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Abstract
Early life exposures to low doses of bisphenol A (BPA), particularly during neonatal periods, are associated with a wide range of adverse health effects in later life. The aim of the present study was to investigate the underlying molecular mechanisms associated with neonatal exposure to BPA on three estrogen responsive genes as tumor necrotic factor-alpha (TNF-Ü), retinoic acid receptor beta (RAR-Ý) and Ý-cell lymphoma-2 (Bcl-2) in mammary and ovarian tissues and assess hepatic tissue injury in female rat offspring. Rat dams (n=9) were gavaged with 0.5 and 50 mg BPA/kg b.w./day throughout lactation until weaning. In our study, we found that BPA exposure was resulted in significant increase in both TNF-Ü and Bcl-2 gene expression, however; RAR-Ý mRNA transcripts were decreased. These events were accompanied by incidence of DNA damage and histopathological lesions in ovary, breast and liver throughout the different pubertal periods. Moreover, BPA induces hepatotoxic effects, which are mediated by the overproduction of free radicals and the deficiency of NO elimination mechanisms resulting in severe oxidative/nitrosative stress in liver. These data suggest BPA causes long-term adverse effect in reproductive and non- reproductive organs of female rat offspring