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作 者:王青山[1] 张翠丽[1] 赵秀兰[1] 朱英建[1] 张利平[1] 郭新[1] 谢克勤[1]
机构地区:[1]山东大学公共卫生学院毒理学研究所,山东济南250012
出 处:《毒理学杂志》2006年第6期350-353,共4页Journal of Toxicology
基 金:国家973课题基金资助项目(2002CB512907);国家自然科学基金课题资助项目(30271138)
摘 要:目的研究氯丙烯(AC)亚慢性中毒大鼠血清脂质过氧化的改变是否存在时间效应关系,探讨其中毒性神经病发病机制。方法选用90只Wistar雄性大鼠随机分为对照组(n=50)和染毒组(n=40),染毒组大鼠以200 mg/kg剂量AC经口灌胃,每周3次,分别在染毒第3、6、9和12周随机从对照组和染毒组取大鼠10只,用生物化学方法测定染毒组与相应时间对照组大鼠血清中丙二醛(MDA)、谷胱甘肽(GSH)含量、抗活性氧能力(anti-ROS)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、超氧化物岐化酶(SOD)和总抗氧化能力(T-AOC)活力等指标。结果随染毒时间的延长和步态评分的增加,MDA呈进行性升高趋势;anti-ROS、GSH、GSH-Px、CAT、SOD、T-AOC呈下降趋势。MDA从染毒第3周和步态评分2分开始升高,与对照组相比差异有统计学意义(P<0.05)。结论AC亚慢性染毒可引起大鼠血清发生脂质过氧化,并且存在明显的时间效应关系,脂质过氧化可能是AC诱导的神经毒性的发病机制之一;MDA改变的最早、最为敏感,可为AC中毒的早期诊断提供了依据。Objective To study the time dependent changes of lipid perexidation in wistar rats serum caused by allyl chloride (AC) .Methods 90 Male wistar rats weighting 180 - 220 g were randomly divided into two groups, experimental group( n = 40) and corresponding time-matched control group ( n = 50). The animals in experimental groups were treated with AC dissolved in corn off (200 mg/kg,3 days/week) by gavage. On completion of 3, 6, 9 and 12 weeks of AG administration, rats( n = 10 per experimental and control group) were chosen at random and sacrificed by cervical decapitation. Lipid perexidation indexes of each group were determined in rats serum on the corresponding deadline. The indexes included measurements of malondialdehyde ( MDA ), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione pemxidase ( GSH-Px ), supemxide dismutase ( SOD ) and total antioxidative capacity ( T-AOC). Results All indexes of lipid peroxidation were changed gradually with time went on and symptom developed in rats serum treated by AC. The results showed that MDA levels in serum significantly increased ( P 〈 0.05) on 3 week of AC treatment and at gait score of 2, and further changes were observed after 6, 9, 12 weeks and at gait score of 3, 4. Conclusion The time dependent changes of lipid pemxidation in wistar rats serum occurred and might be served as one of mechanisms of toxic neuropathy induced by AC. The MDA may be used as the most sensitive indicator to the early diagnosis for the AC toxicosis.
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