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作 者:荆俊杰[1] 谢吉民[1] 陈敏[1] 余龙[1] 吕平[1] 袁富荣[1]
出 处:《中国公共卫生》2009年第10期1242-1244,共3页Chinese Journal of Public Health
基 金:国家自然科学基金(20677025);江苏省社会发展计划项目(BS2006038)
摘 要:目的探讨锰对肺、肝脏的毒作用机制。方法将30只小鼠随机分为5组,腹腔注射氯化锰1,2,4,7 d后,观察肺和肝脏的脂质过氧化作用及部分血清指标与脏器中锰、钙、锌、铁等浓度。结果染锰1 d后,小鼠血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和乳酸脱氢酶(LDH)活性分别为(421.5±85.1),(209.5±47.0),(1 698.1±152.2)U/L,肺和肝脏中脂质过氧化(LPO)值分别为(2.59±0.21),(9.08±2.49)μmol/(g.prot),锰浓度均明显升高,与对照组比较差异有统计学意义(P<0.05);而后各项指标呈明显下降趋势;染锰2 d后肺脏、肝脏中钙浓度达到峰值且明显高于对照组(P<0.05),而铁、锌浓度明显低于对照组(P<0.05),提示锰具有明显的肺、肝脏毒性。结论脂质过氧化及钙、铁、锌等代谢障碍可能是锰致小鼠肺、肝脏毒性的机制之一。Objective To explore the effects of manganese(Mn) on lipid peroxidation and contents of iron and zinc in the lung and liver of mice and the mechanism of manganese toxicity. Methods After single exposure to MnCl2 ( 100mg/kg body weight) via i. p. in 30 mice, the activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lacatate dehydrogenase (LDH) were determined at lst, 2rd, 4th and 7th day. The lipid peroxidation (LPO) and concentrations of Mn, calcium( Ca), zinc (Zn) and iron(Fe) in the lung and liver of the mice were also measured. Results The activity of AST, ALT, LDH, LPO and concentrations of Mn were achieved peak value after one day of Mn administration( P 〈 0. 05 ) and then decreased significantly. Concentrations of Ca in the lung and liver in Mn exposed groups were significantly higher than those of in controls and achieved peak value two days after Mn administration ( P 〈 0. 05 ), but concentrations of Fe and Zn were significantly decreased( P 〈 0. 05 ). Obvious toxicity of Mn to lung and liver of mice was observed. Conclusion Lipid peroxidation and metalbolic obstacle of Ca,Zn and Fe may be important mechanism of lung and liver injury caused by Mn in mice.
分 类 号:R114[医药卫生—卫生毒理学]
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