Zhang Heng, Wang Hua, Ji Yan-Li, Ning Huan, Yu Tao, Zhang Cheng, Zhang Ying, Zhao Xian-Feng, Wang Qun, Liu Ping, Meng Xiu-Hong, Xu De-Xiang
Department of Toxicology, Anhui Medical University, Hefei 230032, China.
Toxicol Lett. 2009 Dec 1;191(1):47-56. doi: 10.1016/j.toxlet.2009.08.007. Epub 2009 Aug 14.
Fenvalerate, a widely used synthetic pyrethroid insecticide, has been associated with poor semen quality in human being. However, little is known about the effects of lactational fenvalerate exposure on testicular development and spermatogenesis. The purpose of the present study was to investigate the effects of maternal fenvalerate exposure during lactation on testicular development and spermatogenesis in male offspring. Maternal mice were administered with fenvalerate (60 mg/kg) by gavage daily from postnatal day (PND) 0 to PND21. Lactational fenvalerate exposure markedly decreased the absolute and relative weights of testes and increased the number of apoptotic cells in testes of pups at weaning. Histological examinations showed abnormal seminiferous tubules with large vacuoles or complete spermatogenic failure in testes of fenvalerate-treated mice at weaning. Additional experiment showed that lactational fenvalerate exposure markedly reduced mRNA and protein levels of testicular P450scc, a testosterone (T) synthesis enzyme. Consistent with down-regulation of testicular P450scc, the level of serum and testicular T at weaning was significantly decreased in pups whose mothers were exposed to fenvalerate during lactation. Although the expression of testicular P450scc and serum and testicular T in adulthood restored to control level, the decreased weight of testes and histological changes were irreversible. Importantly, the percentage of mature seminiferous tubules (stages VII and VIII) and the number of spermatozoa were obviously decreased in adult male mice whose mothers were exposed to fenvalerate during lactation. Taken together, these results suggest that lactational fenvalerate exposure permanently impairs testicular development and spermatogenesis.
氰戊菊酯是一种广泛使用的合成拟除虫菊酯类杀虫剂，与人类精液质量差有关。然而，关于哺乳期接触氰戊菊酯对睾丸发育和精子发生的影响知之甚少。本研究的目的是探讨哺乳期母体接触氰戊菊酯对雄性后代睾丸发育和精子发生的影响。从出生后第0天（PND）至第21天，每天通过灌胃给母鼠施用氰戊菊酯（60 mg/kg）。哺乳期接触氰戊菊酯显著降低了断奶时幼崽睾丸的绝对重量和相对重量，并增加了睾丸中的凋亡细胞数量。组织学检查显示，断奶时经氰戊菊酯处理的小鼠睾丸的生精小管异常，有大液泡或完全生精失败。额外的实验表明，哺乳期接触氰戊菊酯显著降低了睾丸P450scc（一种睾酮（T）合成酶）的mRNA和蛋白水平。与睾丸P450scc的下调一致，哺乳期接触氰戊菊酯的母鼠所生幼崽断奶时血清和睾丸T水平显著降低。尽管成年期睾丸P450scc以及血清和睾丸T的表达恢复到对照水平，但睾丸重量的降低和组织学变化是不可逆的。重要的是，哺乳期接触氰戊菊酯的成年雄性小鼠中成熟生精小管（VII和VIII期）的百分比和精子数量明显减少。综上所述，这些结果表明哺乳期接触氰戊菊酯会永久性损害睾丸发育和精子发生。
