Increase in the expression of inducible nitric oxide synthase on exposure to bisphenol A: A possible cause for decline in steroidogenesis in male mice

Chouhan, Shikha; Yadav, Sanjeev Kumar; Prakash, Jay; Westfall, Susan; Ghosh, Amrita; Agarwal, Neeraj; Singh, Surya Pratap

doi:10.1016/j.etap.2014.09.014

Cited by 38 publications

(26 citation statements)

References 51 publications

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“…In the current study, soy extract treatment did not alter serum levels of testosterone, whereas BPA noticeably reduced this hormone in all exposed BPA groups. Our finding supports previous work by Chouhan et al (2015) who have reported that sperm count and serum testosterone level were reduced in treated mice by 100 μg/kg BPA.…”

Section: Discussionsupporting

confidence: 93%

“…StAR is a transport protein primarily present in steroid-producing cells that is involved in the production of steroid hormones. In addition, BPA can prob-ably suppress testosterone production via activation of oxidative stress (Chouhan et al 2015). Similarly, data from present study revealed that oxidative stress might be responsible for reduced testosterone due to BPA exposure.…”

Section: Discussionsupporting

confidence: 77%

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Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Veissi

Jafarirad

Ahangarpour

et al. 2018

Endocrine Regulations

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 77%

Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Veissi

Jafarirad

Ahangarpour

et al. 2018

Endocrine Regulations

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“…In mammals, BPA at various doses modulates sex hormone levels and changes the expression of steroidogenic genes including StAR, CYP17a, 3β-HSD and CYP19 [47][48][49]. These data could support the present results where BPA significantly down-regulated the expression of mRNA of selected steroidogenic biomarkers with subsequent reduction in the level of testosterone attributing to the direct inhibitory action of BPA on steroidogenesis and potentially disrupts StAR phosphorylation and cholesterol transport to mitochondria [50,51]. Also, the inhibition of testicular steroidogenesis by BPA was associated with decreased steroidogenic enzyme gene expression in rat…”

Section: Discussionsupporting

confidence: 81%

Bisphenol A Down-Regulates The mRNA Expression of Steroidogenic Genes and Induces Histopathological Changes in Testes Of Rats

Marghani

Ateya

Saleh

et al. 2018

JVHC

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Abstract:Bisphenol A (BPA) is an endocrine disruptor with a weak estrogenic effect used in industry as a component of food cans. We aimed to study the toxic effects of BPA on mRNA expression of steroidogenic genes and testicular structure in mature male rats. Animals were divided into 3 groups: vehicle control rats as first group, while second group received 10 µg/kg BW and third group received BPA 15 µg/kg BW orally every alternate day for a period of 105 successive days. Serum testosterone level, mRNA expression of genes related to steroid synthesis, histopathological examination, spermatogenesis index and number of Leydig cells were evaluated in this study. Lower serum hormone levels were observed in both BPA-treated groups as compared to the control group. The gene expression patterns of steroidogenic acute regulatory protein (StAR), cytochrome P450 17a (CYP17a) and 3β-Hydroxysteroid dehydrogenase (3β-HSD) were significantly down-regulated in BPA-treated rats compared to control group. Meanwhile, the expression of aromatase (CYP19) and lutinizing hormone receptor (LHR) was significantly up-regulated. Histopathological lesions were observed in the testes and epididymis of BPA-treated rats. Spermatogenesis index and the number of Leydig cells were significantly decreased in BPA-treated groups compared with the control group. This study highlights negative effect of BPA on steroidogenic genes and testicular structure in male rats.

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“…The enhanced expression of iNOS observed in ETR SCs in the current study may be related to increased presence of cytokine and inflammatory mediators [12,23,24,25,26,29,33,34]. However, the increased expression of iNOS observed in ETR interstitial cells in the current study (most probably by macrophages) may suppress androgen production [47,48,49], which may be an additional factor in enhanced germ cell apoptosis and detachment. In addition, suppression of androgens may be a mechanism of AR downregulation in various somatic cells of the ETRs observed in the current study.…”

Section: Discussionmentioning

confidence: 73%

Upregulated Autophagy in Sertoli Cells of Ethanol-Treated Rats Is Associated with Induction of Inducible Nitric Oxide Synthase (iNOS), Androgen Receptor Suppression and Germ Cell Apoptosis

Horibe

Eid

Ito

et al. 2017

IJMS

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This study was conducted to investigate the autophagic response of Sertoli cells (SCs) to acute ethanol toxicity using in vivo and in vitro models. Adult Wistar rats were intraperitoneally injected with either 5 g/kg ethanol or phosphate-buffered saline (for the control group) and sacrificed 0, 3, 6 and 24 h after injection. Compared to the control group, enhanced germ cell apoptosis was observed in the ethanol-treated rats (ETRs) in association with upregulation of iNOS and reduced expression of androgen receptor protein levels in SCs, which were resistant to apoptosis. Meanwhile, autophagy was upregulated in ETR SCs (peaking at 24 h) compared to the control group, as evidenced by transcription factor EB (TFEB) nuclear translocation, enhanced expression of microtubule-associated protein 1 light chain3-II (LC3-II), lysosome-associated membrane protein-2 (LAMP-2), pan cathepsin protein levels and reduced expression of p62. This upregulation of SC autophagy was confirmed ultrastructurally by enhanced formation of autophagic vacuoles and by immunofluorescent double labelling of autophagosomal and lysosomal markers. Study of cultured SCs confirmed enhanced autophagic response to ethanol toxicity, which was cytoprotective based on decreased viability of SCs upon blocking autophagy with 3-methyladenine (3-MA). The results highlighted the molecular mechanisms of prosurvival autophagy in ETR SCs for the first time, and may have significant implications for male fertility.

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Increase in the expression of inducible nitric oxide synthase on exposure to bisphenol A: A possible cause for decline in steroidogenesis in male mice

Cited by 38 publications

References 51 publications

Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Bisphenol A Down-Regulates The mRNA Expression of Steroidogenic Genes and Induces Histopathological Changes in Testes Of Rats

Upregulated Autophagy in Sertoli Cells of Ethanol-Treated Rats Is Associated with Induction of Inducible Nitric Oxide Synthase (iNOS), Androgen Receptor Suppression and Germ Cell Apoptosis

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