Journal articles: 'Estrogenic stress'

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Krolick, Kristen N., and Haifei Shi. "Estrogenic Action in Stress-Induced Neuroendocrine Regulation of Energy Homeostasis." Cells 11, no. 5 (March 3, 2022): 879. http://dx.doi.org/10.3390/cells11050879.

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Estrogens are among important contributing factors to many sex differences in neuroendocrine regulation of energy homeostasis induced by stress. Research in this field is warranted since chronic stress-related psychiatric and metabolic disturbances continue to be top health concerns, and sex differences are witnessed in these aspects. For example, chronic stress disrupts energy homeostasis, leading to negative consequences in the regulation of emotion and metabolism. Females are known to be more vulnerable to the psychological consequences of stress, such as depression and anxiety, whereas males are more vulnerable to the metabolic consequences of stress. Sex differences that exist in the susceptibility to various stress-induced disorders have led researchers to hypothesize that gonadal hormones are regulatory factors that should be considered in stress studies. Further, estrogens are heavily recognized for their protective effects on metabolic dysregulation, such as anti-obesogenic and glucose-sensing effects. Perturbations to energy homeostasis using laboratory rodents, such as physiological stress or over-/under- feeding dietary regimen prevalent in today’s society, offer hints to the underlying mechanisms of estrogenic actions. Metabolic effects of estrogens primarily work through estrogen receptor α (ERα), which is differentially expressed between the sexes in hypothalamic nuclei regulating energy metabolism and in extrahypothalamic limbic regions that are not typically associated with energy homeostasis. In this review, we discuss estrogenic actions implicated in stress-induced sex-distinct metabolic disorders.

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Blaize, Jonathan, William J. L’Amoreaux, Maureen Downey, and Elena C. McCoy. "Dibutylphthalate and Tween 80 alter ultrastructure inCandida albicans: implications for peroxisome proliferation." Canadian Journal of Microbiology 55, no. 4 (April 2009): 437–49. http://dx.doi.org/10.1139/w08-153.

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Phthalates are ubiquitous environmental pollutants associated with endocrine disruption and peroxisome proliferation in experimental animals. In yeasts exposed to environmental chemicals, including phthalates, alterations in cell growth, cellular morphology, and H2O2detoxification occur. Nutrient availability also influences diverse cellular processes. Differences in responses to environmental stress between Candida albicans and the model yeast, Saccharomyces cerevesiae , have been reported. In this study, we chose C. albicans as an alternate model for testing estrogen-like chemicals because of its high affinity estrogen-binding protein and, in contrast to S. cerevesiae, estrogens are not growth inhibitory for C. albicans. Cultures were grown in either yeast nitrogen dextrose (YND; phosphate limiting) or YNDP (YND plus 100 mmol/L inorganic phosphate). For chemical testing, 0.5% dibutylphthalate (DBP), 0.05% Tween 80, or a combination of the two (DBPT) were incorporated in growth media to investigate the effects of these estrogenic agents on cell proliferation, morphology, and catalase demonstration. We observed significant differences in cell growth related to DBP and changes in cell wall thickness related to both Tween 80 and phosphate. We describe ultrastructural changes including detachment of the outer yeast cell wall layer and presence of putative peroxisomes. Our findings support the proposal that C. albicans may be particularly suitable for use in studies involving cellular responses associated with exposure to estrogenic chemicals contained in complex mixtures.

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Torrens-Mas, Margalida, and Pilar Roca. "Phytoestrogens for Cancer Prevention and Treatment." Biology 9, no. 12 (November 27, 2020): 427. http://dx.doi.org/10.3390/biology9120427.

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Phytoestrogens are a large group of natural compounds found in more than 300 plants. They have a close structural similarity to estrogens, which allow them to bind to both estrogen receptors (ER), ERα and ERβ, presenting a weak estrogenic activity. Phytoestrogens have been described as antioxidant, anti-inflammatory, anti-thrombotic, anti-allergic, and anti-tumoral agents. Their role in cancer prevention has been well documented, although their impact on treatment efficiency is controversial. Several reports suggest that phytoestrogens may interfere with the effect of anti-cancer drugs through the regulation of oxidative stress and other mechanisms. Furthermore, some phytoestrogens could exert a protective effect on healthy cells, thus reducing the secondary effects of cancer treatment. In this review, we have studied the recent research in this area to find evidence for the role of phytoestrogens in cancer prevention and therapy efficacy.

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Chung, S. C., A. H. Goldfarb, A. Jamurtas, S. Hegde, and J. Lee. "ESTROGENIC EFFECT ON EXERCISE-INDUCED OXIDATIVE STRESS 545." Medicine &amp Science in Sports &amp Exercise 29, Supplement (May 1997): 94. http://dx.doi.org/10.1097/00005768-199705001-00544.

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Lundholm, Lovisa, Milica Putnik, Michio Otsuki, Sandra Andersson, Claes Ohlsson, Jan-Åke Gustafsson, and Karin Dahlman-Wright. "Effects of estrogen on gene expression profiles in mouse hypothalamus and white adipose tissue: target genes include glutathione peroxidase 3 and cell death-inducing DNA fragmentation factor, α-subunit-like effector A." Journal of Endocrinology 196, no. 3 (December 21, 2007): 547–57. http://dx.doi.org/10.1677/joe-07-0277.

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Obesity has become a major health problem in many parts of the world. Estrogens are known to reduce adipose tissue mass in both humans and animals but the molecular mechanisms are not well characterized. We used gene expression profiling to study long-term effects of estrogen on gene expression in mouse white adipose tissue and hypothalamus. Overall, the effects of estrogen on hypothalamic gene expression were much smaller than the corresponding effects on white adipose tissue gene expression. We characterize in detail estrogenic regulation of glutathione peroxidase 3 (GPX3). Our studies suggest that GPX3 is a direct estrogen receptor α target gene in white adipose tissue. Since obesity is correlated with oxidative stress, and GPX3 has been demonstrated to be lower in obesity and higher after weight loss, we hypothesize that GPX3 is one important mediator of effects of estrogen in relation to fat mass. Additional genes that were affected by estrogen in adipose tissue include cell death-inducing DNA fragmentation factor, α-subunit-like effector A (CIDEA), a gene shown to be related to body fat in mice. We conclude that estrogen has large effects on gene expression in white adipose tissue and hypothesize that GPX3 and CIDEA could be important mediators of the effects of estrogen on fat mass.

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Cheng, Michelle Y., Guohua Sun, Michael Jin, Heng Zhao, Gary K. Steinberg, and Robert M. Sapolsky. "Blocking Glucocorticoid and Enhancing Estrogenic Genomic Signaling Protects against Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 29, no. 1 (September 17, 2008): 130–36. http://dx.doi.org/10.1038/jcbfm.2008.105.

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Glucocorticoids (GCs) and estrogen can modulate neuron death and dysfunction during neurological insults. Glucocorticoids are adrenal steroids secreted during stress, and hypersecretion of GCs during cerebral ischemia compromises the ability of hippocampal and cortical neurons to survive. In contrast, estrogen can be neuroprotective after cerebral ischemia. Here we evaluate the protective potential of a herpes viral vector expressing a chimeric receptor (ER/GR), which is composed of the ligand-binding domain of the GC receptor (GR) and the DNA-binding domain of the estrogen receptor-α (ER). This novel receptor can transduce an endangering GC signal into a protective estrogenic one. Using an in vitro oxygen glucose deprivation model (OGD), GCs exacerbated neuron death in primary cortical cultures, and this worsening effect was completely blocked by ER/GR expression. Moreover, blocking GC actions with a vector expressing a dominant negative GC receptor promoted neuron survival during postischemia, but not preischemia. Thus, gene therapeutic strategies to modulate GC and estrogen signaling can be beneficial during an ischemic insult.

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Kim, Kangmin, Jin-Sook Kwon, Changhwan Ahn, and Eui-Bae Jeung. "Endocrine-Disrupting Chemicals and Their Adverse Effects on the Endoplasmic Reticulum." International Journal of Molecular Sciences 23, no. 3 (January 29, 2022): 1581. http://dx.doi.org/10.3390/ijms23031581.

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There is growing concern regarding the health and safety issues of endocrine-disrupting chemicals (EDCs). Long-term exposure to EDCs has serious adverse health effects through both hormone-direct and hormone-indirect ways. Accordingly, some EDCs can be a pathogen and an inducer to the susceptibility of disease, even if they have a very low affinity on the estrogen receptor, or no estrogenic effect. Endoplasmic reticulum (ER) stress recently attracted attention in this research area. Because ER and ER stress could be key regulators of the EDC’s adverse effects, such as the malfunction of the organ, as well as the death, apoptosis, and proliferation of a cell. In this review, we focused on finding evidence which shows that EDCs could be a trigger for ER stress and provide specific examples of EDCs, which are known to cause ER stress currently.

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Wang, Long, Zhi-Ping Tang, Wei Zhao, Bing-Hai Cong, Jian-Qiang Lu, Xiao-Lu Tang, Xiao-Han Li, Xiao-Yan Zhu, and Xin Ni. "MiR-22/Sp-1 Links Estrogens With the Up-Regulation of Cystathionine γ-Lyase in Myocardium, Which Contributes to Estrogenic Cardioprotection Against Oxidative Stress." Endocrinology 156, no. 6 (June 1, 2015): 2124–37. http://dx.doi.org/10.1210/en.2014-1362.

