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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 toxic mechanism of manganese on lung and liver. Methods Thirty mice were randomly divided into 5 groups. After intraperitoneal injection of manganese chloride for 1, 2, 4 and 7 days, the lipid peroxidation and some serum indexes of lung and liver were observed. The levels of Mn, Ca, Zn , Iron and other concentrations. Results The activities of AST, ALT and LDH were (421.5 ± 85.1), (209.5 ± 47.0), ( 1 698.1 ± 152.2 U / L, and the values of LPO in lung and liver were (2.59 ± 0.21) and (9.08 ± 2.49) μmol / (g · prot), respectively, The content of calcium in lung and liver peaked at 2 d after manganese dying (P <0.05), while the iron content in the control group was significantly higher than that in the control group (P <0.05) , Zinc concentration was significantly lower than the control group (P <0.05), suggesting that manganese has obvious lung and liver toxicity. Conclusion Lipid peroxidation and metabolic disorders such as calcium, iron and zinc may be one of the mechanisms of lung and liver toxicity induced by manganese in mice.