硫丹对成年大鼠生精功能的影响和氧化损伤

目的　研究硫丹对大鼠生精功能的影响是否与氧化损伤有关。方法　成年雄性SPFWistar大鼠随机分为 6组 ,每组 6只。 1～ 4组ig硫丹 0 ,2 .5 ,5 .0 ,7.5mg·kg- 1,每天 1次 ,每周 6次 ,持续 10周。5～ 6组在给硫丹 7.5mg·kg- 1的同时 ,ip维生素C(VitC) 2 0 ,4 0mg·kg- 1。给药结束时检查各组动物的每日精子生成量 (DSP)、附睾精子数和形态 ,并检测血清和睾丸、肝组织中的过氧化脂质 (LPO)和 8 羟基脱氧鸟苷 (8 OHdG)的含量。结果　给硫丹的5 .0和 7.5mg·kg- 1组出现短暂的中枢神经系统中毒症状。给药结束时 3个单给硫丹组DSP和附睾精子计数都低于对照组 ,精子畸形率则高于对照组。同时ipVitC两组的DSP和精子计数虽然仍低于对照组 ,但都比单给硫丹组有所改善。给硫丹组血清、肝脏和睾丸组织中的LPO和 8 OHdG都高于对照组。同时注射VitC组血清和上述组织中的LPO和8 OHdG都比单给硫丹 7.5mg·kg- 1组低。结论　大鼠长期大剂量接触硫丹能引起精子生成减少 ,异常精子比例增多 ,并能引起肝脏和睾丸组织脂质过氧化和DNA氧化损伤 ,而这些改变都能被抗氧化剂VitC部分改善 ,提示氧化损伤可能是硫丹生殖毒性的作用机理之一。

Effects of endosulfan on the spermatogenesis and oxidative damage in rats

AIM To investigate if the effects of endosulfan on spermatogenesis in rats are related to oxidative damage. METHODS Adult male Wistar rats were randomly divided into 6 groups with 6 rats in each. Animals in the 1 st to 4 th groups were orally administrated with endosulfan of 0, 2.5, 5.0, and 7.5 mg·kg^-1 daily, 6 times a week for 10 weeks. Those in the 5 th and 6 th group were given intraperitoneally with vitamin C 20 and 40 mg·kg^-1 synchronously with the oral administration of 7.5 mg·kg^-1 endosulfan. Daily sperm production (DSP), sperm count and morphology were studied after the treatments. Lipid peroxidation product (LPO) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in serum, liver and testis homogenates were determined with enzyme-linked immunosorbent assay (ELISA). RESULTS The DSP and epididymal sperm count decreased, whereas the incidence of sperm abnormality increased significantly in the endosulfan treated groups compared with those in control group. LPO and 8-OHdG in serum, liver, and testis homogenates increased significantly in the endosulfan treated groups compared with those in control group. The acknowledged antioxidant vitamin C administered simultaneously with endosulfan partly protected against the endosulfan induced sperm toxicity and the oxidative damages to liver and testis. CONCLUSION These results implied that the oxidative damage may be involved in the mechanism of endosulfan induced reproductive toxicities.