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目的探讨硫酸镍(NiSO4)对雄性大鼠生殖系统损伤的可能机制。方法选择雄性大鼠32只,随机分为4组,对照组,NiSO41.25、2.50、5.00 mg/kg组;采集附睾和睾丸样本,分别检测精子活率和密度,睾丸细胞活性氧自由基(ROS)荧光强度及其Bax、caspase-3蛋白表达水平。结果 NiSO42.50和5.00 mg/kg组大鼠精子活率(分别为68.29%、65.29%)和密度(分别为3.03、2.85×106/mL)均明显低于对照组(82.34%和4.80×106/mL)(P<0.05);睾丸细胞ROS荧光强度(98.59和96.43)则明显高于对照组(62.54)(P<0.01)。与对照组比较,NiSO42.50和5.00mg/kg组Bax蛋白表达量明显升高(P<0.01),各NiSO4组大鼠睾丸细胞caspase-3前体蛋白表达量明显升高(P<0.05),且均出现caspase-3切割片段,后者呈剂量效应关系。结论过量NiSO4暴露可诱导睾丸细胞内大量生成ROS,进而上调Bax蛋白表达并激活caspase-3蛋白,终致生殖损伤发生。
Objective To investigate the possible mechanism of nickel sulfate (NiSO4) on the reproductive system of male rats. Methods Thirty-two male SD rats were randomly divided into 4 groups: control group, NiSO41.25, 2.50 and 5.00 mg / kg group; epididymal and testicular samples were collected and tested for sperm motility and density, reactive oxygen species ROS) fluorescence intensity and Bax, caspase-3 protein expression levels. Results The sperm motility (68.29%, 65.29%) and density (3.03, 2.85 × 106 / mL, respectively) in the NiSO42.50 and 5.00 mg / kg groups were significantly lower than those in the control group (82.34% vs 4.80 × 106 (P <0.05). The fluorescence intensity of ROS in testicular cells (98.59 and 96.43) was significantly higher than that in control group (62.54) (P <0.01). Compared with the control group, the protein expression of Bax in NiSO42.50 and 5.00mg / kg groups was significantly increased (P <0.01), while the expression of caspase-3 protein in testis cells in each NiSO4 group was significantly increased (P <0.05) , And all appeared caspase-3 cleavage fragments, which showed a dose-response relationship. Conclusion Excessive exposure of NiSO4 induces massive ROS production in testicular cells, which in turn up-regulates Bax expression and activates caspase-3 protein, leading to reproductive injury.