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Abstract Hydrogen sulfide, generated in the myocardium predominantly via cystathionine-γ-lyase (CSE), is cardioprotective. Our previous study has shown that estrogens enhance CSE expression in myocardium of female rats. The present study aims to explore the mechanisms by which estrogens regulate CSE expression, in particular to clarify the role of estrogen receptor subtypes and the transcriptional factor responsible for the estrogenic effects. We found that either the CSE inhibitor or the CSE small interfering RNA attenuated the protective effect of 17β-estradiol (E2) against H2O2- and hypoxia/reoxygenation-induced injury in primary cultured neonatal cardiomyocytes. E2 stimulates CSE expression via estrogen receptor (ER)-α both in cultured cardiomyocytes in vitro and in the myocardium of female mice in vivo. A specificity protein-1 (Sp-1) consensus site was identified in the rat CSE promoter and was found to mediate the E2-induced CSE expression. E2 increases ERα and Sp-1 and inhibits microRNA (miR)-22 expression in myocardium of ovariectomized rats. In primary cardiomyocytes, E2 stimulates Sp-1 expression through the ERα-mediated down-regulation of miR-22. It was confirmed that both ERα and Sp-1 were targeted by miR-22. In the myocardium of ovariectomized rats, the level of miR-22 inversely correlated to CSE, ERα, Sp-1, and antioxidant biomarkers and positively correlated to oxidative biomarkers. In summary, this study demonstrates that estrogens stimulate Sp-1 through the ERα-mediated down-regulation of miR-22 in cardiomyocytes, leading to the up-regulation of CSE, which in turn results in an increase of antioxidative defense. Interaction of ERα, miR-22, and Sp-1 may play a critical role in the control of oxidative stress status in the myocardium of female rats.

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Surico, Daniela, Alfredo Ercoli, Serena Farruggio, Giulia Raina, Davide Filippini, David Mary, Rosalba Minisini, Nicola Surico, Mario Pirisi, and Elena Grossini. "Modulation of Oxidative Stress by 17 β-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro." Cellular Physiology and Biochemistry 42, no. 3 (2017): 1051–62. http://dx.doi.org/10.1159/000478752.

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Background/Aims: estrogens and phytoestrogens exert hepatoprotection through mechanisms not clearly examined yet. Here, we investigated the protective effects exerted by 17β-estradiol and genistein against oxidative stress in hepatocytes and hepatic stellate cells (HSCs) and the involvement of specific receptors and the intracellular signalling. Methods: Huh7.5 and LX-2, alone or in co-culture with Huh7.5, were treated with 17β-estradiol and genistein alone or in the presence of menadione and of estrogen receptors (ERs) and G protein-coupled-estrogenic-receptors (GPER) blockers. Cell viability, mitochondrial membrane potential and oxidant/antioxidant system were measured by specific kits. Western Blot was used for the analysis of Akt and p38-mitogen-activated-protein kinases (MAPK) activation and α-smooth-muscle actin expression. Results: In Huh7.5, 17β-estradiol and genistein prevented the effects of peroxidation by modulating Akt and p38MAPK activation. Similar antioxidant and protective findings were obtained in LX-2 of co-culture experiments, only. ERs and GPER blockers were able to prevent the effects of 17β-estradiol and genistein. Conclusion: In Huh7.5 and LX-2, 17β-estradiol and genistein counteract the effects of peroxidation through the involvement of ERs and GPER and by an intracellular signalling related to Akt and p38MAPK. As concerning LX-2, paracrine factors released by Huh7.5 play a key role in protection against oxidative stress.

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Liu, Suhuan, and Franck Mauvais-Jarvis. "Minireview: Estrogenic Protection of β-Cell Failure in Metabolic Diseases." Endocrinology 151, no. 3 (December 4, 2009): 859–64. http://dx.doi.org/10.1210/en.2009-1107.

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The prevalence of diabetes is lower in premenopausal women, especially diabetic syndromes with insulin deficiency, suggesting that the female hormone 17β-estradiol protects pancreatic β-cell function. In classical rodent models of β-cell failure, 17β-estradiol at physiological concentrations protects pancreatic β-cells against lipotoxicity, oxidative stress, and apoptosis. In this review, we integrate evidence showing that estrogens and their receptors have direct effects on islet biology. The estrogen receptor (ER)-α, ERβ, and the G-protein coupled ER are present in β-cells and enhance islet survival. They also improve islet lipid homeostasis and insulin biosynthesis. We also discuss evidence that ERs modulate insulin sensitivity and energy homeostasis, which indirectly alter β-cell biology in diabetic and obese conditions.

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Agca, Cansu, James E. Ries, Sarah J. Kolath, Jae-Hwan Kim, Lawrence J. Forrester, Eric Antoniou, Kristin M. Whitworth, et al. "Luteinization of porcine preovulatory follicles leads to systematic changes in follicular gene expression." Reproduction 132, no. 1 (July 2006): 133–45. http://dx.doi.org/10.1530/rep.1.01163.

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The LH surge initiates the luteinization of preovulatory follicles and causes hormonal and structural changes that ultimately lead to ovulation and the formation of corpora lutea. The objective of the study was to examine gene expression in ovarian follicles (n= 11) collected from pigs (Sus scrofa domestica) approaching estrus (estrogenic preovulatory follicle;n= 6 follicles from two sows) and in ovarian follicles collected from pigs on the second day of estrus (preovulatory follicles that were luteinized but had not ovulated;n= 5 follicles from two sows). The follicular status within each follicle was confirmed by follicular fluid analyses of estradiol and progesterone ratios. Microarrays were made from expressed sequence tags that were isolated from cDNA libraries of porcine ovary. Gene expression was measured by hybridization of fluorescently labeled cDNA (preovulatory estrogenic or -luteinized) to the microarray. Microarray analyses detected 107 and 43 genes whose expression was decreased or increased (respectively) during the transition from preovulatory estrogenic to -luteinized (P<0.01). Cells within preovulatory estrogenic follicles had a gene-expression profile of proliferative and metabolically active cells that were responding to oxidative stress. Cells within preovulatory luteinized follicles had a gene-expression profile of nonproliferative and migratory cells with angiogenic properties. Approximately, 40% of the discovered genes had unknown function.

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Liu, Xiaozhen, Yangjie Chen, Shaoping Nie, Fuxiang Li, Zhaoliang Zhu, Gaoyi Peng, Qiang Yu, and Mingyong Xie. "Oxidative Stress and Apoptosis Contributed to Nonylphenol-Induced Cell Damage in Mouse NCTC Clone 1469 Cells." Journal of Chemistry 2020 (September 26, 2020): 1–14. http://dx.doi.org/10.1155/2020/1468071.

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Nonylphenol (NP) is considered an environmental toxicant and endocrine-disrupting compound. The present study aimed to investigate the effects of NP on NCTC Clone 1469, nonparenchymal hepatocytes, and to study the molecular basis of NP-induced liver injury. The results showed that NP decreased cell viability and induced nucleus crenulation and intracellular enzyme leakage in NCTC Clone 1469 cells. Additionally, NP-induced oxidative stress and apoptosis of NCTC Clone 1469 are accompanied by upregulating reactive oxygen species (ROS) production, increase of Bax, decrease of Bcl-2, activation of caspase-3 and caspase-12, and release of cytosolic free Ca2+ in the cells. ROS scavenger, N-acetyl-L-cysteine (NAC), prevented the intracellular enzyme leakage induced by NP. NP induced alteration of estrogen receptor- (ER-) α and ER-β expression, while ER antagonists, ICI 182,780, showed no effect on NP-induced intracellular enzyme leakage. We proposed that NP triggered cell damage via inducing oxidative stress and apoptosis in cells, but not estrogenic effect.

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Dixon, Aaron, Evelyn G. Rowan, Allison N. Yackley, and Erin P. Hines. "PFAS Modulate Osmotic Signaling Independent of Gravimetric Changes in the Rat Uterus." Toxics 12, no. 3 (February 23, 2024): 170. http://dx.doi.org/10.3390/toxics12030170.

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Various PFAS have been identified as potential endocrine-disrupting chemicals due to estrogen receptor activation, impacts on puberty timing, or impacts on hormonally sensitive endpoints in fish. This study screened multiple PFAS in the rat uterotrophic assay to determine potential estrogenic effects on the uterus with PFAS exposure. This study also explored PFAS-dependent uterine signaling with an osmotic stress mRNA gene expression array. Briefly, Sprague–Dawley rats (26–39 days old) were ovariectomized, and uterine tissue was allowed to regress for a 3-week period of recovery. Animals were then exposed daily via oral gavage to PFAS for 4 days, and then uterine weight was determined. In contrast to the positive control estrogens, the PFAS tested (4:2, 6:2, and 8:2FTOH; perfluorooctanesulfonamide (PFOSA), perfluorononanoic acid (PFNA), perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS), nafion byproduct 2 (NBP2), 1H,1H,8H,8H-perfluorooctane-1,8-diol (FC8-diol) and 1H,1H,10H,10H-perfluorodecane-1,10-diol (FC10-diol)) caused no significant changes in the uterine weight. Hormonally active compounds can act as carcinogens, and because earlier rodent work has demonstrated that chronic PFOA exposure is associated with increased risk of uterine cancer, uterine mRNA gene expression was explored with an osmotic stress RT-qPCR array. PFAS exposure significantly upregulated multiple genes across the array, with PFOSA being the compound most similar to the reference estrogens (estradiol benzoate and ethinyl estradiol) in its expression pattern. Also, across all PFAS, pathway analysis revealed that the paxillin pathway, a pathway important in tumor suppressor gene SHP-2 signaling, was significantly upregulated with PFAS exposure. These results demonstrate that in vitro estrogen screens or impacts in fish may show different responses from direct impacts on mammalian uterine weight as assessed with the uterotrophic assay. This study also builds out new mechanisms that may contribute to understanding of carcinogenic changes seen in the uterus after PFAS exposure.

