三氯乙烯致敏豚鼠肾脏丙二醛水平和超氧化物歧化酶活力变化

Changes of MDA content and SOD activity in kidneys of trichloroethylene-sensitized guinea pigs

目的研究三氯乙烯(TCE)致敏豚鼠肾脏中丙二醛(MDA)水平和超氧化物歧化酶(SOD)活力的变化,探讨TCE对豚鼠肾脏的氧化应激水平的影响。方法 50只豚鼠随机分为空白对照组、溶剂(橄榄油)对照组、TCE处理组。根据豚鼠最大值实验(GPMT)方法处理豚鼠。按照《化学品毒性鉴定技术规范》的评分标准对动物的皮肤反应进行评分,评分≥1且总致敏率>9%的判为致敏。在末次激发后24、72 h和1周3个时点分批采血,测定血清中尿素氮(BUN)、肌酐(Cr)水平;取肾脏组织测定MDA水平以及总SOD(T-SOD)活力。结果 TCE组致敏率为65.0%,与溶剂对照组相比较,TCE致敏组24 h血清BUN、Cr都明显升高(P<0.05)。与溶剂对照组相比,TCE致敏24 h组MDA水平明显上升(P<0.05);TCE致敏组与未致敏组比较,24 h组MDA水平差异有统计学意义(P<0.05)。TCE致敏组SOD活力比溶剂对照组明显降低(P<0.05),各时点间有下降或升高的趋势但是差异无统计学意义;24、72 h致敏组SOD活力较非致敏组低,差异有统计学意义(P<0.05)。结论 TCE诱导的致敏豚鼠肾脏有一定程度的损伤,其中氧化应激发挥一定作用。

Objective To study the changes of MDA content and SOD activity in the kidneys of guinea pigs sensitized with trichloroethylene（TCE） and the effect of oxidative stress of TCE.Methods 50 guinea pigs were randomly divided into blank control groups,solvent（olive oil） control groups and TCE sensitized groups.The animals were treated by the method of guinea pig maximization test（GPMT）.The score of skin response was recorded following Technology Standard for Chemical Toxicity Appraisal.The score whichwos higher than or equal to 1 and the total rate of sensitization more than 9 was judged as sensitization.24,72 hours and 1 week after the last challenge,serum BUN,Cr,maleic dialdehyde（MDA）,total superoxide dismutase（T-SOD） in kidney were examined.Results Sensitization rates in TCE treatment groups were 65.0%.Compared with the solvent control group,at the point of 24 hours,serum BUN,Cr and MDA in TCE sensitized groups significantly increased（P0.05）,while T-SOD activity was significantly decreased（P〈0.05）.At the point of 24 hours,the content of MDA in kidney of the TCE sensitized groups was higher than those in the non-sensitized groups（P〈0.05）.Compared with the non-sensitized groups,T-SOD activity was significantly decreased at the point of 24 hours and 72 hours.Conclusion TCE could induce oxidative stress in the kidney of the guinea pigs.The tissue oxidative damage might be one of the primary mechanisms of nephrotoxicity of TCE.