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Endocrine disrupting chemicals (EDC) are exogenous compounds, which can interfere with the hormones action and endocrine pathways, affect the development of female reproductive system and ovarian function, and therefore EDCs are associated with female infertility. Current research mainly focus on EDC exposure and its correlation with the different diseases of the endocrine axes. Studies have shown that EDCs affect female fertility by causing ovarian dysfunction, follicular development abnormality, endometrial receptivity reduction, and embryo quality decline, as well as the lowed clinical outcome of assisted reproduction in infertile women. Accumulating evidence in animal studies has provided important insights into the mechanism of EDC effects. This review summarizes some of the most common EDCs including pesticides, bisphenol A and phthalates, and the effects of EDCs on female fertility and clinical outcomes of assisted reproductive technology. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) as an organic compound widely existing in the environment can interfere with the normal metabolism of the body and participate in the occurrence and development of a variety of diseases. High dose BPA exposure has an acute toxic effect on the reproductive system. Long-term exposure to BPA has more significant damage to the reproductive system, and can even produce intergenerational effects, affecting the growth and development of offspring. BPA damages female reproductive function and reduces female fertility through a variety of mechanisms. Therefore, it is particularly important to develop related drugs to alleviate this adverse reaction. This paper reviews the effects of BPA on female reproductive system, and introduces the research progress of antioxidants, probiotics, vitamins and traditional Chinese medicine on alleviating the effects of BPA on reproductive system. However, the clinical application of related drugs still needs the support of evidence-based medical evidence. [ABSTRACT FROM AUTHOR]

Objective: To study the influence of perinatal exposure of bisphenol A (BPA) at a low dose on the spermatogenesis of male offspring rats. Methods: Pregnant rats were injected subcutaneously with BPA 2 μg/(kg·d) from gestation day 10 through lactation day 7, and the same volume of olive oil was used as the blank control. Their male offspring were served as the BPA group and the control group. Histological structure of the testis and the related regulation genes such as cyclin A1、cyclin B、c-jun and c-fos, as well as the FSH and LH, were tested, and the expressions POA-GnRH or ARC-kiss1 mRNAs were also examined in their male offspring during the postnatal day 18, 21, 24. Results: In comparison with the control group, the seminiferous tubular diameter, the number of round spermatids and the ratio of seminiferous tubule with round spermatids were significantly increased in PND24 BPA rats (P＜0.05). The expression levels of cyclin A1, c-jun and c-fos mRNAs in the testes were significantly elevated in PND21 BPA rats (P＜0.01). Similarly, the levels of plasma FSH and LH were increased in the PND21/24 BPA rats compared with the control rats (P＜0.05). But the levels of plasma T and E2 were no significant in the PND18/21/24 BPA rats and the control rats (P＞0.05). In comparison with control group, the expression levels of POA-GnRH mRNA and ARC-kiss1 mRNA were significantly increased in PND21 BPA rats (GnRH: P＜0.05; kiss1: P＜0.01). Conclusions: In addition to the direct effect of BPA on the testes of male offspring, the perinatal exposure to a low dose of BPA promotes spermatogenesis via advancing the pubertal activation of ARC -kisspeptin, and via further enhancing the expressions of meiotic regulation genes in the testes of male offspring. [ABSTRACT FROM AUTHOR]

Environmental endocrine disruptors (EED) widely exist in daily life, as a kind of exogenous chemicals that can interfere with hormonal behavior. EEDs can bind to different receptors in the human body, to enhance or inhibit the normal endocrine function through a variety of mechanisms, resulting in a variety of diseases. The etiology of polycystic ovary syndrome (PCOS) is complex. Previous studies have shown that the pathogenesis of PCOS is related to environmental factors. The epidemiological and basic experiments showed that EEDs were involved in the pathogenesis of PCOS. However, it is necessary to study furtherly the potential mechanism. In this paper, the relationship between EEDs and PCOS, as well as possible mechanism, was expounded. It provides a new clue for those people to block the development of PCOS by improving their lifestyle. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of bisphenol A (bisphenol A, BPA) on the oocyte chromosome non-disjunction in iNos-/- mice. Methods: Female iNos-/- mice and iNos-/- mice, aged 20-22 days, were treated with BPA (100 or 200 µ g/kg body weight per day) by intragastric administration for 13 days. The isopyknic corn oil was used as control. Results: In the iNos-/- mice groups, the numbers of aneuploidy oocytes at metaphase M II were not increased by BPA treatment. Interestingly, the numbers of those oocytes with the error- prone chromosome segregation and the precocious chromatid separation in the iNos-/- mice groups were significantly increased by BPA treatment. Meanwhile, the expressions of polo-like kinase-1 (PLK1) and RAN GTPase (RAN) in oocytes of the iNos-/- mice were significantly down-regulated by BPA treatment. Conclusions: iNos-/- has a direct or indirect protection against the faithful chromosome segregation during meiosis, possibly by maintaining stable expression of PLK1 and RAN in mammalian oocytes. BPA exposure at low level may induce chromosomal aberrations in those oocytes of iNos-/- mice. [ABSTRACT FROM AUTHOR]