Chemistry. 2000;275(21):16023-16029.

    Not in our library10.1074/jbc.275.21.16023

  67. 67.

    Cheng X., Chapple S. J., Patel B., et al. Gestational diabetes mellitus impairs Nrf2-mediated adaptive antioxidant defenses and redox signaling in fetal endothelial cells in utero. Diabetes. 2013;62(12):4088-4097.

    Not in our library10.2337/db13-0169

  68. 68.

    Lim R., Barker G., Lappas M. The transcription factor Nrf2 is decreased after spontaneous term labour in human fetal membranes where it exerts anti-inflammatory properties. Placenta. 2015;36(1):7-17.

    Not in our library10.1016/j.placenta.2014.11.004

  69. 69.

    Guan L., Zhang L., Gong Z., et al. FoxO3 inactivation promotes human cholangiocarcinoma tumorigenesis and chemoresistance through Keap1-Nrf2 signaling. Hepatology. 2016;63(6):1914-1927.

    Not in our library10.1002/hep.28496

  70. 70.

    Gilmore T. Introduction to NF-κ B: players, pathways, perspectives. Oncogene. 2006;25(51):6680-6684.

    Not in our library10.1038/sj.onc.1209954

  71. 71.

    Hayden M., West A., Ghosh S. NF-κ B and the immune response. Oncogene. 2006;25(51):6758-6780.

    Not in our library10.1038/sj.onc.1209943

  72. 72.

    Cindrova-Davies T., Yung H.-W., Johns J., et al. Oxidative Stress, Gene Expression, and Protein Changes Induced in the Human Placenta during Labor. The American Journal of Pathology. 2007;171(4):1168-1179.

    Not in our library10.2353/ajpath.2007.070528

  73. 73.

    Scheidereit C. I κ B kinase complexes: gateways to NF-κ B activation and transcription. Oncogene. 2006;25(51):6685-6705.

    Not in our library10.1038/sj.onc.1209934

  74. 74.

    Sakamoto Y., Harada T., Horie S., et al. Tumor necrosis factor-α-induced interleukin-8 (IL-8) expression in endometriotic stromal cells, probably through nuclear factor-κB activation: gonadotropin-releasing hormone agonist treatment reduced IL-8 expression. The Journal of Clinical Endocrinology & Metabolism. 2003;88(2):730-735.

    Not in our library10.1210/jc.2002-020666

  75. 75.

    Veillat V., Herrmann Lavoie C., Metz C. N., Roger T., Labelle Y., Akoum A. Involvement of nuclear factor-κB in macrophage migration inhibitory factor gene transcription up-regulation induced by interleukin-1β in ectopic endometrial cells. Fertility and Sterility. 2009;91(5):2148-2156.

    Not in our library10.1016/j.fertnstert.2008.05.017

  76. 76.

    Cao W., Morin M., Sengers V., et al. Tumour necrosis factor-α up-regulates macrophage migration inhibitory factor expression in endometrial stromal cells via the nuclear transcription factor NF-κB. Human Reproduction. 2006;21(2):421-428.

    Not in our library10.1093/humrep/dei315

  77. 77.

    Grund E. M., Kagan D., Tran C. A., et al. Tumor necrosis factor-α regulates inflammatory and mesenchymal responses via mitogen-activated protein kinase kinase, p38, and nuclear factor κB in human endometriotic epithelial cells. Molecular Pharmacology. 2008;73(5):1394-1404.

    Not in our library10.1124/mol.107.042176

  78. 78.

    Brunet A., Bonni A., Zigmond M. J., et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell. 1999;96(6):857-868.

    Not in our library10.1016/s0092-8674(00)80595-4

  79. 79.

    van der Vos K. E., Coffer P. J. The extending network of FOXO transcriptional target genes. Antioxidants & Redox Signaling. 2011;14(4):579-592.

    Not in our library10.1089/ars.2010.3419

  80. 80.

    Goto T., Takano M., Albergaria A., et al. Mechanism and functional consequences of loss of FOXO1 expression in endometrioid endometrial cancer cells. Oncogene. 2008;27(1):9-19.

    Not in our library10.1038/sj.onc.1210626

  81. 81.

