Abstract
The FDA recently announced concern about the safety of bisphenol A (BPA) and the need for more research to regulate the use of BPA. In the current controversy, scant attention is being paid to toxicity at the fundamental, molecular level, which is the topic of this report. BPA is an endocrine-disrupting chemical used in the production of plastic food and beverage containers, leading to ubiquitous low-dose human exposure. It has been suggested that exposure to even low doses of BPA during development may be associated with increased susceptibility to obesity and diabetes later in life. In the present study, timed pregnant BL6 mice were treated on days 6-17 of gestation with BPA (0.1, 1, or 10 mg/kg/day). There were no BPA-related effects on adult mating, fertility or gestational indices, ovarian primordial follicle counts, offspring sex ratios or postnatal survival, or reproductive organ weights or histopathology (ovary). However, BPA (10 mg/kg) significantly reduced the onset of estrous cycle. Moreover, ovarian cysts were significantly increased in the 10 mg/kg BPA group. We observed increased estrus cycle and decreased in vaginal opening day against BPA treatment. At 10 mg/kg, BPA also reduced F1/F2 weanling body weight, reduced weanling spleen and testes weights (with seminiferous tubule hypoplasia), which did not result in adverse effects on adult reproductive structures or functions. After delivery, F1 female pups were held for 24 days; ovary and brain tissues were then evaluated. There were no treatment-related effects in the low-dose region (0.1 and 1 mg/kg/day) on any parameters. BPA should not be considered a selective reproductive toxicant, based on the results of this study.
