Bisphenol A derivatives act as novel coactivator binding inhibitors for estrogen receptor β

Iwamoto, Masaki; Masuya, Takahiro; Hosose, Mari; Tagawa, Kunio; Ishibashi, Tatsuro; Yoshihara, Eiji; Downes, Michael; Evans, Ronald M.; Matsushima, Ayami

doi:10.1101/2021.05.10.443431

Cited by 2 publications

(1 citation statement)

References 50 publications

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“…Hence, BPF is referred to as "weak oestrogen" because it can bind with oestrogen receptors (with lesser affinity) and mimic oestrogens. Unlike BPA, other bisphenols have a higher affinity for ERβ (58). ERα is responsible for promoting cell proliferation, while the activation of ERβ has been associated with apoptosis.…”

Section: Discussionmentioning

confidence: 99%

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Odetayo

Adeyemi

Olayaki

2023

Front. Reprod. Health

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IntroductionBisphenol F (BPF), an alternative to bisphenol A has been implicated as a gonadotoxic substance. BPF has been shown to induce hormonal imbalance and testicular oxidative damage. However, the mechanism associated with BPF-induced testicular toxicity has not been fully explored. This study was designed to explore the role of tumor protein (p53)/ B-cell lymphoma 2 (BCl-2) signaling and oestrogen receptor beta (Erβ) in BPF-induced testicular toxicity.MethodsMale Wistar rats were randomized into control (Cntrl), BPF-treated (10, 30, and 50 mg/kg for low dose (BPF-L), medium dose (BPF-M), and high dose (BPF-H) respectively), and BPF-treated recovery (Cntrl-R, BPF-L-R, BPF-M-R, and BPF-H-R). The administration was via gavage and lasted for 28 days and the animals in the recovery groups were allowed 28-days exposure free period for recovery from BPF exposure.ResultsBPF resulted in the distortion of the testicular histoarchitecture, which was accompanied by a significant rise in testicular gamma-lutamyl transferase and lactate dehydrogenase activities but a decline in sorbitol dehydrogenase activities. Also, BPF caused a significant reduction in plasma gonadotropin-releasing hormone, luteinising hormone, follicle-stimulating hormone, and testosterone, which was associated with the downregulation of testicular 3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase activities. Furthermore, BPF induced testicular inflammation, redox imbalance, and apoptosis, accompanied by distortion in p53/BCl-2 signaling and overexpression of Erβ. Again, the observed toxic effects of BPF were dose-dependent and not completely reversed by BPF cessation.DiscussionBisphenol F induced gonadotoxicity by distorting p53/BCl2 signaling and the expression of Erβ. These observed alterations were not completely reversed after the cessation of BPF exposure.

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Section: Discussionmentioning

confidence: 99%

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Odetayo

Adeyemi

Olayaki

2023

Front. Reprod. Health

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Invisible Hand behind Female Reproductive Disorders: Bisphenols, Recent Evidence and Future Perspectives

Wu,

Tian,

Zhu

et al. 2023

Toxics

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Reproductive disorders are considered a global health problem influenced by physiological, genetic, environmental, and lifestyle factors. The increased exposure to bisphenols, a chemical used in large quantities for the production of polycarbonate plastics, has raised concerns regarding health risks in humans, particularly their endocrine-disrupting effects on female reproductive health. To provide a basis for future research on environmental interference and reproductive health, we reviewed relevant studies on the exposure patterns and levels of bisphenols in environmental matrices and humans (including susceptible populations such as pregnant women and children). In addition, we focused on in vivo, in vitro, and epidemiological studies evaluating the effects of bisphenols on the female reproductive system (the uterus, ovaries, fallopian tubes, and vagina). The results indicate that bisphenols cause structural and functional damage to the female reproductive system by interfering with hormones; activating receptors; inducing oxidative stress, DNA damage, and carcinogenesis; and triggering epigenetic changes, with the damaging effects being intergenerational. Epidemiological studies support the association between bisphenols and diseases such as cancer of the female reproductive system, reproductive dysfunction, and miscarriage, which may negatively affect the establishment and maintenance of pregnancy. Altogether, this review provides a reference for assessing the adverse effects of bisphenols on female reproductive health.

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Bisphenol A derivatives act as novel coactivator binding inhibitors for estrogen receptor β

Cited by 2 publications

References 50 publications

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

Invisible Hand behind Female Reproductive Disorders: Bisphenols, Recent Evidence and Future Perspectives

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