日本毒性学会学術年会
第41回日本毒性学会学術年会
セッションID: P-175
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一般演題 ポスター
Low dose of bisphenol A activates steroidogenic gene via JNK signaling pathway in adrenal cells
*Hsin-Chieh LANI-Wen LINZhi-Jie YANG
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会議録・要旨集 フリー

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抄録
Some artificial chemicals used in our life are classified as endocrine disrupting chemicals (EDCs) since they can interrupt the functions of endogenous hormone. Bisphenol A (BPA) is one of EDCs that made of polycarbonate plastic and constituent of resins used in food packaging and dentistry. This chemical can be accumulated along food chains and is detectable in tissues of both wildlife and humans. In the previous studies of human, BPA levels in serum are around 1-100 nM. It is well known that BPA is involved in development, reproduction, endocrine and malignant diseases by disrupting hormone functions. To investigate the influence of BPA on steroidogenesis pathway in adrenal, we examined the effects of steroidogenic molecules using a mouse adrenocortical tumor cell line (Y1). The data indicate that BPA would not cause cell death until over 100 μM which is much higher than the concentration detected in human serum. In low dose of BPA (1-100nM), the promoter activity of CYP11A1 (P450scc) could be induced. From the immunoblotting results, we demonstrated that BPA would affect steroidogenic signaling pathway. BPA induce P450scc expression and c-Jun phosphorylation in Y1 cells. Furthermore, treatment of SP600125, the specific inhibitor of JNK signaling would reduce the BPA activation on steroidogenic gene. Thus, we demonstrated that low level and long time stimulation of BPA in adrenal endocrine cells may affect steroidogenesis through the JNK/c-Jun signaling pathway.
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