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作 者:齐宝宁[1] 易建华[1] 唐国慧[1] 苗江丽[1] 郭剑锋[1]
机构地区:[1]西安交通大学医学院公共卫生系劳动卫生与环境卫生教研室,陕西西安710061
出 处:《西安交通大学学报(医学版)》2007年第2期145-148,共4页Journal of Xi’an Jiaotong University(Medical Sciences)
摘 要:目的研究正己烷(n-hexane)对大鼠的脂质过氧化作用和肝细胞DNA损伤的影响。方法40只雄性SD大鼠随机分成5组,即阴性对照组、75、150、300 mg/kg染毒组和阳性对照组,每组8只。经腹腔注射染毒4周后,检测肝组织匀浆超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活力,血清还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量;用彗星试验技术(SCGE)检测大鼠肝细胞DNA的损伤。结果大鼠体重随染毒时间而增加,阴性对照组增加最快;随染毒剂量增加,肝组织匀浆中SOD、GSH-Px活力、血清GSH含量明显降低,而血清MDA含量增大,组间比较有显著性差异(P<0.05或P<0.01);肝细胞SCGE检测彗星尾长、尾DNA(%)、尾矩、Olive尾矩均增大,组间比较有显著性差异(P<0.01),尾矩值与染毒剂量作相关分析,相关系数r为0.981,呈正相关(P<0.05)。结论正己烷可引起或增强机体氧自由基反应,导致脂质过氧化损伤和肝细胞DNA损伤。Objective To study the effect of n-hexane on lipid peroxidation and DNA damage of hepatic cell in rats. Methods A total of 40 SD male rats were randomly divided into 5 groups, namely, groups of negative control, 75, 150 and 300 mg/kg and positive control. Rats were administered with n-hexane through intraperitoneal injection; the dosages were given according to the weight of rats for four weeks. The examinations included the activity of GSH-Px, SOD in hepat-homogenate, the concentration of GSH and MDA in blood serum, (indicating lipid peroxidation of n-hexane) and DNA damage of hepatic cell by single cell gel electrophoresis (SCGE). Results With the time lapse, the body weight of the rats increased in each group and the weight of the negative controls increased more quickly than that of others. Along with the increase of the dosage, the activity of GSH-Px and SOD in hepat-homogenate and the concentration of GSH in blood serum reduced and the concentration of MDA increased, and there was a significant different among groups (P〈0.05 or P〈0.01). The SCGE result of hepatic cell showed that tail length, tail DNA(%), tail moment and olive tail moment increased with the dosage increase, and significant difference was found among all groups (P〈0.01). Correlation analysis between tail moment and dosage showed positive correlation (r = 0. 981, P〈0.05). Conclusion n-hexane could induce or enhance the reaction of oxygen free radical in organism, result in damage of lipid peroxdation, and induce DNA damage of hepatic ceils of rats.
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