西维因与氰戊菊酯联合染毒对大鼠肝脏脂质过氧化的影响

Effects of combined exposure to carbaryl and fenvalerate on rat liver lipid peroxidation

目的探讨西维因与氰戊菊酯联合染毒对大鼠肝脏脂质过氧化作用的影响。方法将80只健康成年清洁级SD大鼠按2×2析因设计随机分为4组,分别为阴性对照(玉米油)组、西维因单独染毒组(1/50 LD_(50),11.2 mg/kg)、氰戊菊酯单独染毒组(1/50 LD_(50),9.02 mg/kg)和西维因(11.2 mg/kg)+氰戊菊酯(9.02 mg/kg)染毒组,每组20只,雌雄各半。采用经口灌胃方式进行染毒,每天1次,每周6天,连续染毒8周。末次染毒24 h后,测量大鼠肝组织中超氧化物歧化酶(SOD)、谷胱甘肽S转移酶(GST)活力和还原性谷胱甘肽(GSH)、丙二醛(MDA)含量。结果西维因和氰戊菊酯联合染毒使雄鼠肝脏中SOD活力下降(P<0.05)、MDA含量升高(P<0.05),雌鼠肝脏中GSH含量下降(P<0.05),交互效应均有统计学意义,对SOD、GSH表现为拮抗作用,对MDA表现为协同作用;其它指标交互作用均无统计学意义(P>0.05)。结论西维因和氰戊菊酯联合染毒对大鼠肝脏存在联合毒性作用,可能是通过破坏氧化-抗氧化系统的平衡,产生氧化损伤作用。

Objective To study the combined toxic effects of carbaryl and fenvalerate on liver lipid peroxidation in rates.Methods According to 2 ×2 factorial analysis,forty healthy and clean adult male SD rats and forty healthy and clean adult female SD rats were randomly divided into four groups,including one negative control group（given by corn oil） and carbaryl exposure group（1/50 LD_（50）,11.2 mg/kg）,fenvalerate exposure group（1/50 LD_（50）,9.02 mg/kg） and carbaryl＋fenvalerate combined exposure group（11.2 mg/kg ＋9.02 mg/kg,dissolved in coin oil）,20 rats in each group,and half males and half females.The treatment was conducted through gavage,once a day,six days per week for eight consecutive weeks. After 24 hours of the last exposure, the activity of superoxide dismutase（SOD）,glutathione S-transferase（GST）,the content of reduced glutathione（GSH） and malondialdehyde（MDA） were measured in liver tissue. Results The carbaryl-fenvalerate combined exposure induced decreased SOD activity（P〈 0.05）, increased MDA content（P〈 0.05） in liver of male mice, decreased liver GSH content（P〈 0.05） in liver of female mice. Interaction effects were statistically significant,antagonistic for SOD and GSH,synergistic for MDA. No statistical significance was obsreved in interaction for other indicators（P〉 0.05）. Conclusion The carbaryl-fenvalerate combined exposure has interaction on the organ of rats, which may result in oxidative damage through the destruction of oxidation-antioxidant system balance.