摘要
目的通过研究大鼠急性羰基镍中毒后肺组织SOD活力变化与Cu-Zn SOD基因表达,探讨急性羰基镍中毒对肺脏急性毒性作用机制。方法健康SD大鼠静态吸入染毒,染毒时间为30 min,羰基镍染毒浓度分别为20 mg/m3、135 mg/m3和250 mg/m3,氯气染毒250 mg/m3为染毒对照组,健康大鼠为正常对照组,染毒后1 d、2 d、3 d和7 d分别取材,应用黄嘌呤氧化酶测定法和反转录-聚合酶链式反应(RT-PCR)分别测定各组大鼠不同取材时间段下肺组织SOD活力并分析Cu-Zn SOD基因表达水平。结果在低、中、高剂量羰基镍染毒条件下,肺脏SOD活力均有下降,以中剂量组染毒7 d时和高剂量组染毒3 d时肺SOD降低最为显著(P<0.05);氯气染毒后也显著下降(P<0.05)。与正常对照组相比,羰基镍低、中、高剂量染毒组肺脏Cu-Zn SOD基因表达差异均无统计学意义,而氯气染毒组表达明显降低(P<0.05)。结论羰基镍可诱发肺组织氧化损伤,降低SOD活力。在不同染毒剂量下,以高剂量染毒组肺氧化损伤最为明显;在不同取材时间下,以中剂量染毒7 d时和高剂量染毒3 d时肺氧化损伤最为明显。
Objective To investigate the changes of SOD activity and the expressions of Cu-Zn SOD mRNA in lung tissues of rats poisoned by nickel carbonyl and to discuss the mechanism of acute toxicity.Methods Healthy rats were exposed by inhalation of 20,135,250 mg/m3 nickel carbonyl for 30 min.Rats poisoned by chlorine gas with a concentration 250 mg/m3served as poisoned group and healthy SD rats served as no-treatment control group.The rats were euthanized on 1 d,2 d,3 d and 7 d after the administration of nickel carbonyl or chlorine gas.In various treatment groups,SOD activity was studied by assay of xanthine oxidase and the expressions of Cu-Zn SOD mRNA were determined by RT-PCR.Results SOD activity in lung tissues decreased in all treatment groups and chlorine gas-poisoned group,especially on the 7thday following medium-dose treatment and on the 3rd day following high-dose treatment.Compared with normal no-treatment control group,there was no significant difference for the expressions of Cu-Zn SOD mRNA in lung tissues of rats in all nickel carbonyl treatment group,but there was an obvious decrease in chlorine gas poisioned group（P0.05）.Conclusion Nickel carbonyl could induce oxidative damage and decrease SOD activity in lung especially at high dose.The most obvious oxidative damage was happened at the 3rd day following high-dose treatment and at the 7th day following middle-dose treatment.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2011年第3期180-183,共4页
Journal of Toxicology
基金
金川集团公司与兰州大学产学研合作项目<急性羰基镍中毒救治与防护的研究>
