Bisphenol A modulates inflammation and proliferation pathway in human endometrial stromal cells by inducing oxidative stress

Cho, Yeon Jean; Park, Seung Bin; Park, Jung‐Woo; Oh, Seung Joon; Han, Myoungseok

doi:10.1016/j.reprotox.2018.06.016

Cited by 65 publications

(34 citation statements)

References 32 publications

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“…It could therefore be hypothesized that oxidative stress may underlie the association between bisphenol exposure and enhanced endometriosis risk. In this regard, a recent in vitro study suggested that the induction of oxidative stress by BPA might be mediated by ER-α in endometrial cells, although it is not fully elucidated whether this action would be in concert with or independent of BPA's endocrine-disrupting properties [47]. Among oxidative stress biomarkers, TBARS was selected for the present study because it is a good proxy of oxidative status and is a relatively early event, given that the final products possess reactive properties that continue to cause oxidative macromolecule damage [48].…”

Section: Discussionmentioning

confidence: 99%

Association of Urinary Levels of Bisphenols A, F, and S with Endometriosis Risk: Preliminary Results of the EndEA Study

Peinado

Lendínez

Sotelo

et al. 2020

IJERPH

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Aim: The aim of this study was to explore associations of urinary concentrations of bisphenols A (BPA), S (BPS), and F (BPF) and of thiobarbituric acid reactive substances (TBARS) with the risk of endometriosis in women of childbearing age. Methods: This case–control study enrolled 124 women between January 2018 and July 2019: 35 women with endometriosis (cases) and 89 women without endometriosis undergoing abdominal surgery for other reasons (controls). Endometriosis was diagnosed (cases) or ruled out (controls) by laparoscopic inspection of the pelvis and the biopsy of suspected lesions (histological diagnosis). Fasting urine samples were collected before surgery to determine concentrations of BPA, BPS, BPF, and TBARS. Associations of bisphenol and TBARS concentrations with endometriosis risk were explored with multivariate logistic and linear regression analyses. Results: After adjustment for urinary creatinine, age, BMI, parity, and residence, endometriosis risk was increased with each 1 log unit of BPA [OR 1.5; 95%CI 1.0–2.3] and Σbisphenols [OR 1.5; 95%CI 0.9–2.3] but was not associated with the presence of BPS and BPF. Classification of the women by tertiles of exposure revealed statistically significant associations between endometriosis risk and the second tertile of exposure to BPA [OR 3.7; 95%CI 1.3–10.3] and Σbisphenols [OR 5.4; 95%CI 1.9–15.6]. In addition, TBARS concentrations showed a close-to-significant relationship with increased endometriosis risk [OR 1.6; 95%CI 1.0–2.8], and classification by TBARS concentration tertile revealed that the association between endometriosis risk and concentrations of BPA [OR 2.0; 95%CI 1.0–4.1] and Σbisphenols [OR 2.2; 95%CI 1.0–4.6] was only statistically significant for women in the highest TBARS tertile (>4.23 μM). Conclusion: Exposure to bisphenols may increase the risk of endometriosis, and oxidative stress may play a crucial role in this association. Further studies are warranted to verify these findings.

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Section: Discussionmentioning

confidence: 99%

Association of Urinary Levels of Bisphenols A, F, and S with Endometriosis Risk: Preliminary Results of the EndEA Study

Peinado

Lendínez

Sotelo

et al. 2020

IJERPH

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“…When 1000 pmol of BPA was exposed to ESCs, the cells showed decreased expression of antioxidant enzymes namely SOD, GPx, HO, and CAT suggesting an increase in ROS. The cells also presented an increase in eNOS expression and NO production (Cho, Park, Park, Oh, & Han, 2018) which may be an effect to counteract the increased oxidative stress. Alternatively, increased NO production resulting from BPA exposure might be associated with the impairment of mitochondrial oxidative phosphorylation, which is essential for the production of the energy required to facilitate decidualization (Cecchino, Seli, Alves da Motta, & García‐Velasco, 2018).…”

Section: Bpa Exposure and Oxidative Stressmentioning

confidence: 99%

Bisphenol A‐induced mechanistic impairment of decidualization

Nelson

Adu‐Gyamfi

Czika

et al. 2020

Molecular Reproduction Devel

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Decidualization is a crucial precedent to embryo implantation, as its impairment is a major contributor to female infertility and pregnancy complications. Unraveling the molecular mechanisms involved in the impairment of decidualization has been a subject of interest in the field of reproductive medicine. Evidence from several experimental settings show that exposure to bisphenol A (BPA), an endocrine‐disrupting chemical, affects the expression of several molecules that are involved in decidualization. Both low and high doses of BPA impair decidualization through the dysregulation of estrogen (ER) and progesterone (PR) receptors. Exposure to low doses of BPA leads to decreased levels and activities of several antioxidant enzymes, increased activity of endothelial nitric oxide synthase (eNOS), and increased production of nitric oxide (NO) via the upregulation of ER and PR. Consequently, oxidative stress is induced and decidualization becomes impaired. On the other hand, exposure to high doses of BPA downregulates ER and PR and impairs decidualization through two distinct pathways. One is through the upregulation of early growth response‐1 (EGR1) via increased phosphorylation of extracellular signal‐regulated protein kinases 1 and 2; and the other is through a reduced serum glucocorticoid‐induced kinase‐1 (SGK1)‐mediated downregulation of epithelial sodium channel‐α and the induction of oxidative stress. Thus, regardless of the dose, BPA can impair decidualization to trigger infertility and pregnancy complications. This warrants the need to adopt lifestyles that will decrease the tendency of getting exposed to BPA.

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“…Low BPA concentrations affect human endometrial stromal cell (ESC) physiology. BPA enhanced progesterone-induced decidualization and promoted ESC migration and oxidative stress in vitro [36,37]. Currently, the molecular mechanisms involved in the progression of endometriosis are not well understood.…”

Section: Bisphenol Amentioning

confidence: 99%

Nonpersistent endocrine disrupting chemicals and reproductive health of women

et al. 2020

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Nonpersistent endocrine disrupting chemicals (npEDCs) are exogenous chemicals or mixtures of industrial agents that can interfere with the normal action of hormone with a shorter half-life and lower liposolubility. These are commonly found in plastics, medical equipment, detergents, and cosmetics. Recently, role of npEDCs on the changes of ovary and/or uterus development and alterations in hormonal signaling has been emphasized. However, many controversial results exist on the effects of npEDCs and reproductive health of women. Thus, we have focused to review the scientific evidence of a causal relationship between exposure to npEDCs and representative female reproductive issues such as menstrual cycle, endometriosis, uterine fibroids, polycystic ovarian syndrome and infertility/subfertility. Though not all studies indicated a positive correlation of npEDCs with female reproductive issues, the reviewed data illustrated that the majority of the available data strengthen the evidence of reproductive health-related actions of npEDCs. In future, recommendations should be made in order to reduce human exposure to npEDCs and to protect from steadily increasing reproductive health risks.

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Bisphenol A modulates inflammation and proliferation pathway in human endometrial stromal cells by inducing oxidative stress

Cited by 65 publications

References 32 publications

Association of Urinary Levels of Bisphenols A, F, and S with Endometriosis Risk: Preliminary Results of the EndEA Study

Association of Urinary Levels of Bisphenols A, F, and S with Endometriosis Risk: Preliminary Results of the EndEA Study

Bisphenol A‐induced mechanistic impairment of decidualization

Nonpersistent endocrine disrupting chemicals and reproductive health of women

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