毒死蜱对子代雄鼠性激素相关基因mRNA表达的影响

有机磷类农药毒死蜱 (chlorpyrifos，CPF) 可影响雄性动物生殖系统功能。为探究胚胎早期毒死蜱暴露对雄性小鼠生殖功能的影响，于母鼠妊娠后第7天 (gestational day, GD7) 至分娩前1 d每天给予母鼠灌胃染毒10 mg/kg (b.w.) 剂量的毒死蜱，于子代雄鼠出生后第42 天处死，取血液及睾丸，测定睾丸质量，通过酶联免疫法检测血液中睾酮 (testosterone，T) 及促黄体生成素 (luteinizing hormone，LH) 含量，同时采用RT-qPCR方法检测睾丸中与胆固醇及睾酮合成相关的5个基因mRNA表达的变化。结果显示:与对照组相比，毒死蜱染毒组子代鼠睾丸质量增加了16.5%，差异极显著 (P < 0.01)；血清中睾酮及促黄体生成素含量分别增加了9.9%和6.2%，但与对照差异不显著 (P > 0.05)。睾丸中胆固醇合成基因HMG-CoA synthase的mRNA表达量升高了72.9%，运输基因StAR的mRNA表达量升高了45.3%；此外，睾丸中睾酮合成基因P450scc、P450-17α和3β-HSD的mRNA表达量分别升高了95.5%、68.9%和112.0%。各基因mRNA的表达量在染毒组与对照组间均差异极显著 (P < 0.01)。研究表明，毒死蜱暴露可影响子代雄鼠睾酮合成相关基因mRNA的表达，推测毒死蜱可能是通过该途径发挥其毒性作用。

Effects of chlorpyrifos on mRNA expression of genes related to testosterone synthesis in male offspring of mice

chlorpyrifos (CPF) is an organophosphate pesticide that exhibits adverse effects on male reproductive performance. In this study, its influence on reproductive function in male offspring was investigated by gestational exposure of mother mice to CPF. 10 mg/kg body weight (b.w.) of CPF or vehicle was gavaged to mother mice from the 7th day of pregnancy to the day before delivery, and blood and testes samples from male offspring at 42 days old were collected for analysis. The content of testosterone (T) and luteinizing hormone (LH) in serum were determined by ELISA. And mRNA expression of five genes related to testosterone synthesis in testes were analyzed by RT-qPCR. Compared with the control group, prenatal exposure of CPF resulted in a 16.5% increase in the weight of testis in the offspring (P<0.01). The levels of testosterone and luteinizing hormone in serum were increased by 9.9% and 6.2%, respectively, but the difference was not significant (P>0.05). The mRNA expression level of genes related to testosterone synthesis in testes was increased significantly (P<0.01). Specifically, the expression level of HMG-CoA synthase was increased by 72.9%, and that of StAR was increased by 45.3%. In addition, the expression levels of P450scc, P450-17α, and 3β-HSD were increased by 95.5%, 68.9%, and 112.0%, respectively. These results showed that prenatal exposure to CPF could exert its toxicity to male offspring by affecting mRNA expression of genes related to testosterone synthesis.