    Kajihara T., Brosens J. J., Ishihara O. The role of FOXO1 in the decidual transformation of the endometrium and early pregnancy. Medical Molecular Morphology. 2013;46(2):61-68.

    Not in our library10.1007/s00795-013-0018-z

  82. 82.

    Kajihara T., Jones M., Fusi L., et al. Differential expression of FOXO1 and FOXO3a confers resistance to oxidative cell death upon endometrial decidualization. Molecular Endocrinology. 2006;20(10):2444-2455.

    Not in our library10.1210/me.2006-0118

  83. 83.

    Gellersen B., Brosens J. Cyclic AMP and progesterone receptor cross-talk in human endometrium: a decidualizing affair. The Journal of Endocrinology. 2003;178(3):357-372.

    Not in our library10.1677/joe.0.1780357

  84. 84.

    Dhillon A. S., Hagan S., Rath O., Kolch W. MAP kinase signalling pathways in cancer. Oncogene. 2007;26(22):3279-3290.

    Not in our library10.1038/sj.onc.1210421

  85. 85.

    Matsuzaki S., Darcha C. Co-operation between the AKT and ERK signaling pathways may support growth of deep endometriosis in a fibrotic microenvironment in vitro. Human Reproduction. 2015;30(7):1606-1616.

    Not in our library10.1093/humrep/dev108

  86. 86.

    Andrade S. S., Azevedo A. D. C., Monasterio I. C., et al. 17 β -Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis. Free Radical Biology and Medicine. 2013;60:63-72.

    Not in our library10.1016/j.freeradbiomed.2013.01.034

  87. 87.
    Oxidative stress · 2011
    No notice
  88. 88.

    Sharma D., Shastri S., Sharma P. Intrauterine growth restriction: antenatal and postnatal aspects. Clinical Medicine Insights: Pediatrics. 2016;10, article CMPed.S40070.

    Not in our library10.4137/cmped.s40070

  89. 89.

    Frøen J. F., Gardosi J. O., Thurmann A., Francis A., Stray-Pedersen B. Restricted fetal growth in sudden intrauterine unexplained death. Acta Obstetricia et Gynecologica Scandinavica. 2004;83(9):801-807.

    Not in our library10.1111/j.0001-6349.2004.00602.x

  90. 90.

    Krishna U., Bhalerao S. Placental insufficiency and fetal growth restriction. The Journal of Obstetrics and Gynecology of India. 2011;61(5):505-511.

    Not in our library10.1007/s13224-011-0092-x

  91. 91.

    Hung T.-H., Skepper J. N., Charnock-Jones D. S., Burton G. J. Hypoxia-Reoxygenation. Circulation Research. 2002;90(12):1274-1281.

    Not in our library10.1161/01.res.0000024411.22110.aa

  92. 92.

    Biri A., Bozkurt N., Turp A., Kavutcu M., Himmetoglu Ö., Durak I. Role of oxidative stress in intrauterine growth restriction. Gynecologic and Obstetric Investigation. 2007;64(4):187-192.

    Not in our library10.1159/000106488

  93. 93.

    Wang J., Chen L., Li D., et al. Intrauterine growth restriction affects the proteomes of the small intestine, liver, and skeletal muscle in newborn pigs. The Journal of Nutrition. 2008;138(1):60-66.

    Not in our library10.1093/jn/138.1.60

  94. 94.

    Armengaud J., Yzydorczyk C., Siddeek B., Peyter A., Simeoni U. Intrauterine growth restriction: Clinical consequences on health and disease at adulthood. Reproductive Toxicology. 2021;99:168-176.

    Not in our library10.1016/j.reprotox.2020.10.005

  95. 95.

    Rashid C. S., Bansal A., Simmons R. A. Oxidative stress, intrauterine growth restriction, and developmental programming of type 2 diabetes. Physiology. 2018;33(5):348-359.

    Not in our library10.1152/physiol.00023.2018

  96. 96.

    Garcia-Contreras C., Vazquez-Gomez M., Pardo Z., et al. Polyphenols and IUGR pregnancies: effects of maternal hydroxytyrosol supplementation on hepatic fat accretion and energy and fatty acids profile of fetal tissues. Nutrients. 2019;11(7):p. 1534.

