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目的通过观察丙烯腈(acrylonitrile,AN)对小鼠肝组织脂质过氧化的影响,探讨AN的毒作用机制。方法将200只成年健康SPF级昆明种雄性小鼠按体重随机分为4组,分别为阴性对照(生理盐水)组和低(1.25 mg/kg)、中(2.50 mg/kg)、高(5.00 mg/kg)剂量AN染毒组,每组50只。采用腹腔注射方式进行染毒,染毒容量为10 ml/kg,1次/d,连续染毒5d。于首日染毒后第7、14、21、28和35天测定其肝组织中丙二醛(MDA)含量、过氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活力。结果 AN首日染毒后第28天中、高剂量组MDA含量与阴性对照组比较明显升高,有统计学意义(P<0.05,P<0.01),第35天高剂量组MDA含量高于阴性对照组,有统计学意义(P<0.01);第28天高剂量组SOD活力高于阴性对照组(P<0.01);第28天组高剂量组GSH-Px活力显著高于阴性对照组和中剂量组(P<0.01,P<0.05)。结论 AN可能通过破坏氧化-抗氧化体系的平衡,诱导小鼠肝组织产生氧化损伤,在首日染毒后第28天时比较明显。
Objective To investigate the effect of acrylonitrile (AN) on lipid peroxidation in mouse liver and to explore the toxic mechanism of AN. Methods Two hundred Kunming male SPF Kunming mice were randomly divided into four groups according to body weight: negative control (saline) group and low (1.25 mg / kg) moderate (2.50 mg / kg) mg / kg) dose of AN exposure group, each group of 50. The rats were injected intraperitoneally with a dose of 10 ml / kg once a day for 5 days. The malondialdehyde (MDA) content, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver tissue were measured at the 7th, 14th, 21st, 28th and 35th day after the first day of exposure. Px) vitality. Results On the 28th day after the first day of exposure, the content of MDA in the high-dose group was significantly higher than that in the negative control group (P <0.05, P <0.01), and the MDA content in the high-dose group on the 35th day was higher than that of the negative control group (P <0.01). On the 28th day, the activity of SOD in the high-dose group was higher than that in the negative control group (P <0.01). The GSH-Px activity in the high-dose group on the 28th day was significantly higher than that of the negative control group And middle dose group (P <0.01, P <0.05). Conclusion AN may induce oxidative damage in mouse liver tissue by destroying the balance of oxidation-antioxidant system, which is obvious on the 28th day after the first day of exposure.