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Peng, Shuhan, Shengkun Dong, Chang Gong, Xiaohong Chen, Hongyu Du, Yuehao Zhan, and Changxin Ye. "Identification of Breast-Cancer-Associated Properties of Drinking Water under a Composite-Toxicity Perspective of Mixed Contaminants: A Case Study in a High-Prevalence Area of China." Water 16, no. 5 (February 28, 2024): 702. http://dx.doi.org/10.3390/w16050702.

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Breast cancer is the most frequently diagnosed female cancer worldwide. Environmental contaminant exposure is suspected to be crucial, but the broad-spectrum communal properties that these suspected contaminants all share remain to be explored, especially in source and drinking water. In this work, we focused on the Pearl River Basin, which has the highest breast cancer incidence and mortality in China, and hypothesized that the breast cancer risk in this area is associated with its water source. Our objective was to resolve the possible communal properties that are associated with breast cancer from water mixture extracts of source and drinking water and to identify the key drivers by utilizing the latest epidemiology data, performing an exhaustive water toxicological and chemical characterization, and combining partial least-squares path statistics modeling (PLS-PM). We proposed a path for a drinking water-toxicity-induced breast cancer risk and confirmed its association with estrogen-receptor- and thiol-depletion-relevant mechanisms. The breast cancer incidence risk was associated with water-mixture-promoted mammalian cell proliferation (i.e., estrogenic effect), while the mortality risk was associated with a greater thiol depletion (i.e., oxidative stress). Endocrine-disrupting chemicals (EDCs) and dissolved organic matter (DOM) from anthropogenic sources in drinking water are key drivers for estrogenic effects and oxidative stress, respectively. The PLS-PM standardized effects of the DOM and EDCs in treated water on the breast cancer incidence and mortality were −0.07 and 0.31, and 0.35 and 0.31, respectively, further revealing that EDCs strongly influence the incidence risk, whereas the mortality risk resulted from the joint effects of EDCs and DOM. This study clearly shows an association between the breast cancer risk and drinking water toxicity in a high-prevalence area of China, broadening the future perspectives for water-contaminant-specific breast cancer prevention research.

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Bell, James R., Gabriel B. Bernasochi, Upasna Varma, Wah Chin Boon, Stuart J. Ellem, Gail P. Risbridger, and Lea M. D. Delbridge. "Aromatase transgenic upregulation modulates basal cardiac performance and the response to ischemic stress in male mice." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 9 (May 1, 2014): H1265—H1274. http://dx.doi.org/10.1152/ajpheart.00012.2014.

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Estrogen in females is conventionally considered a cardioprotective influence, but a role for estrogen in male cardioprotection has yet to be defined. Estrogen biosynthesis from testosterone is regulated by aromatase. Aromatase has recently been shown to be expressed in the adult heart, although little is known about its involvement in the regulation of myocardial function and stress responses. The goal of this study was to determine whether upregulation of tissue aromatase expression could improve ischemic resilience in male hearts. Isolated hearts from male transgenic aromatase-overexpressing (AROM+; high estrogen, low testosterone) mice and wild-type (WT) mice (12 wk) were Langendorff perfused and subjected to ischemia-reperfusion (25 min ischemia and 60 min of reperfusion). Basal systolic function was lower in AROM+ hearts (dP/d tmax: 4,121 ± 255 vs. 4,992 ± 283 mmHg/s, P < 0.05) and associated with augmented Akt phosphorylation, consistent with a suppressor action of estrogen on contractility. Ischemic contracture was attenuated in AROM+ hearts (43 ± 3 vs. 55 ± 4 mmHg, P < 0.05), yet AROM+ hearts were more arrhythmic in early reperfusion. At the end of 60 min of reperfusion, AROM+ systolic functional recovery was lower (left ventricular developed pressure: 39 ± 6 vs. 56 ± 5 %basal, P < 0.05) and diastolic dysfunction was accentuated (36 ± 4 vs. 24 ± 2 mmHg, P < 0.05). This is the first study to show that in vivo aromatase upregulation modulates basal cardiac performance and the response to ischemic stress. These data suggest that while chronic exposure to enhanced estrogenic influence may have benefits in limiting ischemic contracture severity, acute functional recovery in reperfusion is compromised. A temporally targeted, tissue-specific intervention combining aromatase treatment with inotropic support may offer therapeutic potential for men and women.

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Jordan, V. Craig. "The new biology of estrogen-induced apoptosis applied to treat and prevent breast cancer." Endocrine-Related Cancer 22, no. 1 (October 22, 2014): R1—R31. http://dx.doi.org/10.1530/erc-14-0448.

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The successful use of high-dose synthetic estrogens to treat postmenopausal metastatic breast cancer is the first effective ‘chemical therapy’ proven in clinical trial to treat any cancer. This review documents the clinical use of estrogen for breast cancer treatment or estrogen replacement therapy (ERT) in postmenopausal hysterectomized women, which can either result in breast cancer cell growth or breast cancer regression. This has remained a paradox since the 1950s until the discovery of the new biology of estrogen-induced apoptosis at the end of the 20th century. The key to triggering apoptosis with estrogen is the selection of breast cancer cell populations that are resistant to long-term estrogen deprivation. However, estrogen-independent growth occurs through trial and error. At the cellular level, estrogen-induced apoptosis is dependent upon the presence of the estrogen receptor (ER), which can be blocked by nonsteroidal or steroidal antiestrogens. The shape of an estrogenic ligand programs the conformation of the ER complex, which, in turn, can modulate estrogen-induced apoptosis: class I planar estrogens (e.g., estradiol) trigger apoptosis after 24 h, whereas class II angular estrogens (e.g., bisphenol triphenylethylene) delay the process until after 72 h. This contrasts with paclitaxel, which causes G2 blockade with immediate apoptosis. The process is complete within 24 h. Estrogen-induced apoptosis is modulated by glucocorticoids and cSrc inhibitors, but the target mechanism for estrogen action is genomic and not through a nongenomic pathway. The process is stepwise through the creation of endoplasmic reticulum stress and inflammatory responses, which then initiate an unfolded protein response. This, in turn, initiates apoptosis through the intrinsic pathway (mitochondrial) with the subsequent recruitment of the extrinsic pathway (death receptor) to complete the process. The symmetry of the clinical and laboratory studies now permits the creation of rules for the future clinical application of ERT or phytoestrogen supplements: a 5-year gap is necessary after menopause to permit the selection of estrogen-deprived breast cancer cell populations to cause them to become vulnerable to apoptotic cell death. Earlier treatment with estrogen around menopause encourages growth of ER-positive tumor cells, as the cells are still dependent on estrogen to maintain replication within the expanding population. An awareness of the evidence that the molecular events associated with estrogen-induced apoptosis can be orchestrated in the laboratory in estrogen-deprived breast cancers now supports the clinical findings regarding the treatment of metastatic breast cancer following estrogen deprivation, decreases in mortality following long-term antihormonal adjuvant therapy, and the results of treatment with ERT and ERT plus progestin in the Women's Health Initiative for women over the age of 60. Principles have emerged for understanding and applying physiological estrogen therapy appropriately by targeting the correct patient populations.

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Roach, Crystal M., Edith J. Mayorga, Lance H. Baumgard, Jason W. Ross, and Aileen F. Keating. "81 Zearalenone Affects the Ovarian Proteome During Heat Stress in Prepubertal Gilts." Journal of Animal Science 99, Supplement_1 (May 1, 2021): 107–8. http://dx.doi.org/10.1093/jas/skab054.175.

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Abstract Zearalenone (ZEA), an estrogenic mycotoxin, causes hormonal disruption and reproductive dysfunction in pigs. Heat stress (HS) occurs when exogenous and metabolic heat accumulation exceeds heat dissipation; a scenario negatively impacting gilt reproduction. Our objective was to identify differentially abundant ovarian proteins in gilts exposed to HS +/- ZEA. We hypothesized that ZEA exposure would negatively impact the prepubertal gilt ovarian proteome and HS would be additive to ZEA-induced toxicity. Prepubertal gilts (n = 38) were assigned to one of six treatment groups: thermoneutral (TN) ad libitum control (TNCtl; n = 6); TN + ZEA (TNZea; 2 ppm; n = 6); pair-fed (PF) control (PFCtl; n = 6); PF+ ZEA (PFZea; 2 ppm; n = 6); cyclical HS control (HSCtl; n = 7); and HS + ZEA (HSZea; 2 ppm; n = 7). Gilts were subjected to TN (20 ± 1°C) or cyclic HS (35 ± 1°C for 12 h/31.6° for 12 h) conditions for 7 d. Liquid chromatography-mass spectrometry (LC-MS/MS) was performed on ovarian protein homogenates. Exposure to ZEA altered (P < 0.05) abundance of 93 proteins in TN gilts (48 increased and 45 decreased). In PF gilts, ZEA increased 50 and decreased 47 proteins (P < 0.05). During HS, ZEA differentially affected (P < 0.05) 126 proteins: 58 increased and 68 increased. Pathways impacted by either HS or ZEA alone or in combination included cellular stress, metabolic pathways, and estrogenic pathways. Thus, ZEA and HS, either alone or in combination, impact the ovarian proteome in prepubertal gilts in ways that could contribute to seasonal infertility. This project was supported by the Iowa Pork Producers Association.

