Bisphenol A disrupts granulosa cell function

Grasselli, Francesca; Baratta, L; Baioni, Laura; Bussolati, Simona; Ramoni, Roberto; Grolli, Stefano; Basini, Giuseppina

doi:10.1016/j.domaniend.2010.01.004

Cited by 112 publications

(69 citation statements)

References 36 publications

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“…These findings contrast those which found that neonatal treatment with BPA increased estradiol [Fernandez et al 2010]. However, it was reported that low doses of BPA induced estrogen but high doses inhibited estrogen levels in porcine ovarian cells in vitro [Grasselli et al 2010]. Similarly, low dose exposure (2µg/ kg) not only reduced reproductive hormones but also reduced GnRH and FSH mRNA in rats [Jin et al 2013].…”

Section: Discussioncontrasting

confidence: 53%

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

Jahan

Ain

Ullah

2016

Systems Biology in Reproductive Medicine

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The present study was designed to investigate protective effects of quercetin against bisphenol A (BPA) induced testicular toxicity in male Sprague Dawley rats. Twenty adult male rats were divided into four groups. The first group served as the control and was provided with normal saline. The second group of rats was treated with 50 mg/kg of BPA dissolved in alcoholic saline. The third group received oral gavage of 50 mg/kg quercetin while the fourth group was treated with quercetin (50 mg/kg) along with BPA (50 mg/kg). All of the treatments were carried out for 52 days. Testicular tissues and epididymis were used for histology while blood plasma was used for hormonal and biochemical analysis. BPA administration resulted in a significant reduction in seminiferous tubule diameter and epithelial height with impaired spermatogenesis. Quercetin treatment resulted in restoration of spermatogenesis and reversal of histological damage. In addition, BPA treatment significantly reduced (p < 0.05) plasma testosterone level (ng/ml) while estrogen was not affected. Similarly, BPA caused a significant alteration in the lipid profile. Interestingly, quercetin treatment led to a marked increase in plasma testosterone, decrease in estrogen concentration, as well as a normalized lipid profile. In conclusion, results indicated that BPA administration induces toxic effects on testis and epididymis, impairs spermatogenesis, with an imbalance in hormonal levels and lipid profile while quercetin amended these toxic effects by restoring normal spermatogenesis, testicular tissue damage, and hormonal levels. This suggests that quercetin may be a potential therapeutic against BPA induced testicular toxicity. ARTICLE HISTORY

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Section: Discussioncontrasting

confidence: 53%

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

Jahan

Ain

Ullah

2016

Systems Biology in Reproductive Medicine

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“…Recent studies have been focused on the effects of BPA on steroid biosynthesis in different animal models. 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].…”

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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“…In granulosa cells, BPA (0.1-10 mM, 48 h) increased progesterone and Cyp11a1 levels, but decreased E 2 and Cyp19a1 levels when given at concentrations among 1, 10, and 100 mM (Zhou et al 2008). In cultured porcine granulosa cells, all doses of BPA (0.1-10 mM) decreased progesterone production, while a low dose of 0.1 mM increased E 2 levels and high doses ranging from 1 to 100 mM BPA decreased E 2 production (Grasselli et al 2010). Another study with porcine granulosa cells showed that, depending on the dose given, BPA increased basal (1 mM) and FSHinduced (10 mM) progesterone production, while it inhibited (1-100 mM) FSH-induced E 2 production (Mlynarcíková et al 2005).…”

Section: Plasticizers: Bisphenol a And Phthalatesmentioning

confidence: 98%

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

Craig¹,

Wang²,

Flaws³

2011

Reproduction

217

123

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Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).

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Bisphenol A disrupts granulosa cell function

Cited by 112 publications

References 36 publications

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

Therapeutic effects of quercetin against bisphenol A induced testicular damage in male Sprague Dawley rats

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

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

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