小鼠丙酮预处理对丙烯腈氧化应激效应的影响  

Effects of acetone pretreatment on oxidative stress induced by acrylonitrile in mice

作　　者：邢光伟[1] 王苏华[1] 陆荣柱[1] 韩方岸[1] 

机构地区：[1]江苏大学医学技术学院临床化学与卫生检验教研室,江苏镇江212013

出　　处：《毒理学杂志》2007年第6期458-460,共3页Journal of Toxicology

基　　金：江苏大学青年基金(JDQ03026);江苏大学高级人才启动基金(JDG0406);江苏省自然科学基金(BK2004061);江苏省社会发展基金(BS2005049)

摘　　要：目的探讨细胞色素P450 2E1诱导对丙烯腈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:空白对照组、(丙酮)诱导组、单纯丙烯腈染毒组(AN)和(丙酮)诱导加丙烯腈染毒组(诱导+AN)。诱导组和诱导+AN组小鼠饮用体积分数为1%的丙酮溶液预处理7 d。4组分别给予丙烯腈0、01、0和10 mg/kg,经腹腔注射染毒24 h后测定小鼠全脑和肝脏的丙二醛(MDA)和谷胱甘肽(GSH)含量以及超氧化歧化酶(SOD)活力。结果4组脑的脏器系数及肝脏的脏器系数性差异无统计学意义;AN染毒组小鼠脑组织中的MDA含量显著高于对照组,诱导+AN组的MDA水平较AN组有所降低;诱导+AN组组小鼠脑组织GSH和SOD含量均高于AN组,其中GSH水平升高具有统计学意义(P<0.05);和空白对照组相比,诱导+AN组、AN组小鼠肝组织中的MDA含量均有所增高,非酶性抗氧化剂GSH含量有所降低,特别是诱导+AN组和AN组相比又有所上升,但差异无统计学意义(P>0.05)。单纯AN组的SOD活力较单纯对照组明显降低(P<0.05),诱导+AN组的SOD活力有所回升,接近单纯对照组水平。结论CYP 2E1诱导表达可减轻丙烯腈的氧化应激损伤,提示丙烯腈原形可能是小鼠引起氧化损伤的主要机制。Objective To explore the effects of cytochrome P450 induction by acetone pretreatment on the oxidative stress produced by acrylonitrile （AN） in mice. Methods Forty Kuming mice were randomly divided into4 groups： Control group, AN group, Acetone group, and AN following acetone pretreatment group （AN ＋ acetone）. The mice were treated with acetone in drinking water （1%v/v） in Acetone group and AN ＋ Acetone group. 7 days later,AN（0, 10,0, 10 mg/kg） were administered by i.p. in the control group, AN group, acetone group and AN ＋ Acetone group, respectively, malondialdehyde （ MDA ）, reduced glutathione （ GSH ） and superoxide dismutase（SOD） in mice brains and livers were determined. Results The changes of brain/body weight ratios and liver/body weight ratios of all treatment groups were not significant compared with control group. The level of MDA in brain of mice in AN group was significantly higher than that of control group（ P 〈 0.05 ） , The level of MDA in AN ＋ Acetone group were lower than that of AN group though the difference was not significant ; The GSH contents of brain in AN group were significantly lower than that of control group and AN ＋ Acetone group （ P 〈 0.05） ; The activities of SOD in mice brain in AN ＋ Acetone group were increased compared with control and AN group but without statistical significance . The level of MDA in mice liver were increased compared with control group with no significance. Though the level of MDA and GSH in liver of mice in AN ＋ Acetone group were higher than that of AN group, the differences were not significant; The activities of SOD in mice liver were decreased compared with control, with a significant decreasing in the group of AN （ P 〈 0.05 ）, but the difference between the Acetone ＋ AN group was not significant. Conclusion Acetone pretreatment in the mice can alleviate oxidative damage of AN and it can be implied that the parent AN may be mainly responsible for oxidative stress in the mice.

关 键 词：丙酮诱导 丙烯腈 脑组织 肝组织 氧化应激 

分 类 号：R99[医药卫生—毒理学]