小鼠四氯化碳预处理对丙烯腈氧化应激的影响

Carbon tetrachloride pretreatemt on the oxidation stress in mice resulted from administering acrylonitrile

目的以四氯化碳(CCl4)预处理为模型,探讨细胞色素P450抑制对丙烯腈(AN)氧化应激效应的影响。方法将40只小鼠雌雄各半随机分成4组,正常对照组、CCl4对照组、CCl4+AN、AN,CCl4组和CCl4+AN组腹腔注射CCl4(1.28 ml/kg)预处理24 h,分别给予AN 0、0、20、20 mg/kg,经腹腔染毒24 h。测定小鼠脑、肝组织中丙二醛(MDA)和谷胱甘肽(GSH)的含量及超氧化歧化酶(SOD)活力。结果CCl4+AN组脑体系数明显高于CCl4组(P<0.05)。CCl4+AN组的肝脏脏器系数明显高于各组(P<0.05);各剂量组脑组织中MDA含量高于对照组,CCl4+AN组与对照组差异有统计学意义(P<0.05);AN组GSH含量明显高于对照组(P<0.05);各剂量组中SOD含量与对照组比较,有不同程度的下降,但差异无统计学意义。各剂量组肝组织中的MDA、GSH含量和SOD活力低于对照组。结论CCl4预处理增强CN的氧化应激效应,推断CN原形可能是小鼠氧化应激主要机制。

Objective To explore the effects of P450 inhibition with carbon tetrachloride pretreatment on the oxidative stress of acrylonitrile（AN） in mice. Methods Forty Kuming mice were randomly divided into four groups, control group, carbon tetrachloride group （CC14）, AN following CC14 pretreatrnent group （AN ＋ CC14 ）and AN group. The mice were pretreated CC14 （1.28 ml/kg） by intraperitoneal injection in CCl4 group and AN ＋ CCl4 group. Twenty-four h later, 0, 0, 20, 20 mg/kg. AN were administered by intraperitoneal injection respectively, malondialdehyde （ MDA）, glutathione （ GSH ） and superoxide dismutase （SOD） in brain and liver were determined in all mice. Results The brain/body weight ratios of AN ＋ CCl4 group were significantly increased than that of CCl4 group （P 〈 0.05）; The liver/body weight ratios of AN ＋ CCl4 group were significantly increased than other groups（ P 〈 0.05）. The level of MDA in mice brains were dose-dependently increased, The level of MDA in AN ＋ CCl4 group were significantly higher than that of control group （ P 〈 0.05） ; The activities of GSH in AN group were significantly higher than that of control group （ P 〈 0.05） ; The activities of SOD in mice brain were dose-dependently decreased without statistical significance . The level of MDA and the activities of GSH and SOD in mice liver were dose-dependently decreased. Conclusion Enhanced oxidative stress of AN following CCl4 pretreatment in the mice, The parent AN may be result in oxidative stress in the mice.