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Ciribilli, Yari, Virginia Andreotti, Daniel Menendez, Jan-Stephan Langen, Gilbert Schoenfelder, Michael A. Resnick, and Alberto Inga. "The Coordinated P53 and Estrogen Receptor Cis-Regulation at an FLT1 Promoter SNP Is Specific to Genotoxic Stress and Estrogenic Compound." PLoS ONE 5, no. 4 (April 21, 2010): e10236. http://dx.doi.org/10.1371/journal.pone.0010236.

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Kowalska, Karolina, Dominika Ewa Habrowska-Górczyńska, Marta Justyna Kozieł, Kinga Anna Urbanek, Kamila Domińska, and Agnieszka Wanda Piastowska-Ciesielska. "Mycotoxin Alternariol (AOH) Affects Viability and Motility of Mammary Breast Epithelial Cells." International Journal of Molecular Sciences 22, no. 2 (January 12, 2021): 696. http://dx.doi.org/10.3390/ijms22020696.

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Mycotoxins are present in everyday diet as common food and feed pollutants. A part of them is still concerned as so-called emerging mycotoxins. Due to the lack of toxicity data, the safety limits and detail molecular mechanism have been not established yet for all of them. Alternariol (AOH), as one of these mycotoxins, produced by Alternaria species, is so far reported as an estrogenic, genotoxic, and immunomodulatory agent; however, its direct effect on human health is not known. Especially, in the case of hormone-dependent tissues which are sensitive to both endogenic, as well as external estrogenic agents, it might be crucial to assess the effect of AOH. Thus, this study evaluated how exposure to AOH affects viability and motility of the human normal mammary gland epithelial in vitro model. We observed that AOH significantly affects viability of cells in a time- and dose-dependent manner. Moreover, the induction of oxidative stress, DNA damage, and cell cycle arrest in the G2/M cell cycle phase was observed. The motility of 184A1 cells was also significantly affected. On the molecular level, AOH induced antioxidative stress response via activation of Nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway agents, as well as decrease in the phosphorylation of protein kinase B (Akt) and p44/42 (ERK 1-2) molecules, indicating that AOH might affect crucial signaling pathways in both physiological and pathophysiological processes in breast tissue.

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Jabłońska-Trypuć, Agata, Urszula Wydro, Elżbieta Wołejko, Marcin Makuła, Rafał Krętowski, Monika Naumowicz, Gabriela Sokołowska, et al. "Selected Fungicides as Potential EDC Estrogenic Micropollutants in the Environment." Molecules 28, no. 21 (November 5, 2023): 7437. http://dx.doi.org/10.3390/molecules28217437.

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An increasing level of pesticide exposition is being observed as a result of the consumption of large amounts of fruits, vegetables and grain products, which are key components of the vegetarian diet. Fungicides have been classified as endocrine-disrupting compounds, but their mechanisms of action have not yet been clarified. The effect of boscalid (B), cyprodinil (C) and iprodione (I) combined with Tamoxifen (T) and 17β-estradiol (E2) on cell viability, cell proliferation, reporter gene expression, ROS content, the cell membrane’s function, cell morphology and antioxidant enzymes gene expression in MCF-7 and T47D-KBluc cell lines were investigated. The cell lines were chosen due to their response to 17β -estradiol. The selected fungicides are commonly used in Poland to protect crops against fungi. Our results revealed that the studied fungicides caused significant increases in cell viability and proliferation, and estrogenic activity was present in all studied compounds depending on their concentrations. Oxidative stress activated uncontrolled cancer cell proliferation by inducing ROS production and by inhibiting antioxidant defense. Our findings verify that the studied fungicides could possibly exhibit endocrine-disrupting properties and exposure should be avoided.

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Grassi, D., N. Lagunas, M. Amorin, H. Pinos, G. C. Panzica, L. M. Garcia-Segura, and P. Collado. "Estrogenic regulation of NADPH-diaphorase in the supraoptic and paraventricular nuclei under acute osmotic stress." Neuroscience 248 (September 2013): 127–35. http://dx.doi.org/10.1016/j.neuroscience.2013.05.024.

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Yoo, Jisu, Jin Hur, and Jinho Jung. "Identification of oxidative stress and estrogenic activity induced by polarity fractions of effluent organic matter." Journal of Hazardous Materials 375 (August 2019): 264–72. http://dx.doi.org/10.1016/j.jhazmat.2019.05.008.

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De Luliis, Geoffry N., Katherine Zelski, and R. John Aitken. "Estrogenic Compounds Induce Oxidative Stress in Human Spermatozoa: Implications for DNA Integrity and Fertilization Success." Biology of Reproduction 78, Suppl_1 (May 1, 2008): 296. http://dx.doi.org/10.1093/biolreprod/78.s1.296c.

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Agil, Rania, Chloé Gilbert, Hamed Tavakoli, and Farah Hosseinian. "Redefining Unusable Weeds to Beneficial Plants: Purslane as a Powerful Source of Omega-3 for the Future." Journal of Food Research 4, no. 6 (November 3, 2015): 39. http://dx.doi.org/10.5539/jfr.v4n6p39.

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<p>With global consumer demand shifting towards the consumption of healthier foods, it is crucial to discover new sources of edible plants with high nutritional value and low cost. Unique weeds such as purslane have the potential to be used as an untapped source of unconventional food with diverse nutrients and beneficial bioactive properties. Inflammation can cause oxidative stress related diseases including cardiovascular disorders, aging and cancer. One key nutrient of purslane is omega-3 with potential of inhibitory properties against inflammatory and estrogenic mediators. Purslane is known to be a rich source of a-linolenic acid, 18:3 ω-3, an essential fatty acid, carotenes, antioxidants and minerals. However, the precise mechanism of action of its individual components in disease prevention is unknown. This review provides a summary on the role of purslane bioactives, particularly omega-3 fatty acids as one of purslane’s main constituents with potential of anti-inflammatory and anti-estrogenic properties. The discovery of new sources of plants rich in omega-3 fatty acids may be a useful strategy in utilizing natural alternative sources of foods that can enhance human health and wellbeing.</p>

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Akter, Reshmi, Dong Uk Yang, Jong Chan Ahn, Muhammad Awais, Jinnatun Nahar, Zelika Mega Ramadhania, Jong Yun Kim, et al. "Comparison of In Vitro Estrogenic Activity of Polygoni multiflori Radix and Cynanchi wilfordii Radix via the Enhancement of ERα/β Expression in MCF7 Cells." Molecules 28, no. 5 (February 27, 2023): 2199. http://dx.doi.org/10.3390/molecules28052199.

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Postmenopausal women experience several symptoms, including inflammation and a sharp rise in oxidative stress caused by estrogen deprivation. Although estrogen replacement therapy (ERT) is generally regarded as an effective treatment for menopause, it has been used less frequently due to some adverse effects and high costs. Therefore, there is an immediate need to develop an effective herbal-based treatment that is affordable for low-income populations. Acordingly, this study explored the estrogen-like properties of methanol extracts from Cynanchum wilfordii (CW) and Poligonum multiflorum (PM), two important medicinal plants in Republic of Korea, Japan, and China. Due to the similar names and morphologies of these two radixes, they are frequently confused in the marketplace. Our previous colleagues discriminated between these two plants. In this study, we investigated the estrogenic activity of PM and CW using several in vitro assays with their possible mechanism of action. First, their phytochemical contents, such as gallic acid, 2,3,5,4′-tetrahydroxystilbene-2-O-glucoside (TSG) and emodin, were quantified using high-performance liquid chromatography (HPLC). Secondly, estrogen-like activity was assessed utilizing the well-known E-screen test and gene expression analysis in estrogen receptor (ER)-positive MCF7 cells. ROS inhibition and anti-inflammatory effects were analyzed using HaCaT and Raw 264.7 cells, respectively. Our findings demonstrate that PM extracts significantly increased the expression of the estrogen-dependent genes (ERα, ERβ, pS2) and boosted MCF7 cell proliferation in comparison to CW extracts. Additionally, PM extract demonstrated a significant reduction in reactive oxygen species (ROS) production as well as an enhanced antioxidant profile compared to the CW extract. Further, the PM extract treatment significantly reduced the generation of nitric oxide (NO) in RAW 264.7 cells, a murine macrophage cell line, demonstrating the anti-inflammatory properties of the extract. Finally, this research offers an experimental foundation for the use of PM as a phytoestrogen to minimize menopausal symptoms.

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Litschauer, Brigitte, Georg Schaller, and Michael Wolzt. "Naloxone does not influence cardiovascular responses to mild mental stress in postmenopausal women." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H2120—H2125. http://dx.doi.org/10.1152/ajpheart.01113.2004.

