Maternal Exposure to Xenoestrogen Bisphenol a on Embryo Fetal Development and Teratogenic Potential in Rattus Norvegicus

In recent years, the association between alterations in animal hormonal regulation and exposure to estrogenic endocrine – disrupting chemicals (EEC), such as xenoestrogens has led to increasing public and scientific concern. EEDs reportedly have the potential to produce widespread adverse effects through their endocrine disrupting activity, such as carcinogenicity, neurotoxicity, immunotoxicity, interference with the cardiovascular system, reproductive abnormalities, developmental toxicity, and so on (Kavlock et al., 1996; Witorsch, 2002). Many studies in animal models have reported that prenatal exposure to EEDs could induce birth defects (Richter et al., 2007; Sone et al., 2004), and the embryo toxic and teratogenic potential of EEDs have been of particular concern among researchers. Among the endocrine disrupting chemicals, bisphenol a (BPA, C 15 H 16 O 2 ), an estrogen – activity compound has received much attention. Bisphenol A (2, 2bis (4-hydroxyphenol) propane; BPA), a chemical compound found in plastic products, is being used increasingly in industrial manufacturing materials. Numerous reports state that BPA production was 2, 214, 000 metric tons worldwide per year in 2003 and 3, 200, 000 tons in 2005 (Calafat et al., 2005). Because BPA is used to manufacture polycarbonate plastic, epoxy resins and certain dental sealants (Kang et al., 2006), humans are frequently exposed to BPA released from plastics and food cans in daily life (Richter et al., 2007). Therefore, through these daily exposures BPA potentially affects human health. Estrogenic activity of BPA has been reported for over 50 years. Krishnan et al., (1993) reported BPA is released from autoclaved polycarbonate flasks and estrogenic activity of BPA is mediated via estrogen receptor (ER). Steinmetz et al., (1998) indicated that BPA induced the molecular and morphological alterations in the uterus and vagina of adult rats. Low dose of BPA in utero accelerated vaginal opening in mice and a large dose of BPA given neonatally induced ovary – independent vaginal epithelial changes (Honna et al., 2002). Previous studies through analyses of BPA in the serum of pregnant women and in cord blood collected at birth have indicated that BPA accumulates early in fetuses (Takahashi and Oishi, 2000). Developing fetus is more sensitive to estrogenic chemicals than adults in various induction of abnormalities (Iguchi, 1992). Pregnant rats were orally administered BPA at a dose of 10 mg/kg/day resulting in a decreased number of neonates and decreased survival rate (Tachibana et al., 2007). In this study, therefore, we investigated embryo toxicity and/ or foeto toxicity of BPA through maternal exposure.