Objective To investigate the underlying mechanism of alcohol-induced damage involving nitric oxide (NO) in the reproductive system of male mice.Methods C57BL/6J male mice (10 weeks old) were randomly divided into 2 groups:the con-trol group ( orally treated with 10%sucrose daily for 15 weeks) and the alcohol group ( orally treated with 8 g/kg daily for 15 weeks) . Fifteen weeks later, epididymises were collected for the observation of sperm number and activity.At the same time, blood samples were taken to detect the level of serum testosterone.Testes were also collected for the detection of serum testosterone levels, the levels of NO and OONO-, as well as the expression levels of inducible nitric oxide synthase ( iNOS ) , endothelial nitric oxide synthase (eNOS), and neural nitric oxide synthase (nNOS).Results As compared with that of the control group (221 ±55) ×106/ml)(P<0.05), the number of sperms in the animals of the alcohol group was obviously decreased (394 ±60) ×106/ml) (P<0.05), and the activity (P<0.05) of sperms in the animals of the alcohol group was also decreased (54 ±13)%, as compared with(23 ±8)%of the control group(P<0.05).Laboratory tests also revealed that the levels of testosterone in serum and testes were all decreased (P<0.05).The levels of NO and OONO-were all increased in the alcohol-treated mice (P<0.05), and the expression levels of iNOS and nNOS were also up-regulated in the testes of the alcohol-treated mice.Conclusion Enhanced synthesis of NO in the testis of male mice following prolonged consumption of alcohol was one of the important mechanisms involved in the injury of the reproductive system of adult male mice.%目的 探讨酒精摄入损伤成年雄性小鼠生殖系统的一氧化氮机制. 方法 选用10周龄的C57BL/6J小鼠,按数字表法随机分为2组:对照组(10%蔗糖,口服)和酒精摄入组(8 g/kg体质量,口服). 持续15周后,取附睾观察精子数目及活力;取血分离血清检测其中睾酮含量;取睾丸组织检测组织中睾酮含量,检测睾丸中一氧化氮( NO)水平和过氧化亚硝基阴离子( OONO-)含量,同时检测睾丸组织中诱导型一氧化氮合酶( iNOS)、内皮型一氧化氮合酶( eNOS)、神经型一氧化氮合酶(nNOS)蛋白表达水平. 结果 酒精摄入组与对照组相比,酒精摄入组小鼠精子数目减少[(394 ±60) ×106/ml比(221 ±55) ×106/ml](P<0.05),精子活力下降[(54 ±13)%比(23 ±8)%](P<0.05);血清中睾酮含量下降(P<0.05),睾丸中睾酮含量下降(P<0.05),睾丸中NO水平增加(P<0.05),OONO-含量增加(P<0.05),睾丸中iNOS(P<0.05)和nNOS蛋白(P<0.05)表达增加. 结论 长期酒精摄入后小鼠睾丸中NO合成增加是导致成年小鼠雄性生殖系统损伤的重要机制之一.
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