Department of Toxicology, Anhui Medical University, Hefei, 230032, China.
Arch Toxicol. 2010 Jan;84(1):53-61. doi: 10.1007/s00204-009-0479-y. Epub 2009 Oct 28.
Cypermethrin is a widely used synthetic pyrethroid insecticide. Previous studies showed that cypermethrin significantly decreased the fertility and reduced the number of implantation sites and viable fetuses in females impregnated by males exposed to cypermethrin. As yet, little is known about the mechanism of cypermethrin-induced reproductive toxicity. In the present study, we investigated the effects of cypermethrin exposure during puberty on steroidogenesis in mice. Young male mice were administered with cypermethrin (25 mg/kg) by gavage daily from postnatal day (PND) 35 to PND70. Results showed that the level of serum and testicular testosterone (T) was markedly decreased in cypermethrin-treated mice. Additional experiment showed that cypermethrin exposure during puberty markedly downregulated mRNA level of steroidogenic acute regulatory protein (StAR) in testes. Correspondingly, protein level of testicular StAR was significantly decreased in cypermethrin-treated mice. Cypermethrin exposure during puberty did not affect the number of Leydig cells in testes. Although cypermethrin exposure during puberty did not affect the weight of testes and epididymides, the number of sperm in the cauda epididymides was significantly decreased in cypermethrin-treated mice. Taken together, these results indicate that cypermethrin exposure during puberty significantly disrupts T synthesis via downregulating the expression of testicular StAR. The decreased T synthesis might be associated with cypermethrin-induced impairment in spermatogenesis in mice.
氯菊酯是一种广泛使用的合成拟除虫菊酯类杀虫剂。先前的研究表明，氯菊酯会显著降低雄性亲代暴露于氯菊酯的雌性的生育能力，并减少着床部位和活胎数量。然而，目前对于氯菊酯引起的生殖毒性的机制知之甚少。本研究探讨了青春期暴露于氯菊酯对小鼠类固醇生成的影响。雄性幼鼠从出生后第 35 天（PND）至第 70 天（PND）每天通过灌胃给予氯菊酯（25mg/kg）。结果显示，氯菊酯处理组小鼠血清和睾丸睾酮（T）水平明显降低。进一步的实验表明，青春期暴露于氯菊酯可显著下调睾丸中类固醇急性调节蛋白（StAR）的 mRNA 水平。相应地，氯菊酯处理组小鼠睾丸中 StAR 的蛋白水平也显著降低。青春期暴露于氯菊酯并不影响睾丸中莱迪希细胞的数量。尽管青春期暴露于氯菊酯并不影响睾丸和附睾的重量，但氯菊酯处理组小鼠附睾尾部的精子数量明显减少。综上所述，这些结果表明，青春期暴露于氯菊酯通过下调睾丸 StAR 的表达显著破坏了 T 的合成。T 合成的减少可能与氯菊酯诱导的小鼠精子发生损伤有关。
