微囊藻毒素对雄性大鼠生殖系统的影响

目的通过观察微囊藻毒素（MC-dLR）对雄性大鼠生殖系统的影响，以明确MC-dLR的生殖毒性并分析其作用机制。方法雄性SD大鼠40只，月龄为12月，随机分为对照组和实验1、2、3组，每组10只。实验组各组每日腹腔注射不同剂量的MC-dLR，对照组每日注射相同剂量的生理盐水。染毒后分别检测实验大鼠的体质量、睾丸质量、睾丸组织学变化、血清激素、氧化损伤指标。结果与对照组相比，3组实验组大鼠体质量、体质量净增长下降（P〈0．05），睾丸质量、睾丸系数下降（P〈0．01）；组织学检测示睾丸曲细精管萎缩，堵塞，排列紊乱；实验2、3组血清睾酮（T）浓度下降（P〈0．05），促黄体生成激素（LH）、促滤泡生成激素（FSH）水平升高；各实验组血清、睾丸组织丙二醛（MDA）含量增加，实验2、3组超氧化物歧化酶（SOD）活性下降（P〈0．05）。结论本研究表明，暴露于MC-dLR可导致雄性大鼠生殖系统的损伤，其损伤机制可能是MC-dLR进入体内可能引起机体及睾丸的氧化压力的改变，从而导致睾丸功能严重受损。

Effects of microcystin-LR on reproductive system of male rats

Objective To investigate the effects of MC-dLR on reproductive system of male rats, and to explore the mechanism. Methods Forty male rats were divided at random into four groups： control group and experiment group 1, 2 and 3, with 10 animals in each group. The animals in control group received peritoneal injection of normal saline, and the experiment group 1, 2 and 3 received peritoneal injection of 5 μg/（kg·d） ,10 μg/（kg·d）, 15 μg（kg·d） of MC-dLR, respectively. After 2 weeks, the body weight and testes weight of the rats were measured, and the pathological changes of testes observed, the serum levels of hormone and the oxidative stress index detected. Results The body weight and net weight gain of the rats were decreased （P 〈 0. 05 ）, the mean absolute weight of the testes and the mean relative weight of the testes were decreased （P 〈 0. 01 ） in the 3 experiment groups. By histological examination, the semi niferous tubules were atrophied and obstructed, and disorder form was observed. The serum testosterone level was decreased in the experiment group 2 and 3 （ P 〈0.05 ）. The levels of MDA in serum and testis tissue were increased in all rats of the experiment groups,while the SOD activity was decreased in the experiment group 2 and 3, compared with the control group（P 〈 0. 05）. Conclusions These findings suggest that long-time exposure to MC-dLR may induce reproductive damage of rats. The mechanism may be that MC-dLR could change the oxidative stress of body and testis, then inducing the reproductive toxicity.