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首页> 外文期刊>The Journal of toxicological sciences >Effect of in utero exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis: a study in rats using different ways of administration
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Effect of in utero exposure to endocrine disruptors on fetal steroidogenesis governed by the pituitary-gonad axis: a study in rats using different ways of administration

机译：宫内暴露于内分泌干扰物对垂体-性腺轴控制的胎儿类固醇生成的影响：一项使用不同给药方式的大鼠研究

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The effects of endocrine disruptors on testicular steroidogenesis in fetal rats were investigated in a study involving in utero exposure. In the major part of this study, pregnant rats at gestational day (GD)15 were given a single oral administration of the test substance, and then the expression of the following mRNAs in GD20 fetuses was determined: testicular steroidogenic acute-regulatory protein (StAR), a cholesterol transporter mediating the rate-limiting step of steroidogenesis, a ?-subunit of pituitary luteinizing hormone (LH), and a regulator of gonadal steroidogenesis. Among the substances tested, only di(2-ethylhexyl)phthalate (DEHP) reduced the expression of fetal testicular StAR. The others listed below exhibited little effect on fetal StAR: 2,2’,4,4’-tetrabromodiphenylether, tributyltin chloride, atrazine, permethrin, cadmium chloride (Cd), lead acetate (Pb) and methylmercury (CH3HgOH). None of them, including DEHP, lacked the ability to reduce the expression of pituitary LH? mRNA. The present study also examined the potential of metals as modifiers of fetal steroidogenesis by giving them to pregnant dams in drinking water during GD1 and GD20. Under these conditions, Cd and Pb at a low concentration (0.01 ppm) significantly attenuated the fetal testicular expression of StAR mRNA without a concomitant reduction in LH?. No such effect was detected with CH3HgOH even at 1 ppm. These results suggest that: 1) DEHP, Cd and Pb attenuate the fetal production of sex steroids by directly acting on the testis, and 2) chronic treatment during the entire gestational period is more useful than a single administration for determining the hazardous effect of a suspected endocrine disruptor on fetal steroidogenesis.
机译：在一项涉及子宫暴露的研究中，研究了内分泌干扰物对胎鼠睾丸类固醇生成的影响。在这项研究的主要部分中，妊娠大鼠（GD）15一次口服受试物质，然后确定GD20胎儿中以下mRNA的表达：睾丸类固醇生成性急性调节蛋白（StAR） ），介导类固醇形成的限速步骤的胆固醇转运蛋白，垂体促黄体生成激素（LH）的β亚基和性腺类固醇生成的调节剂。在测试的物质中，只有邻苯二甲酸二（2-乙基己基）酯（DEHP）降低胎儿睾丸StAR的表达。以下列出的其他对胎儿StAR的影响很小：2,2'，4,4'-四溴二苯醚，三丁基氯化锡，chloride去津，苄氯菊酯，氯菊酯，氯化镉（Cd），乙酸铅（Pb）和甲基汞（CH 3 < / sub> HgOH）。它们，包括DEHP，都不缺少降低垂体LH表达的能力。 mRNA。本研究还通过在GD1和GD20期间将金属添加到饮用水中的孕妇水坝中，研究了金属作为胎儿类固醇生成修饰剂的潜力。在这些条件下，低浓度（0.01 ppm）的Cd和Pb会显着减弱StAR mRNA的胎儿睾丸表达，而LHα却不会随之降低。 CH 3 HgOH即使在1 ppm时也未检测到这种作用。这些结果表明：1）DEHP，Cd和Pb通过直接作用于睾丸而减弱了性类固醇的胎儿产生; 2）在整个妊娠期进行长期治疗比单次给药更能确定胎儿的性激素危害。可疑内分泌干扰物对胎儿类固醇生成的影响。

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