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The interaction between central opioid activity, sex hormones, and the cardiovascular reactivity to stress is unknown. Twenty-eight healthy postmenopausal women, 16 without, and 12 with hormone replacement therapy (HRT) participated in this randomized, double-blind, cross-over study. The opioid receptor antagonist naloxone or placebo was administered intravenously on 2 different days and mild mental stress was induced by the Stroop Color-Word Test. Cardiovascular responses were assessed noninvasively by impedance cardiography. Stress significantly increased stroke volume, cardiac output, blood pressure, and heart rate, which was not influenced by opioid receptor blockade. Whereas naloxone increased cortisol plasma concentrations irrespective of HRT status, luteinizing hormone concentrations, which were higher in non-HRT compared with HRT women, were increased by naloxone in women with HRT only. These data suggest that the opioidergic tone of the hypothalamus-pituitary-adrenal axis persists in postmenopausal women, irrespective of HRT use, while the opioidergic tone on the hypothalamus-pituitary-gonadal axis seems to depend on an estrogenic milieu. Naloxone does not alter cardiovascular mental stress reactions in postmenopausal women independent of their hormone substitution status.

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Mukhtar, Fatima, Kashif Jilani, Ismat Bibi, Zahid Mushataq, Maham Abdul Bari Khan, and Maria Fatima. "Stimulation of Erythrocyte Membrane Blebbing by Bifenthrin Induced Oxidative Stress." Dose-Response 20, no. 1 (January 2022): 155932582210767. http://dx.doi.org/10.1177/15593258221076710.

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Background Bifenthrin is an insecticide and anti-estrogenic compound primarily used to control residential pests by depolarizing sodium gated voltage channels in the nervous system. Eryptosis, the suicidal death of erythrocytes, featured by PS exposure, membrane blebbing and cell shrinkage. Anemia is an outcome of uncontrolled eryptosis. Research Design In this study, erythrocytes were treated with different concentrations (.5-1-1.5 μM) of bifenthrin over a period of 48 hours. In order to investigate the oxidative stress induced by bifenthrin, catalase, superoxide dismutase, and glutathione peroxidase activities were investigated. Results Obtained data indicated the decrease in the enzymes (superoxide dismutase, glutathione peroxidase, and catalase) activities in bifenthrin treated cells at 1 μM concentration. In addition, measurement of cell size and confirmation of the role of calcium in the stimulation of the eryptotic activity of bifenthrin were performed. A significant increase in mean cell volume was found in the presence of bifenthrin and a decrease in mean cell volume in the presence of calcium channel blocker was observed. Similarly, there was also a significant increase in the percentage of hemolysis indicating the necrotic activity of bifenthrin. Conclusions It is concluded that the indicated doses of bifenthrin triggered oxidative stress which may lead to early cell death by eryptosis and hemolysis.

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Hassan, Zeinab K., Mai A. Elobeid, Promy Virk, Sawsan A. Omer, Maha ElAmin, Maha H. Daghestani, and Ebtisam M. AlOlayan. "Bisphenol A Induces Hepatotoxicity through Oxidative Stress in Rat Model." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/194829.

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Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity.

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Oliveira, Phablo Wendell C., Mariana R. Couto, Glauciene J. de Sousa, Pollyana Peixoto, Flávia S. A. Moraes, Tadeu U. de Andrade, and Nazaré S. Bissoli. "Effects of Drugs, Phytoestrogens, Nutrients and Probiotics on Endothelial Dysfunction in the Estrogen-Deficient State." Current Pharmaceutical Design 26, no. 30 (September 4, 2020): 3711–22. http://dx.doi.org/10.2174/1381612826666200331084338.

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Background: Endothelial dysfunction is commonly present in estrogen-deficient states, e.g., after menopause. In the search for alternatives to hormone replacement therapy (HRT), treatments based on phytoestrogens or in non-hormonal mechanisms have been under evaluation. Objective: Here we aim to present an overview of innovative potential treatments for endothelial dysfunction in estrogen-deficient states, introducing our own preliminary data about the probiotic kefir. Methods: We conducted a review based on a PubMed database search for keywords of interest (Menopause, Ovariectomy, Vascular dysfunction, Hot flashes, Metformin, Statins, Phytoestrogens, Omega-3, Vitamin D, Probiotics). Results: Vascular parameters were found to be improved by both metformin and statins through pleiotropic effects, being related to a decrease in oxidative stress and restoration of the nitric oxide pathway. Phytoestrogens such as genistein and resveratrol have also been shown to improve vascular dysfunction, which seems to involve their estrogenic-like actions. Omega-3, vitamin D and its analogues, as well as probiotics, have shown similar vascular beneficial effects in both postmenopausal women and an animal model of ovariectomy (OVX), which could be related to antioxidant and/or anti-inflammatory effects. Moreover, our preliminary data on the probiotic kefir treatment in OVX rats suggested a vascular antioxidant effect. In particular, some evidence points to statins and vitamin D having anti-atherogenic effects. Conclusion: Pleiotropic effects of common medications and natural compounds could have therapeutic potential for endothelial dysfunction in estrogen-deficient states. They could, therefore, work as future complementary or alternative treatments to HRT.

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Mengue Ngadena, Yolande Sandrine, Pascal Emmanuel Owona, Michel Noubom, Michel Arnaud Mbock, Lohik MbolangNguegan, Madeleine Chantal Ngoungouré, Rodrigue Ngapout Fifen, et al. "Estrogenic and Antioxidant Activities of Pterocarpus soyauxii (Fabaceae) Heartwood Aqueous Extract in Bilateral Oophorectomized Wistar Rat." Evidence-Based Complementary and Alternative Medicine 2021 (September 30, 2021): 1–18. http://dx.doi.org/10.1155/2021/6759000.

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Phytoestrogens are used to ease postmenopausal symptoms, a property probably due to estrogenic and antioxidant effects. Pterocarpus soyauxii (P. soyauxii) is empirically used in Cameroon to treat among others primary and secondary amenorrhea. The aim of this study is to evaluate estrogenic and antioxidant activities of P. soyauxii heartwood aqueous extract in bilateral oophorectomized Wistar rats. Firstly, a characterization of the extract was carried out. For that, flavonoids, phenols, and tannins levels in P. soyauxii extract were evaluated by colorimetric assays and UHPLC-MS analysis was realized. In vitro antioxidant analysis of P. soyauxii was conducted using DPPH, ABTS, and FRAP assays. Secondly, 2 sets of pharmacologic tests were carried out. The results revealed that P. soyauxii aqueous extract contains, respectively, 229.42 ± 3.62 mg EAG/g, 63.42 ± 2.16 mg EQ/g, and 27.88 ± 0.23 mg ETA/g of polyphenols, flavonoids, and tannins. UHPLC-MS enabled identifying seven components including mono(2-ethylhexyl) phthalate, cembrene, 3′,5′-dimethoxy-4-stilbenol, and linoleic acid. DPPH, ABTS, and FRAP assays revealed that P. soyauxii extract possessed a high antioxidant activity with IC50 value of 730.20 µg/mL, 892.90 µg/mL, and 765.75 mEAG/g of extract, respectively. In the uterotrophic assay, P. soyauxii extract induced significant increase of fresh uterine weight, uterine and vaginal epithelial size, and mammary glands differentiation compared to Ovx control. In the postmenopausal model, compared to the sham control, vagina and uterine dystrophies were observed in Ovx rats treated with distilled water. P. soyauxii aqueous extract expressed estrogenic-like effects on vagina and did not affect uterine epithelial height compared with vehicle groups. On the back of these vaginotrophic effects, the extract displayed antiatherogenic properties by reducing ( p < 0.001) AI and LDL cholesterol level as compared to Ovx control group. The extract at 200 mg/kg significantly prevented the increase of MDA ( p < 0.01) level and decreased nitrites ( p < 0.001) and GSH ( p < 0.01) levels compared to Ovx rats. These beneficial effects are related at least in part to the presence of compound such as mono(2-ethylhexyl) phthalate, 3′,5′-dimethoxy-4-stilbenol, and linoleic acid. Overall, P. soyauxii aqueous extract exhibits estrogenic and antioxidant effects which can inhibit postmenopausal symptoms by providing vaginal stratification, improving lipid profile and insulin sensitivity, and reducing oxidative stress without side effects on the endometrium and mammary gland in 84-day Ovx rats.

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Santos-Cruz, Luis Felipe, Alberto Ponciano-Gómez, Juan Tomás Torres-Gregorio, Bertha Guadalupe Ramírez-Cruz, Gerardo Vázquez-Gómez, Luis Barbo Hernández-Portilla, Cesar Mateo Flores-Ortiz, et al. "Zearalenone Does Not Show Genotoxic Effects in the Drosophila melanogaster Wing Spot Test, but It Induces Oxidative Imbalance, Development, and Fecundity Alterations." Toxins 15, no. 6 (May 25, 2023): 358. http://dx.doi.org/10.3390/toxins15060358.

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Zearalenone (ZEN) is a non-steroidal mycoestrogen produced by the Fusarium genus. ZEN and its metabolites compete with 17-beta estradiol for cytosolic estrogen receptors, causing reproductive alterations in vertebrates. ZEN has also been associated with toxic and genotoxic effects, as well as an increased risk for endometrial adenocarcinomas or hyperplasia, breast cancer, and oxidative damage, although the underlying mechanisms remain unclear. Previous studies have monitored cellular processes through levels of transcripts associated with Phase I Xenobiotic Metabolism (Cyp6g1 and Cyp6a2), oxidative stress (hsp60 and hsp70), apoptosis (hid, grim, and reaper), and DNA damage genes (Dmp53). In this study, we evaluated the survival and genotoxicity of ZEN, as well as its effects on emergence rate and fecundity in Drosophila melanogaster. Additionally, we determined levels of reactive oxygen species (ROS) using the D. melanogaster flare and Oregon R(R)-flare strains, which differ in levels of Cyp450 gene expression. Our results showed that ZEN toxicity did not increase mortality by more than 30%. We tested three ZEN concentrations (100, 200, and 400 μM) and found that none of the concentrations were genotoxic but were cytotoxic. Taking into account that it has previously been demonstrated that ZEN administration increased hsp60 expression levels and apoptosis gene transcripts in both strains, the data agree with an increase in ROS and development and fecundity alterations. Since Drosophila lacks homologous genes for mammalian estrogen receptors alpha and beta, the effects of this mycotoxin can be explained by a mechanism different from estrogenic activity.