    Not in our library10.3390/nu11071534

  97. 97.
    The effects of oxidative stress on female reproduction: a review · 2012
    No notice
  98. 98.

    Jauniaux E., Gulbis B., Burton G. J. Physiological implications of the materno-fetal oxygen gradient in human early pregnancy. Reproductive Biomedicine Online. 2003;7(2):250-253.

    Not in our library10.1016/s1472-6483(10)61760-9

  99. 99.

    Benjamin D., Sharma R. K., Moazzam A., Agarwal A. Methods for the detection of ROS in human sperm samples. Studies on men's health and fertility. 2012;257-273.

    Not in our library

  100. 100.

    El Hachem H., Crepaux V., May-Panloup P., Descamps P., Legendre G., Bouet P. E. Recurrent pregnancy loss: current perspectives. International Journal of Women's Health. 2017;Volume 9:331-345.

    Not in our library10.2147/ijwh.s100817

  101. 101.

    Homer H. A. Modern management of recurrent miscarriage. Australian and New Zealand Journal of Obstetrics and Gynaecology. 2019;59(1):36-44.

    Not in our library10.1111/ajo.12920

  102. 102.

    Coughlan M., Vervaart P., Permezel M., Georgiou H., Rice G. Altered placental oxidative stress status in gestational diabetes mellitus. Placenta. 2004;25(1):78-84.

    Not in our library10.1016/s0143-4004(03)00183-8

  103. 103.

    Sacks D. A., Hadden D. R., Maresh M., et al. Frequency of gestational diabetes mellitus at collaborating centers based on IADPSG consensus panel–recommended criteria: the hyperglycemia and adverse pregnancy outcome (HAPO) study. Diabetes Care. 2012;35(3):526-528.

    Not in our library10.2337/dc11-1641

  104. 104.

    Gauster M., Desoye G., Tötsch M., Hiden U. The placenta and gestational diabetes mellitus. Current Diabetes Reports. 2012;12(1):16-23.

    Not in our library10.1007/s11892-011-0244-5

  105. 105.

    Lekva T., Norwitz E. R., Aukrust P., Ueland T. Impact of systemic inflammation on the progression of gestational diabetes mellitus. Current Diabetes Reports. 2016;16(4):p. 26.

    Not in our library10.1007/s11892-016-0715-9

  106. 106.

    Pendeloski K. P. T., Mattar R., Torloni M. R., Gomes C. P., Alexandre S. M., Daher S. Immunoregulatory molecules in patients with gestational diabetes mellitus. Endocrine. 2015;50(1):99-109.

    Not in our library10.1007/s12020-015-0567-0

  107. 107.

    Xie B. G., Jin S., Zhu W. J. Expression of toll-like receptor 4 in maternal monocytes of patients with gestational diabetes mellitus. Experimental and Therapeutic Medicine. 2014;7(1):236-240.

    Not in our library10.3892/etm.2013.1360

  108. 108.

    Robakis T. K., Aasly L., Williams K. E., Clark C., Rasgon N. L. Roles of inflammation and depression in the development of gestational diabetes. Current Behavioral Neuroscience Reports. 2017;4(4):369-383.

    Not in our library10.1007/s40473-017-0131-8

  109. 109.

    Lappas M., Hiden U., Desoye G., Froehlich J., Mouzon S. H. D., Jawerbaum A. The role of oxidative stress in the pathophysiology of gestational diabetes mellitus. Antioxidants & Redox Signaling. 2011;15(12):3061-3100.

    Not in our library10.1089/ars.2010.3765

  110. 110.

    Ruder E. H., Hartman T. J., Blumberg J., Goldman M. B. Oxidative stress and antioxidants: exposure and impact on female fertility. Human Reproduction Update. 2008;14(4):345-357.

    Not in our library10.1093/humupd/dmn011

  111. 111.
    The effects of oxidative stress on female reproduction: a review · 2012
    No notice
  112. 112.

    Mironczuk-Chodakowska I., Witkowska A. M., Zujko M. E. Endogenous non-enzymatic antioxidants in the human body. Advances in Medical Sciences. 2018;63(1):68-78.

