中文摘要：

目的研究氯化锰导致的大鼠生精细胞caspase-9及Apaf-1表达中XIAP和Smac的调节机制,探讨锰导致的雄性不育机制。方法雄性SD大鼠随机分为对照组、低剂量（15 mg/kg MnCl2）和高剂量（30 mg/kg MnCl2）组,腹腔注射MnCl24周和6周,免疫组织化学检测生精细胞caspase-9、Apaf-1、XIAP和Smac表达。结果 （1）各组生精细胞caspase-9、Apaf-1和Smac表达均显著升高（P〈0.01）,XIAP表达降低（P〈0.01）。（2）同时间的高剂量组与低剂量组比较,同剂量的6周组与4周组比较,生精细胞caspase-9、Apaf-1和Smac表达均显著升高（P〈0.01）,XIAP表达降低（P〈0.01）。（3）各组caspase-9与Apaf-1表达呈正相关（r=0.862,P〈0.05）,XIAP与Smac表达呈负相关（r=-0.887,P〈0.01）。结论锰可促进生精细胞caspase-9、Apaf-1和Smac表达,抑制XIAP表达,导致细胞凋亡,产生雄性生殖毒性效应。

英文摘要：

Objective To determine the regulatory effects of XIAP and Smac on the expressions of caspase-9and Apaf-1 in spermatogenic cells of rats exposed to manganese and further explore the mechanisms through which male sterility caused by manganese. Methods Male Sprague Dawley rats were divided into control and MnCl2（ 15 and 30 mg/kg） groups. After exposed to manganese for 4 or 6 weeks,the expressions of caspase-9,Apaf-1,XIAP and Smac were detected by immunohistochemistry（ SABC） assay. Results 1） The caspase-9-positive-cell rate,the Apaf-1-positive-cell rate and the Smac-positive-cell rate were increased（ P〈0.01） while the XIAP-positive-cell rate was decreased（ P〈0.01）. 2） Among the same dose and same time manganese groups,caspase-9-positive-cell rate,the Apaf-1-positive-cell rate and the Smac-positive-cell rate were increased（ P〈0.01） while the XIAP-positive-cell rate was decreased（ P〈0.01）. 3） There was a positive correlation between caspase-9-positive-cell rate and Apaf-1-positive-cell rate（ r = 0. 862,P 0. 05）,and a negative correlation between XIAP-positive-cell rate and Smac-positive-cell rate（ r =-0. 887,P〈0.01）. Conclusion Manganese could promote the expressions of caspase-9,Apaf-1 and Smac and inhibit the expression of XIAP,which might lead to male reproductive toxicity.