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Mike, Nóra, Gábor Papp, Milan Čertik, Zsuzsanna Czibulya, Sándor Kunsági-Máté, István Ember, Csaba Vágvölgyi, Miklós Pesti, and Zoltán Gazdag. "Regulation of cytotoxic, non-estrogenic, oxidative stress-induced processes of zearalenone in the fission yeast Schizosaccharomyces pombe." Toxicon 73 (October 2013): 130–43. http://dx.doi.org/10.1016/j.toxicon.2013.07.015.

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Tou, Janet C. L., Richard E. Grindeland, and Charles E. Wade. "Effects of diet and exposure to hindlimb suspension on estrous cycling in Sprague-Dawley rats." American Journal of Physiology-Endocrinology and Metabolism 286, no. 3 (March 2004): E425—E433. http://dx.doi.org/10.1152/ajpendo.00287.2003.

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Various factors can disrupt the female reproductive cycle resulting in subfertility. The primary objective of this study was to determine whether physiological changes associated with exposure to hypogravity disrupt reproductive cycles. The hindlimb suspension (HLS) model was used to simulate the major physiological effects of hypogravity in female Sprague-Dawley rats. Also, to determine whether diet may influence reproductive results, rats were fed purified American Institute of Nutrition (AIN)-93G or chow diet. Rats ( n = 9-11/group) subjected to HLS had lengthened estrous cycles due to prolonged diestrus, indicating hypoestrogenism. Interestingly, HLS rats fed AIN-93G but not chow diet had significantly reduced time spent in estrus and decreased plasma estradiol. Attenuation of hypoestrogenism in the chow-fed rats suggested that diet provided an exogenous source of estrogen. The mechanism involved in the disruption of estrous cycling remains to be determined. HLS increased urinary corticosterone (CORT) levels during the initial 4 days of HLS, suggesting that physiological responses to acute stress may be a potential mechanism in the disruption of estrous cycles. Higher basal urinary CORT was observed in rats fed chow vs. AIN-93G diet. HLS resulted in increased urinary CORT. However, two-way ANOVA indicated a significant HLS effect ( P < 0.001) but no effect of HLS × diet effect on urinary CORT levels, suggesting that estrogenic activity associated with the chow diet did not enhance the stress response. The results of this study indicate that HLS, diet, and the combination of HLS and diet influence estrous cycling. This has important implications for future reproductive success in the hypogravity environment of space.

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Li, HongCheng, WenRu Luo, Yong Tao, Yuan Wu, XueFei Lv, QunFang Zhou, and GuiBin Jiang. "Effects of nanoscale quantum dots in male Chinese loaches (Misgurnus anguillicaudatus): Estrogenic interference action, toxicokinetics and oxidative stress." Science in China Series B: Chemistry 52, no. 10 (October 2009): 1683–90. http://dx.doi.org/10.1007/s11426-009-0226-5.

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Micioni Di Bonaventura, Maria Vittoria, Thomas A. Lutz, Adele Romano, Mariangela Pucci, Nori Geary, Lori Asarian, and Carlo Cifani. "Estrogenic suppression of binge-like eating elicited by cyclic food restriction and frustrative-nonreward stress in female rats." International Journal of Eating Disorders 50, no. 6 (February 23, 2017): 624–35. http://dx.doi.org/10.1002/eat.22687.

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Gundacker, Claudia, Karine Audouze, Raimund Widhalm, Sebastian Granitzer, Martin Forsthuber, Florence Jornod, Maria Wielsøe, et al. "Reduced Birth Weight and Exposure to Per- and Polyfluoroalkyl Substances: A Review of Possible Underlying Mechanisms Using the AOP-helpFinder." Toxics 10, no. 11 (November 12, 2022): 684. http://dx.doi.org/10.3390/toxics10110684.

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Prenatal exposure to per- and polyfluorinated substances (PFAS) may impair fetal growth. Our knowledge of the underlying mechanisms is incomplete. We used the Adverse Outcome Pathway (AOP)-helpFinder tool to search PubMed for studies published until March 2021 that examined PFAS exposure in relation to birth weight, oxidative stress, hormones/hormone receptors, or growth signaling pathways. Of these 1880 articles, 106 experimental studies remained after abstract screening. One clear finding is that PFAS are associated with oxidative stress in in vivo animal studies and in vitro studies. It appears that PFAS-induced reactive-oxygen species (ROS) generation triggers increased peroxisome proliferator-activated receptor (PPAR)γ expression and activation of growth signaling pathways, leading to hyperdifferentiation of pre-adipocytes. Fewer proliferating pre-adipocytes result in lower adipose tissue weight and in this way may reduce birth weight. PFAS may also impair fetal growth through endocrine effects. Estrogenic effects have been noted in in vivo and in vitro studies. Overall, data suggest thyroid-damaging effects of PFAS affecting thyroid hormones, thyroid hormone gene expression, and histology that are associated in animal studies with decreased body and organ weight. The effects of PFAS on the complex relationships between oxidative stress, endocrine system function, adipogenesis, and fetal growth should be further explored.

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Shimizu, Takashi, Izumi Ohshima, Manabu Ozawa, Satoko Takahashi, Atsushi Tajima, Masayuki Shiota, Hitoshi Miyazaki, and Yukio Kanai. "Heat stress diminishes gonadotropin receptor expression and enhances susceptibility to apoptosis of rat granulosa cells." Reproduction 129, no. 4 (April 2005): 463–72. http://dx.doi.org/10.1530/rep.1.00502.

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Heat stress inhibits ovarian follicular development in mammalian species. We hypothesized that heat stress inhibits the function of follicular granulosa cells and suppresses follicular development. To test this, immature female rats were injected with pregnant mare serum gonadotropin (PMSG) at 48 h after the start of temperature treatment (control: 25 °C, 50% RH; heat stress: 35 °C, 70% Relative Humidity). The ovaries and granulosa cells of follicles at different developmental stages were analyzed for gonadotropin receptor levels and aromatase activity; estradiol levels were measured in follicular fluid. Before injection, heat stress diminished only the amount of FSH receptor on granulosa cells of antral follicles. During PMSG-stimulated follicular development, heat stress strongly inhibited gonadotropin receptor levels and aromatase activity in granulosa cells, and estradiol levels in the follicular fluid of early antral, antral and preovulatory follicles. To examine apoptosis and mRNA levels of bcl-2 and bax in granulosa cells, follicles harvested 48 h after PMSG injection were cultured in serum-free conditions. Heat-stressed granulosa cells showed a time-dependent increase in apoptosis. The bcl-2 mRNA levels were similar in control and heat-stressed granulosa cells; bax mRNA levels were increased in heat-stressed granulosa cells. According to these results, heat stress inhibits expression of gonadotropin receptors in granulosa cells and attenuates estrogenic activity of growing follicles, granulosa cells of heat-stressed follicles are susceptible to apoptosis, and the bcl2/bax system is not associated with heat-stress-induced apoptosis of granulosa cells. Our study suggests that decreased numbers and function of granulosa cells may cause ovarian dysfunction in domestic animals in summer.

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Ouanes-Ben Othmen, Z., S. Essefi, and H. Bacha. "Mutagenic and epigenetic mechanisms of zearalenone: prevention by Vitamin E." World Mycotoxin Journal 1, no. 3 (August 1, 2008): 369–74. http://dx.doi.org/10.3920/wmj2008.1036.

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It has been suggested that zearalenone, a non-steroidal estrogenic mycotoxin produced by Fusarium graminearium, causes DNA damage. However, the mutagenic properties of this toxin are controversial. The purpose of this study was to investigate both genotoxic and epigenetic effects of zearalenone in vitro. The effects of zearalenone on unscheduled DNA synthesis (UDS), induction of chromosome aberrations and inhibition of gap junctional intercellular communication were determined using Vero cells. The results show that in Vero cells, zearalenone treatment caused a concentration-dependent increase in UDS, induced chromosome aberrations and inhibited gap junctional intercellular communication. All of these effects were either prevented or reduced by co-treatment with the antioxidant vitamin E. The results support the hypothesis that in Vero cells zearalenone-induced oxidative stress is involved in and precedes all of the studied effects.

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Tiwari, Dinesh, and Geeta Vanage. "Bisphenol A Induces Oxidative Stress in Bone Marrow Cells, Lymphocytes, and Reproductive Organs of Holtzman Rats." International Journal of Toxicology 36, no. 2 (March 2017): 142–52. http://dx.doi.org/10.1177/1091581817691224.

