二硫化碳对大鼠生精细胞线粒体呼吸链的影响

Effect of carb on disulfide on mitochondrial respiratory chain in spermatogenic cells in male rats

目的 观察二硫化碳（CS2）染毒对大鼠睾丸生殖细胞中线粒体呼吸链的影响,探索CS2染毒对雄性大鼠生殖系统的损伤机制.方法 选取24只清洁级雄性SD大鼠随机分为3个不同浓度CS2染毒组（50、250、1250 mg/m3）和1个对照组,每日静式吸入CS22 h,每周5d,共染毒10周,对照组仅吸入空气.染毒结束后断颈处死大鼠,取睾丸组织,分离睾丸组织细胞中的线粒体,提取线粒体中的蛋白,用酶联免疫吸附法（EIISA）检测大鼠生精细胞线粒体中呼吸酶复合物Ⅰ～Ⅴ的含量.结果 与对照组相比,各浓度的CS2染毒均可引起大鼠生殖细胞线粒体内呼吸酶复合物Ⅰ～Ⅴ水平明显上升,差异有统计学意义（P＜0.05）；各浓度CS2染毒组比较,呼吸酶复合物Ⅰ～Ⅳ水平的差异无统计学意义（P＞0.05）,而呼吸酶复合物水平则随着CS2染毒浓度的增加明显上升,差异有统计学意义（P＜0.05）.结论 各浓度的CS2暴露均可引起雄性大鼠睾丸生殖细胞线粒体呼吸链复合物水平上升,影响线粒体正常的氧化磷酸化过程.

Objective To investigate the effect of carbon disulfide （CS2） on the mitochondrial respiratory chain in testicular spermatogenic cells in male rats and to explore the possible mechanism of reproductive system damage caused by CS2 in male rats.Methods Twenty-four male Sprague-Dawley rats （clean grade）were randomly divided into four groups：three CS2 exposure groups （CS2 concentrations：50,250,and 1250 mg/m3）and a control group.The rats in CS2 exposure groups were exposed to CS2 by static inhalation for 10 weeks （2 h/d,5 d/w）,while the rats in control group were exposed to air.Then,all rats were sacrificed by decapitation;testicular tissues were collected,and mitochondrial protein in spermatogenic cells were extracted; the levels of mitochondrial respiratory chain enzyme complex Ⅰ～Ⅴ were measured by enzyme-linked immunosorbent assay.Results Compared with the control group,all CS2 exposure groups had significantly increased levels of mitochondrial respiratory chain enzyme complex Ⅰ～Ⅴ in spermatogenic cells （P＜0.05）.There were no significant differences in the levels of respiratory chain enzyme complex Ⅰ～Ⅳ between the CS2 exposure groups （P＜0.05）,but the level of respiratory chain enzyme complex Ⅴ rose significantly as the concentration of CS2 increased （P＜0.05）.Conclusion Various levels of CS2 exposure may increase the levels of mitochondrial respiratory chain enzyme complex in testicular spermatogenic cells among male rats,thus affecting the normal oxidative phosphorylation in mitochondria.