    Not in our library10.1016/j.advms.2017.05.005

  113. 113.

    Ledee-Bataille N., Olivennes F., Lefaix J. L., Chaouat G., Frydman R., Delanian S. Combined treatment by pentoxifylline and tocopherol for recipient women with a thin endometrium enrolled in an oocyte donation programme. Human Reproduction. 2002;17(5):1249-1253.

    Not in our library10.1093/humrep/17.5.1249

  114. 114.

    Thomson R. L., Spedding S., Buckley J. D. Vitamin D in the aetiology and management of polycystic ovary syndrome. Clinical Endocrinology. 2012;77(3):343-350.

    Not in our library10.1111/j.1365-2265.2012.04434.x

  115. 115.

    Showell M. G., Mackenzie-Proctor R., Jordan V., Hart R. J. Antioxidants for female subfertility. Cochrane Database of Systems Review. 2017;7, article CD007807.

    Not in our library10.1002/14651858.cd007807.pub3

  116. 116.

    Smits R. M., Mackenzie-Proctor R., Fleischer K., Showell M. G. Antioxidants in fertility: impact on male and female reproductive outcomes. Fertility and Sterility. 2018;110(4):578-580.

    Not in our library10.1016/j.fertnstert.2018.05.028

  117. 117.

    Mahmood N., Hameed A., Hussain T. Vitamin E and Selenium Treatment Alleviates Saline Environment-Induced Oxidative Stress through Enhanced Antioxidants and Growth Performance in Suckling Kids of Beetal Goats. Oxidative Medicine and Cellular Longevity. 2020;2020:16.

    Not in our library10.1155/2020/4960507

  118. 118.

    Afzal A., Hussain T., Hameed A. Moringa oleifera supplementation improves antioxidant status and biochemical indices by attenuating early pregnancy stress in Beetal goats. Frontiers in Nutrition. 2021;8:p. 444.

    Not in our library10.3389/fnut.2021.700957

  119. 119.

    Abdul-Barry J., Al-Rubai S. A., Qasim Q. A. Study of Oxidant-Antioxidant status in recurrent spontaneous abortion. TQMJ. 2011;5:35-46.

    Not in our library

  120. 120.

    al-Kunani A. S., Knight R., Haswell S. J., Thompson J. W., Lindow S. W. The selenium status of women with a history of recurrent miscarriage. British Journal of Obstetrics and Gynaecology. 2001;108(10):1094-1097.

    Not in our library10.1111/j.1471-0528.2001.00253.x

  121. 121.

    Reece E. A. Maternal Fuels, Diabetic Embryopathy: Pathomechanisms and Prevention. Seminars in Reproductive Medicine. 1999;17(2):183-194.

    Not in our library10.1055/s-2007-1016225

  122. 122.

    Malvy E., Thiébaut R., Marimoutou C., Dabis F., the Groupe d’Epidémiologie Clinique du Sida en Aquitaine. “Weight loss and body mass index as predictors of HIV disease progression to AIDS in adults”, Aquitaine cohort, France, 1985-1997. Journal of American College Nutrition. 2001;20(6):609-615.

    Not in our library10.1080/07315724.2001.10719065

  123. 123.

    Maged A. M., Torky H., Fouad M. A., et al. Role of antioxidants in gestational diabetes mellitus and relation to fetal outcome: a randomized controlled trial. Journal of Maternal-Fetal & Neonatal Medicine. 2016;29(24):4049-4054.

    Not in our library10.3109/14767058.2016.1154526

  124. 124.

    Nath B., Roy H. Antioxidants in Female Reproductive Biology. Antioxidants-Benefits, Sources, Mechanisms of Action. 2021.

    Not in our library10.5772/intechopen.95937

  125. 125.

    Parraguez V. H., Sales F., Peralta O. A., et al. Maternal Supplementation with Herbal Antioxidants during Pregnancy in Swine. Antioxidants. 2021;10(5):p. 658.

    Not in our library10.3390/antiox10050658

  126. 126.

    Taravati A., Tohidi F. Comprehensive analysis of oxidative stress markers and antioxidants status in preeclampsia. Taiwanese Journal of Obstetrics and Gynecology. 2018;57(6):779-790.

