Abstract
Exposure to environmental toxicants may affect reproduction and development of subsequent generations. This study was aimed at determining the male-mediated F1 effects induced following 8-weeks of subchronic exposure of F0 male mice to bisphenol A (BPA) alone and in a combination with X-rays irradiation (IR) started during their puberty.4.5 weeks old F0 male mice were exposed to BPA dissolved in ethyl alcohol and diluted in drinking water at the following doses: 5 mg/kg bw, 10 mg/kg bw, 20 mg/kg bw or irradiated with X-rays (0.05 Gy) or exposed to a combination of low doses of both agents (0.05 Gy + 5 mg/kg bw BPA). Immediately after the end of the 8 weeks exposure F0 males were caged with two unexposed females each. Three quarters of the mated females from each group were sacrificed 1 day before expected parturition for examination of prenatal development of the offspring. The remainder of the females from each group were allowed to deliver and rear litters. Pups of exposed males were monitored for postnatal development for 8 weeks. At 8–9 weeks of age 6–8 males from each group of F1 generation were sacrificed to determine sperm count and quality.The current results, compared to the earlier results, showed that exposure of pubescent males to BPA alone or in combination with irradiation may be more damaging to their offspring than the exposure of adult males. The exposure of pubescent males to BPA alone and in combination with irradiation significantly increased the frequency of abnormal skeletons of surviving fetuses, increased the percent of mortality of pups in the F1 generation, reduced the sperm motility of F1 males and may induce obesity. Additionally, the combined BPA and irradiation exposure reduced the number of total and live implantations, whereas the exposure to BPA alone disturbed the male:female sex ratio. The above results may be caused by genetic or by epigenetic mechanisms. Limitation of use of products including BPA, especially by children and teenagers, is strongly recommended.
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