Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats

Jin, Pengpeng; Wang, Xiaoli; Fei, Chang; Bai, Yinyang; Li, Yingchun; Zhou, Rong; Chen, Ling

doi:10.7555/jbr.27.20120076

Cited by 101 publications

(32 citation statements)

References 43 publications

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“…Other rodent studies suggest that BPA exposure can affect T production with one report suggesting developmental exposure to BPA increases this hormone [84], whereas other studies suggest this chemical decreases T production [85; 86; 87; 88; 89]. Similar to the BPA-analogue studies reported above, BPA can also affect sperm production and quality and increase sperm DNA damage in rodent models [90; 91; 92; 93; 94]. Some of the effects of BPAF and BPS in the CNS and other systems might be due to non-genomic actions [68; 69; 70].…”

Section: Neuroendocrine Disruption Due To Exposure Of Rodent Models Tmentioning

confidence: 77%

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Rosenfeld

2017

Frontiers in Neuroendocrinology

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Animal and human studies provide evidence that exposure to the endocrine disrupting chemical (EDC), bisphenol A (BPA), can lead to neurobehavioral disorders. Consequently, there is an impetus to identify safer alternatives to BPA. Three bisphenol compounds proposed as potential safer alternatives to BPA are bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF). However, it is not clear whether these other compounds are safer in terms of inducing less endocrine disrupting effects in animals and humans who are now increasingly coming into contact with these BPA-substitutes. In the past few years, several animal studies have shown exposure to these other bisphenols induce similar neurobehavioral disruption as BPA. We will explore in this review article the current studies suggesting these other bisphenols result in neuroendocrine disruptions that may be estrogen receptor-dependent. Current work may aide in designing future studies to test further whether these BPA-substitutes can act as neuroendocrine disruptors.

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Section: Neuroendocrine Disruption Due To Exposure Of Rodent Models Tmentioning

confidence: 77%

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Rosenfeld

2017

Frontiers in Neuroendocrinology

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“…6B, E ). We decided to use a concentration of 0.05 µM of NP and BPA for the following experiments as this concentration was found to significantly increase the AP activity and is within the range of levels detected in human samples [28] , [30] , [53] , [54] . The AP activity started to increase in the culture medium as early as 1 h after treatment with 0.05 µM BPA or NP ( Fig.…”

Section: Resultsmentioning

confidence: 99%

A Mechanism of Male Germ Cell Apoptosis Induced by Bisphenol-A and Nonylphenol Involving ADAM17 and p38 MAPK Activation

2014

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Germ cell apoptosis regulation is pivotal in order to maintain proper daily sperm production. Several reports have shown that endocrine disruptors such as Bisphenol-A (BPA) and Nonylphenol (NP) induce germ cell apoptosis along with a decrease in sperm production. Given their ubiquitous distribution in plastic products used by humans it is important to clarify their mechanism of action. TACE/ADAM17 is a widely distributed extracellular metalloprotease and participates in the physiological apoptosis of germ cells during spermatogenesis. The aims of this work were: 1) to determine whether BPA and NP induce ADAM17 activation; and 2) to study whether ADAM17 and/or ADAM10 are involved in germ cell apoptosis induced by BPA and NP in the pubertal rat testis. A single dose of BPA or NP (50 mg/kg) induces germ cell apoptosis in 21-day-old male rats, which was prevented by a pharmacological inhibitor of ADAM17, but not by an inhibitor of ADAM10. In vitro, we showed that BPA and NP, at similar concentrations to those found in human samples, induce the shedding of exogenous and endogenous (TNF-α) ADAM17 substrates in primary rat Sertoli cell cultures and TM4 cell line. In addition, pharmacological inhibitors of metalloproteases and genetic silencing of ADAM17 prevent the shedding induced in vitro by BPA and NP. Finally, we showed that in vivo BPA and NP induced early activation (phosphorylation) of p38 MAPK and translocation of ADAM17 to the cell surface. Interestingly, the inhibition of p38 MAPK prevents germ cell apoptosis and translocation of ADAM17 to the cell surface. These results show for the first time that xenoestrogens can induce activation of ADAM17 at concentrations similar to those found in human samples, suggesting a mechanism by which they could imbalance para/juxtacrine cell-to-cell-communication and induce germ cell apoptosis.

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“…In vivo study with adult rats suggests that low dosage (2 μg/kg body weight) of BPA after oral administration impairs spermatogenesis by reducing reproductive hormones to stop meiosis of germ cells and activating the Fas/FasL pathway to induce the apoptosis of germ cells, lowers the biosynthesis and secretion of testosterone via inhibiting the activity of GnRH neurons, and decreases the expression of steroidogenic enzymes. Subsequently, declining testosterone rate was accompanied by reduction of sperm concentration [90]. Another recent in vivo study with experimental rats evaluated the potential impact of BPA in the doses of 1, 5, 10 and 100 mg/kg body weight on spermatogenesis.…”

Section: Spermatogenesis and Sperm Function Affected By Bpamentioning

confidence: 99%

Male Reproduction: One of the Primary Targets of Bisphenol

Jambor¹,

Bistakova²,

Greifova³

et al. 2017

Bisphenol a Exposure and Health Risks

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Infertility is a major health issue affecting human life. The most notable factors causing male infertility is exposure to environmental contaminants. Bisphenol A (BPA) is a common toxic environmental contaminant. Human population is exposed to bisphenol A through air, water, food and a variety of industrial products. Growing evidence from research on laboratory animals supports the hypothesis that bisphenol A is able to adversely affect male reproductive function. The specific mechanisms of action of bisphenol A are wide but not definite. Bisphenol A interferes with the hormonal metabolism and regulation, binding affinity or enzymatic activity, resulting in a deviation from a normal reproductive behaviour. Binding ability to androgen and oestrogen receptors, as well as other properties, is currently investigated. A decreased sperm count, inhibition of sperm motility and reduction of organ weights were observed and linked with oxidative stress after bisphenol A treatment. In addition, prenatal exposure to bisphenol A may lead to adverse effects in the offspring. In this review, we address the topic of BPA effects on male reproductive function and emphasize its effects on testicular steroidogenesis and spermatogenesis. A considerably more detailed and systematic research focusing on bisphenol A toxicology is required for a better understanding of risks associated with exposure to this endocrine disruptor.

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Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats

Cited by 101 publications

References 43 publications

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

A Mechanism of Male Germ Cell Apoptosis Induced by Bisphenol-A and Nonylphenol Involving ADAM17 and p38 MAPK Activation

Male Reproduction: One of the Primary Targets of Bisphenol

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