    Not in our library10.1016/j.tjog.2018.10.002

  127. 127.

    Idogun E. S., Odiegwu M. E., Momoh S. M., Okonofua F. E. Effect of pregnancy on total antioxidant capacity in Nigerian women. Pakistan Journal of Medical Sciences. 2008;24(2):p. 292.

    Not in our library

  128. 128.

    Ly C., Yockell-Lelièvre J., Ferraro Z. M., Arnason J. T., Ferrier J., Gruslin A. The effects of dietary polyphenols on reproductive health and early development. Human Reproduction Update. 2015;21(2):228-248.

    Not in our library10.1093/humupd/dmu058

  129. 129.

    Al-Gubory K. H., Fowler P. A., Garrel C. The roles of cellular reactive oxygen species, oxidative stress and antioxidants in pregnancy outcomes. The International Journal of Biochemistry & Cell Biology. 2010;42(10):1634-1650.

    Not in our library10.1016/j.biocel.2010.06.001

  130. 130.

    Ni H., Yu X. J., Liu H. J., et al. Progesterone regulation of glutathione S-transferase Mu2 expression in mouse uterine luminal epithelium during preimplantation period. Fertility and Sterility. 2009;91(5):2123-2130.

    Not in our library10.1016/j.fertnstert.2008.04.053

  131. 131.

    Garrel C., Fowler P. A., Al-Gubory K. H. Developmental changes in antioxidant enzymatic defences against oxidative stress in sheep placentomes. Journal of Endocrinology. 2010;205:107-116.

    Not in our library10.1677/joe-09-0362

  132. 132.

    Borchert A., Wang C. C., Ufer C., Schiebel H., Savaskan N. E., Kuhn H. The Role of Phospholipid Hydroperoxide Glutathione Peroxidase Isoforms in Murine Embryogenesis∗. Journal of Biological Chemisry. 2006;281(28):19655-19664.

    Not in our library10.1074/jbc.m601195200

  133. 133.

    Warren A. Y., Matharoo-Ball B., Shaw R. W., Khan R. N. Hydrogen peroxide and superoxide anion modulate pregnant human myometrial contractility. Reproduction. 2005;130(4):539-544.

    Not in our library10.1530/rep.1.00437

  134. 134.

    al-Gubory K.¨. H., Bolifraud P., Germain G., Nicole A., Ceballos-Bicot I.`. Antioxidant enzymatic defence systems in sheep corpus luteum throughout pregnancy. Reproduction. 2004;128(6):767-774.

    Not in our library10.1530/rep.1.00389

  135. 135.

    Lapointe J., Bilodeau J. F. Antioxidant defenses are modulated in the cow oviduct during the estrous cycle. Biology of Reproduction. 2003;68(4):1157-1164.

    Not in our library10.1095/biolreprod.102.007476

  136. 136.

    Sugino N., Takiguchi S., Kashida S., Karube A., Nakamura Y., Kato H. Superoxide dismutase expression in the human corpus luteum during the menstrual cycle and in early pregnancy. Molecular Human Reproduction. 2000;6(1):19-25.

    Not in our library10.1093/molehr/6.1.19

  137. 137.

    Jauniaux E., Watson A. L., Hempstock J., Bao Y. P., Skepper J. N., Burton G. J. Onset of Maternal Arterial Blood Flow and Placental Oxidative Stress: A Possible Factor in Human Early Pregnancy Failure. American Journal of Pathology. 2000;157(6):2111-2122.

    Not in our library10.1016/s0002-9440(10)64849-3

  138. 138.

    Qanungo S., Mukherjea M. Ontogenic profile of some antioxidants and lipid peroxidation in human placental and fetal tissues. Molecular and Cellular Biochemistry. 2000;215(1/2):11-19.

    Not in our library10.1023/a:1026511420505

  139. 139.

    Baiza-Gutman L. A., Flores-Sánchez M. M., Díaz-Flores M., Hicks J. J. Presence of uterine peroxidase activity in the rat early pregnancy. International Journal of Biochemistry & Cellular Biology. 2000;32(2):255-262.

    Not in our library10.1016/s1357-2725(99)00061-8

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