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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra
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Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra

机译：塑料和口服避孕药中的雌激素化学物质会破坏胎儿小鼠前列腺和尿道的发育

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Exposure of human fetuses to man-made estrogenic chemicals can occur through several sources. For example, fetal exposure to ethinylestradiol occurs because each year ≈3% of women taking oral contraceptives become pregnant. Exposure to the estrogenic chemical bisphenol A occurs through food and beverages because of significant leaching from polycarbonate plastic products and the lining of cans. We fed pregnant CD-1 mice ethinylestradiol (0.1 μg/kg per day) and bisphenol A (10 μg/kg per day), which are doses below the range of exposure by pregnant women. In male mouse fetuses, both ethinylestradiol and bisphenol A produced an increase in the number and size of dorsolateral prostate ducts and an overall increase in prostate duct volume. Histochemical staining of sections with antibodies to proliferating cell nuclear antigen and mouse keratin 5 indicated that these increases were due to a marked increase in proliferation of basal epithelial cells located in the primary ducts. The urethra was malformed in the colliculus region and was significantly constricted where it enters the bladder, which could contribute to urine flow disorders. These effects were identical to those caused by a similar dose (0.1 μg/kg per day) of the estrogenic drug diethylstilbestrol (DES), a known human developmental teratogen and carcinogen. In contrast, a 2,000-fold higher DES dose completely inhibited dorsolateral prostate duct formation, revealing opposite effects of high and low doses of estrogen. Acceleration in the rate of proliferation of prostate epithelium during fetal life by small amounts of estrogenic chemicals could permanently disrupt cellular control systems and predispose the prostate to disease in adulthood.
机译：人类胎儿暴露于人造雌激素化学物质可通过多种途径发生。例如，胎儿暴露于乙炔雌二醇的发生是因为每年约有3％服用口服避孕药的妇女怀孕。由于聚碳酸酯塑料产品和罐壁的大量浸出，食品和饮料中会暴露于雌激素性双酚A。我们喂养了怀孕的CD-1小鼠乙炔雌二醇（每天0.1μg/ kg）和双酚A（每天10μg/ kg），其剂量低于孕妇的暴露范围。在雄性小鼠胎儿中，炔雌醇和双酚A都会增加背外侧前列腺导管的数量和大小，并总体上增加前列腺导管的体积。用抗增殖细胞核抗原和小鼠角蛋白5抗体切片的组织化学染色表明，这些增加是由于位于初级导管中的基底上皮细胞的增殖显着增加所致。尿道在大肠区域畸形，进入膀胱的位置明显狭窄，这可能导致尿流异常。这些作用与由类似剂量（0.1μg/ kg /天）的雌激素药物己烯雌酚（DES），已知的人类发育性致癌物和致癌物引起的作用相同。相反，高2,000倍的DES剂量完全抑制了背外侧前列腺导管的形成，揭示了高剂量和低剂量雌激素的相反作用。少量雌激素化学物质在胎儿生命中加速前列腺上皮的增殖速率可能会永久破坏细胞控制系统，并使前列腺易患成年疾病。

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