中文摘要：

目的：探讨S-腺苷蛋氨酸（SAM）对丙烯腈（AN）染毒小鼠急性毒性的影响及可能机制。方法：雄性小鼠80只,随机分成8组,分别为空白对照（生理盐水）、单纯SAM对照、20 mg/kg丙烯腈、40 mg/kg丙烯腈、60 mg/kg丙烯腈、SAM＋20 mg/kg丙烯腈、SAM＋40 mg/kg丙烯腈、SAM＋60 mg/kg丙烯腈。SAM剂量为50 mg/kg,每隔12 h腹腔注射1次,连续3天,最后一次注射12 h后给予不同剂量的丙烯腈,对照组则腹腔注射生理盐水。观察丙烯腈染毒后3 h内动物的行为变化和死亡情况,并测定细胞色素P450 2E1（CYP2E1）活性,氰氢根离子（CN-）含量、细胞色素C氧化酶（CcOx）活性以及还原性谷胱甘肽（GSH）水平。结果：丙烯腈染毒3 h内,同等剂量丙烯腈染毒组与SAM预处理组相比较,翻正反射消失动物数、翻正反射消失时间、死亡数和死亡时间等观察指标未见明显差异;各组间CYP 2E1活性亦无显著差异;随着染毒剂量的增加,肝脑组织中CN-含量有着不同程度的升高,与同等剂量的丙烯腈组相比较,SAM预处理组脑组织中CN-含量未见明显降低,但中、高剂量组肝组织CN-含量则有显著性下降;肝脑组织中CcOx活性与染毒剂量间显示出明显的剂量-效应关系,SAM预处理后脑组织CcOX活性略高于同等剂量的染毒组;SAM预处理可升高GSH水平,其中SAM＋20 mg/kg丙烯腈组肝组织GSH水平较单纯20 mg/kg丙烯腈明显上升,脑组织中、高剂量预处理组与同等剂量丙烯腈比较有显著差异。结论：SAM预处理可增加组织GSH水平,但并未显著抑制CYP2E1活性,对丙烯腈的急性毒性也未见保护作用,SAM的应用价值有待进一步探讨。

英文摘要：

Objective： To examine the potential protective effect of S-adenosyl-L-methionine（SAM） on acute acrylonitrile（AN） toxicity in mice.Methods： Eighty male Kun-ming mice were randomly divided into eight groups： normal control,SAM alone,20 mg/kg AN alone,40 mg/kg AN alone,60mg/kg AN alone,SAM＋20 mg/kg AN,SAM＋40 mg/kg AN and SAM＋60 mg/kg AN.Mice were intraperitoneally（i.p.） preinjected with SAM at dosage of 50 mg/kg body weight every 12 h for 3 day,AN was i.p.administered at 12 h after the last SAM injection.The behavior on mice after injection with AN was recorded,CYP2E1 activity in liver microsomes was measured,the cyanide concentrations and Cytochrome c Oxidase（CcOx） activity in brain and liver homogenates were determined by Conway microdiffusion and spectrophotometer respectively.Results： No significant change in the CYP2E1 activity was observed in mice treated with AN compared with the normal control group and SAM alone group.The CN-levels were dose-dependently increased,the hepatic CN-content in SAM＋40mg/kg acrylonitrile,and SAM＋60mg/kg AN group was significantly lower than that in rats treated with AN alone,respectively.The CcOx activities in mice pretreated with SAM were higher than those in mice treated with the same dose of AN alone.SAM increased the level of GSH,with significant increment in liver of low dose group and in brain of middle and high dose group compared to the same dose of AN alone respectively.Conclusion： The protection by SAM against acute toxicity of AN was not significant,though SAM can prevent the GSH depletion by AN.