摘要
目的通过观察急性羰基镍中毒大鼠组织中丙二醛(MDA)含量的变化,探讨急性羰基镍中毒机制。方法 SD大鼠静态吸入不同浓度羰基镍,设氯气对照组和正常对照组,染毒后不同时间取材,用硫代巴比妥显色法(TBA)测定MDA的含量。结果在大鼠肺组织中,20 mg/m3染毒组中MDA含量明显升高,与对照组比较,差异有统计学意义(P<0.01);在肝组织中,250 mg/m3染毒组中的MDA含量明显升高,与其他各组比较,差异均有统计学意义(P<0.01);在肾组织中,20 mg/m3染毒组中MDA含量明显升高,与其他各组比较,差异均有统计学意义(P<0.05);在脑组织中,各个染毒剂量组中MDA含量与对照组比较,差异有统计学意义(P<0.05)。结论羰基镍可诱发组织脂质过氧化,引起MDA含量明显升高,并存在组织差异。
Objective To investigate the contents of malondialdehyde(MDA)in various rat organs poisoned by nickel carbonyl and to explore the mechanism of acute toxicity of nickel carbonyl.Methods Healthy SD rats were acutely exposed by statically inhaling different concentrations of nickel carbonyl.A chlorine poisoned rat group and a normal group were established in same way taken as the controls.The tissues of animal organs were taken at different time periods after nickel carbonyl exposure.The contents of MDA in every group were measured by thiobarbituric acid(TBA).Results The MDA contents in rat lung in 20 mg/m^3 exposure group increased significantly compared with controls(P〈0.01).The MDA contents in rat livers in 250 mg/m^3 exposure group were significantly higher than those of other exposed groups and the controls(P〈0.01).The MDA contents of kidneys in 20 mg/m^3 exposure group were significantly higher than those of other exposed groups and the controls(P〈0.05).The MDA contents in brain tissues in various doses groups were significantly higher than those of the controls(P〈0.05).Conclusions Nickel carbonyl could induce lipid peroxidation of the tissues and increase the contents of MDA,but the changes were different in different organ tissues.
出处
《工业卫生与职业病》
CAS
CSCD
北大核心
2010年第6期321-324,共4页
Industrial Health and Occupational Diseases
基金
金川集团公司与兰州大学合作项目<急性羰基镍中毒救治与防护的研究>(金科综2009-12)
关键词
羰基镍
氯气
丙二醛
脂质过氧化
Nickel carbonyl
Chlorine
Malondialdehyde(MDA)
Lipid peroxidation