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Bisphenol A (BPA) is an estrogenic chemical used in the production of polycarbonate plastics and epoxy resins. Our earlier studies have demonstrated that BPA is a potent reproductive and genotoxic agent and affects the normal physiological functions. The objective of this study was to evaluate whether exposure to BPA induces oxidative stress. The male Holtzman rats were orally gavaged with BPA (0.01 mg and 5.0 mg/kg/bw) over the period of 6 days. Animals were euthanized by cervical dislocation at the end of the treatments; bone marrow cells and blood lymphocytes were aspirated; testis and epididymis were collected, immediately frozen in liquid nitrogen, and stored at −80°C. These samples were utilized for the determination of lipid peroxidation and various antioxidant enzymes such as superoxide dismutase, catalase, and nonenzymatic reduced glutathione. The results demonstrated that BPA caused an increase in lipid peroxidation and a decrease in activity of various enzymatic and nonenzymatic antioxidants in bone marrow cells, blood lymphocytes, and testicular and epididymal tissues. The findings of the current study suggest that BPA exposure induced oxidative stress, which could be one of the possible mechanisms causing reproductive and genetic toxicity.

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Liu, Liu, Shreya Kashyap, Brennah Murphy, Dillion D. Hutson, Rebecca A. Budish, Emma H. Trimmer, Margaret A. Zimmerman, et al. "GPER activation ameliorates aortic remodeling induced by salt-sensitive hypertension." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 8 (April 15, 2016): H953—H961. http://dx.doi.org/10.1152/ajpheart.00631.2015.

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The mRen2 female rat is an estrogen- and salt-sensitive model of hypertension that reflects the higher pressure and salt sensitivity associated with menopause. We previously showed that the G protein-coupled estrogen receptor (GPER) mediates estrogenic effects in this model. The current study hypothesized that GPER protects against vascular injury during salt loading. Intact mRen2 female rats were fed a normal (NS; 0.5% Na+) or high-salt diet (HS; 4% Na+) for 10 wk, which significantly increased systolic blood pressure (149 ± 5 vs. 224 ± 8 mmHg; P < 0.001). Treatment with the selective GPER agonist G-1 for 2 wk did not alter salt-sensitive hypertension (216 ± 4 mmHg; P > 0.05) or ex vivo vascular responses to angiotensin II or phenylephrine ( P > 0.05). However, G-1 significantly attenuated salt-induced aortic remodeling assessed by media-to-lumen ratio (NS: 0.43; HS+veh: 0.89; HS+G-1: 0.61; P < 0.05). Aortic thickening was not accompanied by changes in collagen, elastin, or medial proliferation. However, HS induced increases in medial layer glycosaminoglycans (0.07 vs. 0.42 mm2; P < 0.001) and lipid peroxidation (0.11 vs. 0.51 mm2; P < 0.01), both of which were reduced by G-1 (0.20 mm2 and 0.23 mm2; both P < 0.05). We conclude that GPER's beneficial actions in the aorta of salt-loaded mRen2 females occur independently of changes in blood pressure and vasoreactivity. GPER-induced attenuation of aortic remodeling was associated with a reduction in oxidative stress and decreased accumulation of glycosaminoglycans. Endogenous activation of GPER may protect females from salt- and pressure-induced vascular damage.

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HUANG, Q., H. ZHU, D. FISCHER, and J. ZHOU. "An estrogenic effect of 5α-androstane-3β, 17β-diol on the behavioral response to stress and on CRH regulation." Neuropharmacology 54, no. 8 (June 2008): 1233–38. http://dx.doi.org/10.1016/j.neuropharm.2008.03.016.

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Xu, Jiehuan, Lingwei Sun, Mengqian He, Shushan Zhang, Jun Gao, Caifeng Wu, Defu Zhang, and Jianjun Dai. "Resveratrol Protects against Zearalenone-Induced Mitochondrial Defects during Porcine Oocyte Maturation via PINK1/Parkin-Mediated Mitophagy." Toxins 14, no. 9 (September 16, 2022): 641. http://dx.doi.org/10.3390/toxins14090641.

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Mitochondria hold redox homeostasis and energy metabolism as a crucial factor during oocyte maturation, while the exposure of estrogenic mycotoxin zearalenone causes developmental incapacity in porcine oocyte. This study aimed to reveal a potential resistance of phytoalexin resveratrol against zearalenone during porcine oocyte maturation and whether its mechanism was related with PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy. Porcine oocytes were exposed to 20 μM zearalenone with or without 2 μM resveratrol during in vitro maturation. As for the results, zearalenone impaired ultrastructure of mitochondria, causing mitochondrial depolarization, oxidative stress, apoptosis and embryonic developmental incapacity, in which mitophagy was induced in response to mitochondrial dysfunction. Phytoalexin resveratrol enhanced mitophagy through PINK1/Parkin in zearalenone-exposed oocytes, manifesting as enhanced mitophagy flux, upregulated PINK1, Parkin, microtubule-associated protein light-chain 3 beta-II (LC3B-II) and downregulated substrates mitofusin 2 (MFN2), voltage-dependent anion channels 1 (VDAC1) and p62 expressions. Resveratrol redressed zearalenone-induced mitochondrial depolarization, oxidative stress and apoptosis, and accelerated mitochondrial DNA copy during maturation, which improved embryonic development. This study offered an antitoxin solution during porcine oocyte maturation and revealed the involvement of PINK1/Parkin-mediated mitophagy, in which resveratrol mitigated zearalenone-induced embryonic developmental incapacity.

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Agrawal, Neha. "Urinary Incontinence: The Distressing Problem." Journal of SAFOMS 2, no. 2 (2014): 83–86. http://dx.doi.org/10.5005/jp-journals-10032-1048.

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ABSTRACT The prevalence of urinary incontinence (UI) in India is as high as 30%. Since, patients do not directly report the problem of incontinence leading questions regarding incontinence should be a routine part of history taking in gynecology. Older patients may assume that UI is a normal consequence of aging. Incontinence is not a normal part of ageing, but it becomes a clinical problem in ageing women due to trauma of child birth, acute and chronic illnesses, loss of estrogenic stimulation at menopause and weaker pelvic support. A stepped management strategy is recommended beginning with lifestyle modification, then behavioral therapy, then medications and finally surgery. First-line treatment to women with stress or mixed UI is pelvic floor exercises.1 Bladder training lasting for a minimum of 6 weeks should be offered as first-line treatment to women with urge or mixed UI. Most urinary incontinence can be evaluated and treated in the primary care setting after careful history and simple clinical assessment. Initial treatment, for both urge urinary incontinence and stress urinary incontinence, is lifestyle modification and pelvic floor muscle treatment. Urinary urgency responds to bladder training and pharmacotherapy with anticholinergic medication. Pharmacotherapy has a limited place in stress incontinence. How to cite this article Singh S, Garg R, Agrawal P, Agrawal N. Urinary Incontinence: The Distressing Problem. J South Asian Feder Menopause Soc 2014;2(2):83-86.

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Eliana Estrella, Akselrad, Cabeza Fernández María de la, Moyano Paula, and Naval María Victoria. "Unveiling the connections: Chlorpyrifos and its association with breast cancer." Journal of Clinical Microbiology and Biochemical Technology 9, no. 1 (December 22, 2023): 022–29. http://dx.doi.org/10.17352/jcmbt.000055.

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Chlorpyrifos, a broad-spectrum insecticide categorized within the organophosphate family, is recognized for its potent inhibition of the enzyme Acetylcholinesterase (AChE), resulting in the manifestation of cholinergic syndrome in humans. Beyond its well-established toxicity in the central nervous system, recent studies have explored additional pathways through which this pesticide may adversely impact human health. Breast cancer, characterized by the uncontrolled proliferation of epithelial cells in the mammary gland, stands as the most diagnosed cancer in women and is a leading global cause of female cancer-related deaths. Chlorpyrifos, extensively employed worldwide for pest control in agriculture, domestic settings, and industries, has notably faced recent bans in the European Union, marking a significant regulatory shift. This bibliographical review aims to unravel the intricate mechanisms by which chlorpyrifos may contribute to the development of breast cancer. Collating findings from human studies, as well as in vitro and in vivo research spanning the past decade, the review sheds light on chlorpyrifos as a potent endocrine disruptor. It influences female sex hormones, exhibits estrogenic effects on breast cancer cells, and induces alterations in breast tissue. Additionally, chlorpyrifos acts as an agonist of Estrogen Receptor α(ERα) and Aryl hydrocarbon Receptor (AhR), contributing to cell proliferation, oxidative stress, and engaging epigenetic and angiogenic mechanisms. This comprehensive review underscores the compelling association between chlorpyrifos exposure and mammary cancer. It emphasizes the urgent need for further research on pesticide usage to mitigate potential adverse health consequences.

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Reznikov, A. G., O. V. Sachynska, A. A. Lymareva, L. I. Polyakova, and I. G. Perchyk. "ENVIRONMENTAL POLLUTANT BISPHENOL DISRUPTS THE PROGRAMMING OF SEXUAL BEHAVIOR IN FEMALE RAT OFFSPRING." Fiziolohichnyĭ zhurnal 69, no. 1 (February 28, 2023): 3–12. http://dx.doi.org/10.15407/fz69.01.003.

