Imbalance of Testosterone Level in Male Offspring of Rats Perinatally Exposed to Bisphenol A

Abstract

The purpose of this study was to investigate whether exposure to bisphenol A (BPA) through the placenta and milk has any effect on the reproductive system in male offspring. Pregnant rats were treated with BPA at 0, 4, 40 and 400 mg/kg body weight, from gestation day 6 through lactation day 20 by gavage. Plasma testosterone concentrations in offspring at 9 weeks old were significantly high in BPA groups as compared with those of the control. At the age of 36 weeks the hormone concentrations showed an increase in a dose-dependent manner, although without statistical significance. Testosterone content in testes showed a similar tendency to that in plasma, though statistically insignificant. Little alteration in testes weight was seen in BPA-exposed offspring. There was no remarkable change in plasma concentrations of luteinizing hormone and follicle-stimulating hormone at 9 weeks old. The pathway of E 2 (17β β β β β-estradiol) formation from testosterone seemed not to be affected by BPA. The results indicate that exposure to BPA during the perinatal period has a significant effect on testosterone homeostasis in male offspring of rats.

Impairment in protein expression profile of testicular steroid receptor coregulators in male rat offspring perinatally exposed to Bisphenol A

“…There are only two reports in the literature documenting the effects of perinatal exposure of male rats to BPA leading to a significant increase in the plasma testosterone levels in adult male rats, a decrease in the exvivo synthesis of testosterone by the Leydig cells and a decline in leutinizing hormone levels in the pituitary culture (Akingbemi et al 2004;Watanabe et al 2003). In our recent study, we observed that the perinatal exposure of rats (F 0 ) to BPA leads to perturbations in the hormonal profile of adult F 1 male rats.…”

Effects of in Utero and Lactational Exposure to Bisphenol A on Thyroid Status in F1 Rat Offspring

“…Kwon et al showed that exposure at 320 mg/ kg/day from GD 11 through PND 20 resulted in no apparent change in male and female pubertal development and reproductive function in SD rats 18) . We previously reported that exposure at 4 or 40 mg/kg/day from GD 6 through PND 20 did not cause changes in somatic growth or anogenital distance in rat offspring of both sexes 16) , but these doses did affect testosterone homeostasis in the male testis 19) . Thus, much of the interest in BPA toxicity has focused on its putative effects on reproductive organs and genital glands.…”

Adverse Effects of Bisphenol A on Male Reproductive Function

“…Protein expression of the LHR is also compromised following BPA exposure, and may lead to decreasing androgen secretion by testicular Leydig cells (Nanjappa et al 2012 ). The testosterone concentration increased in 9-week-old male pups exposed to BPA in utero and through lactation (Watanabe et al 2003 ), and this could be attributed to in utero BPA-induced proliferative activity (mitogenic effect) on testosterone-producing Leydig cells (Nanjappa et al 2012 ). In addition to modulating the Leydig cells, BPA also induced downregulation of several genes associated with Sertoli cell function (Msi1h, Ncoa1, Nid1, Hspb2, and Gata6) in 6-week-old male mice after prenatal exposure (Tainaka et al 2012 ), thereby disrupting the blood-testis barrier (BTB) and impairing spermatogenesis Su et al 2011 ).…”