西维因致男性工人精子DNA损伤的机制初探

Preliminary study on carbaryl induced sperm DNA damage in male workers

目的:探讨西维因农药暴露与男性工人精子DNA损伤的关系,并探讨其可能的机制。方法:选择某农药厂西维因生产男工31名为暴露组;该厂行政区男性员工36名为内对照组;同地区男性行政人员22名为外对照组。检测3组人群精子DNA损伤、精浆超氧化物歧化酶(SOD)活性及精子活性氧(ROS)含量。选用培养的小鼠精母细胞(GC2-spd细胞)进行体外功能学验证,在不同浓度西维因染毒条件下,分析细胞存活率、凋亡及SOD活性,ROS含量的变化。结果:与内、外对照组相比,暴露组男性精子DNA断裂损伤显著增加(P<0.05)、精浆SOD活性降低及精子ROS增加(P<0.05)。相关性分析的结果显示,精子DNA损伤与精浆SOD的活性负相关(r=-0.53,P<0.001),与精子ROS水平呈正相关(r=0.32,P=0.002)。小鼠精母细胞随西维因染毒剂量增加细胞存活率显著下降,凋亡增多并且细胞SOD减少及ROS增加(P<0.05)。结论:西维因可影响男性精液质量,其可能的机制是通过氧化应激导致精子DNA的损伤。

Objective：To detect the effects of carbaryl exposure on sperm DNA damage ,and explore the mechanism of carbaryl induced sperm DNA damage. Methods：A case-ontrol analysis was conducted,including 31 male carbaryl exposure workers （exposure group）, 36 male administrators in the office in a pesticide factory （internal control group） and 22 male administrators in same area （external control group）. The activity of semen SOD, the level of sperm ROS and the sperm apoptosis in three groups were compared. In cytotoxic experiments, GC2-spd ceils were cultured with different doses of earbaryl. The cell survival rate, apoptosis rate ,the production of ROS and the activity of SOD were measured. Results：The sperm DNA apoptosis and the level of sperm ROS in the exposure group were significantly higher than those in the internal and external control groups （P 〈 0.05）. In addition, a negative correlation between the sperm apoptosis and semen SOD was found （r=-0.53,P 〈 0.001）,while there was a positive correlation between the sperm apoptosis and sperm ROS （r=0.32,P = 0.002）. Cytotoxic experiments showed that cell apoptosis rate and production of ROS increased,while the cell survival rate and the activity of SOD decreased at higher dose of carbaryl. Conclusion：Our findings suggested that occupational exposure to carbaryl production can cause the sperm DNA damage by oxidative stress.