【摘 要】
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Bisphenol A (BPA) is an environmental estrogen that shows carcinogenicity, yet its research on percutaneous exposure is not widespread.The aim was to investigate the effects and possible mechanisms of
【机 构】
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Department of Toxicology, School of Public Health, Peking University, Beijing Key Laboratory of Toxi
【出 处】
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2016(第二届)毒性测试替代方法与转化毒理学(国际)学术研讨会暨有害结局路径(AOP)与风险评估培训会议
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Bisphenol A (BPA) is an environmental estrogen that shows carcinogenicity, yet its research on percutaneous exposure is not widespread.The aim was to investigate the effects and possible mechanisms of BPA on gap junctional intercellular communication (GJIC) of human normal skin cells HaCat.Results showed that BPA increased cell proliferation rates, prolonged fluorescence recovery times and reduced fluorescence recovery rates at 1.0 × 108-1.0 × 1 0-6 mol/L.Estrogen receptor (ER) inhibitor ICI182780 partially blocked the above effects.MAPK/ERK kinase (MEK) 1/2 inhibitor U0126 completely blocked the promoting effects on cell proliferation,but didnt rescue the inhibition of GJIC.BPA 1.0 × 10-7 mol/L down-regulated Cx26 rnRNA level.ICI182780 and U0126 inhibited this effect.BPA 1.0 × 10-7 and 1.0 × 10-6 mol/L combined with U0126 up-regulated extracellular regulated protein kinases (ERK) 1/2 mRNA levels.BPA 1.0 × 10-7 mol/L combined with ICI182780 had similar but weaker effects.These results suggest that BPA can promote HaCat proliferation through ER-ERK pathway, inhibit HaCat GJIC function through ER pathway, and down-regulate Cx26 mRNA level through ER-ERK pathway.Complete inhibition of ERK pathway can stimulate BPA to promote ERK1/2 mRNA expression, and ER plays an important role in this effect.
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