氯氰菊酯对成年雄性大鼠生殖系统及雄激素受体表达的影响

目的 研究氯氰菊酯（CYP）对雄性大鼠生殖系统的损伤作用,并阐明其与雄激素受体（AR）表达的关系.方法 选择成年雄性SD大鼠60只,随机分为5组（对照组及氯氰菊酯6.25、12.5、25和50 mg·kg-1·d-1组）.灌胃染毒15天后处死大鼠,分离睾丸,称重,一侧用于精子头计数,另一侧用于普通病理和免疫组化检测.结果 12.5 和 25 mg·kg-1·d-1组睾丸脏器系数增加,与对照组比较差异有统计学意义（P＜0.05）.50 mg·kg-1 ·d-1组睾丸每日精子生成量减少,与对照组比较差异有统计学意义（P＜0.05）.染毒组大鼠睾丸曲细精管变形、皱缩,出现坏死管腔伴随细胞层数减少,染毒组AR表达减少.结论 氯氰菊酯可引起大鼠雄性生殖系统的损伤,而AR表达受到抑制可能是损伤的重要机制之一.

Toxic effects of cypermethrin on the reproductive system and the expression of androgen receptor in male rats

Objective To investigate the possible toxicity of cypermethrin （CYP） on the reproductive system in male rats, to elucidate the relationship between eypermethrin - induced toxicity and the expression of androgen receptors （AR） and to provide basis for the revelation of the anti - androgen effect of pyrethriod insecticides. Methods 60 male Sprague- Dawley rats were randomized into 5 groups： 0, 6.25, 12.5, 25 and 50 mg· kg^-1 · d^-1groups. 15 days after gavage for toxieation, the rats were sacrificed, followed by excision and measurement of the testes. One testis was used for testicular sperm head counts, and the other was for immunohistochemical test to characterize the expression of AR. Resuits The visceral coefficient of testis increased in 12.5 and 25 mg· kg^-1 · d^-1groups compared with the control group, the relative weights of testes in 12.5 and 25 mg · kg^-1 · d^-1 groups increased, with statistical differences as compared to the control group （ P 〈 0.05 ）. Testicular sperm head counts reduced significantly in 50 mg· kg^-1 · d^-1 group, with statistical differences as compared to the control group （ P 〈 0.05 ）. In CYP group, malformation and distortion in the architecture of testieular seminiferous tubules were evident as well as the appearance of necrotic lumen accompanied by reduced cell stratification of the scminiferous tubules in CYP treatment groups, and decrease in AR expression. Conclusion Cypermethrin can induce impairment to the reproductive system in male rats, and the inhibition of AR expression may be attributed to one of the mechanisms of impairment.