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Bisphenol A (BPA) is a common environmental pollutant and, due to its estrogenic properties, can cause disorders of the reproductive and other physiological systems of the body, especially in males. It is known that in male rats it disrupts the sexual differentiation of the brain (SDB) of the fetus in utero. Studies of the effects of perinatal exposure of fetuses and newborn females through the mother’s body under the conditions of long-term administration of BPA during pregnancy and lactation did not reveal significant changes in SDB. Identification of long-term endocrine, neuromorphological, and behavioral consequences of exposure of female rat fetuses to a low dose of BPA administered to mothers during the last week of pregnancy, which corresponds to the temporal period of SDB, was the aim of this study. Rats were orally administered BPA suspended in Dorfman gel at a daily dose of 25 μg/kg b.w., which is 200 times less than the NOAEL (no observed adverse effect level) for rats, via a gavage, or, as a positive control, estradiol diacetate (E2D) subcutaneously at a dose of 10 μg/kg b.w., during 15-21 days of pregnancy. Control animals received gel without BPA. The levels of estradiol, testosterone, and corticosterone in blood plasma, the response of the hypothalamic-pituitary-adrenal (HPA) axis to acute immobilization stress, sexual behavior, and the histological structure and karyometric parameters of neurocytes of the medial-preoptic nuclei (MPN) of the hypothalamus were studied in adult female offspring. Prenatal exposure to BPA or E2D decreased the concentration of estradiol in the blood plasma, while the levels of testosterone and corticosterone remained normal. In the females of the BPA and E2D groups, a masculinization of sexual behavior (mounting to a receptive female, approaching her, etc.) was observed, which, according to the number of lordosis reactions in the presence of a sexually experienced male, not accompanied by her defeminization. Changes in the morphology of the MPN, which belongs to the sex-dimorphic area of the brain, conformed to the masculinization of female sexual behavior due to prenatal exposure to a low dose of BPA. Karyometry of neurocytes of the hypothalamic MPN of rats revealed no difference between the control and the BPA group. The response of the HPA axis to immobilization stress did not change in both experimental groups. It is found for the first time that maternal exposure of in utero female rat fetuses to an ultra-low relative to the NOAEL dose of BPA during the last gestational week, which corresponds to the critical period of SDB impairs programming of sexual behavior in the direction of its masculinization and causes hypoestrogenemia at adulthood. Disorders of sexual behavior conformed to morphological changes of the hypothalamic MPN. The unidirectionality of functional disorders induced by prenatal exposure to BPA and the reference estrogenic drug E2D indicates that they are caused by the estrogenic properties of both substances.

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Zhang, Lian-Dong, He-Cheng Li, Tie Chong, Ming Gao, Jian Yin, De-Lai Fu, Qian Deng, and Zi-Ming Wang. "Prepubertal Exposure to Genistein Alleviates Di-(2-ethylhexyl) Phthalate Induced Testicular Oxidative Stress in Adult Rats." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/598630.

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Di-(2-ethylhexyl) phthalate (DEHP) is the most widely used plastizer in the world and can suppress testosterone production via activation of oxidative stress. Genistein (GEN) is one of the isoflavones ingredients exhibiting weak estrogenic and potentially antioxidative effects. However, study on reproductive effects following prepubertal multiple endocrine disrupters exposure has been lacking. In this study, DEHP and GEN were administrated to prepubertal male Sprague-Dawley rats by gavage from postnatal day 22 (PND22) to PND35 with vehicle control, GEN at 50 mg/kg body weight (bw)/day (G), DEHP at 50, 150, 450 mg/kg bw/day (D50, D150, D450) and their mixture (G + D50, G + D150, G + D450). On PND90, general morphometry (body weight, AGD, organ weight, and organ coefficient), testicular redox state, and testicular histology were studied. Our results indicated that DEHP could significantly decrease sex organs weight, organ coefficient, and testicular antioxidative ability, which largely depended on the dose of DEHP. However, coadministration of GEN could partially alleviate DEHP-induced reproductive injuries via enhancement of testicular antioxidative enzymes activities, which indicates that GEN has protective effects on DEHP-induced male reproductive system damage after prepubertal exposure and GEN may have promising future in its curative antioxidative role for reproductive disorders caused by other environmental endocrine disruptors.

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Rodríguez-Fuentes, Gabriela, Juan J. Sandoval-Gío, Anita Arroyo-Silva, Elsa Noreña-Barroso, Karla S. Escalante-Herrera, and Francisco Olvera-Espinosa. "Evaluation of the estrogenic and oxidative stress effects of the UV filter 3-benzophenone in zebrafish (Danio rerio) eleuthero-embryos." Ecotoxicology and Environmental Safety 115 (May 2015): 14–18. http://dx.doi.org/10.1016/j.ecoenv.2015.01.033.

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Maiuolo, Jessica, Irene Bava, Cristina Carresi, Micaela Gliozzi, Vincenzo Musolino, Miriam Scicchitano, Roberta Macri, et al. "The Effect of Ferula communis Extract in Escherichia coli Lipopolysaccharide-Induced Neuroinflammation in Cultured Neurons and Oligodendrocytes." International Journal of Molecular Sciences 22, no. 15 (July 24, 2021): 7910. http://dx.doi.org/10.3390/ijms22157910.

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In recent decades, interest in natural compounds has increased exponentially due to their numerous beneficial properties in the treatment of various acute and chronic diseases. A group of plant derivatives with great scientific interest is terpenic compounds. Among the plants richest in terpenes, the genus Ferula L. is one of the most representative, and ferutinin, the most common sesquiterpene, is extracted from the leaves, rhizome, and roots of this plant. As reported in the scientific literature, ferutinin possesses antioxidant and anti-inflammatory properties, as well as valuable estrogenic properties. Neurodegenerative and demyelinating diseases are devastating conditions for which a definite cure has not yet been established. The mechanisms involved in these diseases are still poorly understood, and oxidative stress is considered to be both a key modulator and a common denominator. In the proposed experimental system, co-cultured human neurons (SH-SY5Y) and human oligodendrocytes (MO3.13) were treated with the pro-inflammatory agent lipopolysaccharide at a concentration of 1 μg/mL for 24 h or pretreated with ferutinin (33 nM) for 24 h and subsequently exposed to lipopolysaccharide 1 μg/mL for 24 h. Further studies would, however, be needed to establish whether this natural compound can be used as a support strategy in pathologies characterized by progressive inflammation and oxidative stress phenomena.

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Jasińska, Anna, Adrian Soboń, Sylwia Różalska, and Paulina Średnicka. "Bisphenol A Removal by the Fungus Myrothecium roridumIM 6482—Analysis of the Cellular and Subcellular Level." International Journal of Molecular Sciences 22, no. 19 (October 1, 2021): 10676. http://dx.doi.org/10.3390/ijms221910676.

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Bisphenol (BPA) is a key ingredient in the production of epoxy resins and some types of plastics, which can be released into the environment and alter the endocrine systems of wildlife and humans. In this study, the ability of the fungus M. roridumIM 6482 to BPA elimination was investigated. LC-MS/MS analysis showed almost complete removal of BPA from the growth medium within 72 h of culturing. Products of BPA biotransformation were identified, and their estrogenic activity was found to be lower than that of the parent compound. Extracellular laccase activity was identified as the main mechanism of BPA elimination. It was observed that BPA induced oxidative stress in fungal cells manifested as the enhancement in ROS production, membranes permeability and lipids peroxidation. These oxidative stress markers were reduced after BPA biodegradation (72 h of culturing). Intracellular proteome analyses performed using 2-D electrophoresis and MALDI-TOF/TOF technique allowed identifying 69 proteins in a sample obtained from the BPA containing culture. There were mainly structural and regulator proteins but also oxidoreductive and antioxidative agents, such as superoxide dismutase and catalase. The obtained results broaden the knowledge on BPA elimination by microscopic fungi and may contribute to the development of BPA biodegradation methods.

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Li, Yina, Yujin Gao, Dan Yao, Zongshuai Li, Jiamian Wang, Xijun Zhang, Xingxu Zhao, and Yong Zhang. "Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells." International Journal of Molecular Sciences 25, no. 5 (February 23, 2024): 2578. http://dx.doi.org/10.3390/ijms25052578.

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Zearalenone (ZEA) is a common non-steroidal estrogenic mycotoxin found in a range of animal feeds and poses a serious threat to the reproductive health of farm animals and humans. However, the mechanism underlying ZEA-induced reproductive toxicity in sheep remains unknown. Granulosa cells are crucial for egg maturation and the fertility of female sheep. In this study, we aimed to examine the impact of different ZEA concentrations on sheep follicular granulosa cells and to elucidate the potential molecular mechanism underlying ZEA-induced toxicity using transcriptome sequencing and molecular biological approaches. Treating primary sheep follicular granulosa cells with different concentrations of ZEA promoted the overproduction of reactive oxygen species (ROS), increased lipid peroxidation products, led to cellular oxidative stress, decreased antioxidant enzyme activities, and induced cell apoptosis. Using transcriptome approaches, 1395 differentially expressed genes were obtained from sheep follicular granulosa cells cultured in vitro after ZEA treatment. Among them, heme oxygenase-1 (HMOX1) was involved in 11 biological processes. The protein interaction network indicated interactions between HMOX1 and oxidative and apoptotic proteins. In addition, N-acetylcysteine pretreatment effectively reduced the ZEA-induced increase in the expression of HMOX1 and Caspase3 by eliminating ROS. Hence, we suggest that HMOX1 is a key differential gene involved in the regulation of ZEA-induced oxidative stress and apoptosis in follicular granulosa cells. These findings provide novel insights into the prevention and control of mycotoxins in livestock.

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Journal articles on the topic 'Estrogenic stress'

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