Mutagenic effect of Bisphenol A on adult rat male germ cells and their fertility

Tiwari, D. C.; Vanage, Geeta

doi:10.1016/j.reprotox.2013.05.013

Cited by 103 publications

(73 citation statements)

References 46 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: 76%

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: 76%

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

Rosenfeld

2017

Frontiers in Neuroendocrinology

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“…Our in vitro data were also consistent with previous in vivo findings. BPA exposure ( 50 mg/kg) consistently induced impairments of sperm production and quality, and alteration of steroidogenesis (D'Cruz et al, 2012;Tiwari and Vanage, 2013). Whereas BPS, BPAF, and TBBPA exerted some adverse reproductive effects, including alterations of hormone levels, decreases in sperm count and changes of seminiferous epithelium morphology, Future study will be important to validate these findings (Feng et al, 2012;Kuriyama et al, 2005;Ullah et al, 2016).…”

Section: Discussionmentioning

confidence: 92%

“…As a known endocrine disruptor, BPA has been shown to interfere with hormonal and homeostatic systems, and BPA levels in human urine have been correlated with various diseases and adverse health outcomes (Braun et al, 2011;Carwile and Michels, 2011;Ehrlich et al, 2012;Lang et al, 2008;Lassen et al, 2014). BPA exposure has also been associated with reproductive dysfunctions, including reduction of testicular weight and sperm count, alterations of hormone levels, and impairment of spermatogenesis (Jin et al, 2013;Pacchierotti et al, 2008;Sakaue et al, 2001;Tiwari and Vanage, 2013;Wang et al, 2016). The mechanism of action of BPA has been investigated with respect to its estrogenic activity, such as effects on steroid hormone synthesis, and androgen receptor (AR) antagonism (Kitamura et al, 2005;Lee et al, 2003;Vinggaard et al, 2008;Zhang et al, 2011).…”

mentioning

confidence: 99%

High-Content Analysis Provides Mechanistic Insights into the Testicular Toxicity of Bisphenol A and Selected Analogues in Mouse Spermatogonial Cells

Liang

Yin

et al. 2016

Toxicol. Sci.

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Bisphenol A (BPA), an endocrine-disrupting compound, was found to be a testicular toxicant in animal models. Bisphenol S (BPS), bisphenol AF (BPAF), and tetrabromobisphenol A (TBBPA) were recently introduced to the market as alternatives to BPA. However, toxicological data of these compounds in the male reproductive system are still limited so far. This study developed and validated an automated multi-parametric high-content analysis (HCA) using the C18-4 spermatogonial cell line as a model. We applied these validated HCA, including nuclear morphology, DNA content, cell cycle progression, DNA synthesis, cytoskeleton integrity, and DNA damage responses, to characterize and compare the testicular toxicities of BPA and 3 selected commercial available BPA analogues, BPS, BPAF, and TBBPA. HCA revealed BPAF and TBBPA exhibited higher spermatogonial toxicities as compared with BPA and BPS, including dose-and time-dependent alterations in nuclear morphology, cell cycle, DNA damage responses, and perturbation of the cytoskeleton. Our results demonstrated that this specific culture model together with HCA can be utilized for quantitative screening and discriminating of chemical-specific testicular toxicity in spermatogonial cells. It also provides a fast and cost-effective approach for the identification of environmental chemicals that could have detrimental effects on reproduction.

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“…Exposing the adult male rats to BPA resulted in the decrease of testicular weight, daily sperm production and efficiency of spermatogenesis (18). Furthermore, prenatal exposure of pregnant rats to BPA causes breast cancer in adult female offsprings and hyperplasia of prostate in male rats, and this hyperplasia may result in greater risk of prostate cancer (19).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the Effects of Bisphenol A on the Histology and Ultrastructure of Prostate and Seminal Vesicle Glands in Rats

Hasanluyi

Khojasteh

Nejhad

2016

Thrita

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Background: Bisphenol A is a xenoestrogen, synthesized in large quantities for the production of polymers (polycarbonates, epoxy resins) and thermal paper, and is widely used in products of everyday use (packaging, containers and bottles). Data concerning the occurrence of BPA in food, water and indoor environments as well as its appearance in tissues and body fluids of the human body are available in the literature. Male accessory sex glands are also vulnerable to environmental endocrine disruptors with adverse effects in adulthood. The developing prostate gland is particularly sensitive to estrogens and high-dose exposures during a critical developmental window results in intraepithelial prostatic neoplasia (PIN) in adult rodent models. Bisphenol A is also an endocrine disruptor. High levels of BPA exposure correlate with increased risk of mammary gland, brain and prostate cancers and have adverse effects on the tissues of the prostate and seminal vesicles. Objectives: The aim of this study was to investigate the effects of BPA doses on the histological structure and ultrastructure of prostate and seminal vesicle glands. Methods: Forty male Wistar rats were randomly divided into four groups (n = 10): A control group and three treatment groups,

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Mutagenic effect of Bisphenol A on adult rat male germ cells and their fertility

Cited by 103 publications

References 46 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

High-Content Analysis Provides Mechanistic Insights into the Testicular Toxicity of Bisphenol A and Selected Analogues in Mouse Spermatogonial Cells

Investigation of the Effects of Bisphenol A on the Histology and Ultrastructure of Prostate and Seminal Vesicle Glands in Rats

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