摘要
目的探讨锰对小鼠肺脏和睾丸的急性致毒作用,防治锰中毒。方法测定锰染毒1、2、4、7d后小鼠的乳酸脱氢酶(LDH)活力、肺脏与睾丸脂质过氧化物(LPO)值和组织中锰、钙、锌、铁等浓度。结果染锰1d后小鼠血清LDH活力、肺脏和睾丸中LPO值和锰的浓度均达峰值,而后各项指标呈明显下降趋势;染锰2d后肺脏、睾丸中钙浓度达到峰值且明显高于对照组,而铁、锌浓度明显低于对照组,提示锰具有明显的肺脏、睾丸毒性。结论脂质过氧化及钙等代谢障碍可能是锰引起肺脏和睾丸损害的重要机制。
Objective To study the mechanism of Mn-indueed toxieities in lung and testis to prevent or to treat manganese (Mn) poisoning. Methods After a single exposure to MnCl2( 100 mg/kg body weight) via i. p. , the activity of serum laeatate dehydrogenase (LDH) of mice were determined at day 1,2, 4 and 7. Lipid peroxidation (LPO) and the concentrations of manganese ( bin), calcium ( Ca), zinc (Zn) and iron (Fe) in lungs and testes of the mice were also measured. Results The activity of LDH in mice serum, LPO and concentrations of Mn achieved their peak values 1 day after Mn administration and then significantly decreased. Concentrations of Ca in lung and testis of Mn exposed groups were significantly higher than those of controls and achieved their peak values 2 days after Mn administration, but concentrations of Fe and Zn were significantly decreased. Mn had obvious toxieities to the lung and testis. Conclusion LPO and metabolic obstacle of Ca may be the important mechanism of lung and testis injury caused by Mn.
出处
《中国职业医学》
CAS
北大核心
2009年第2期98-101,共4页
China Occupational Medicine
基金
国家自然科学基金资助项目(20677025)
江苏省社会发展计划资助项目(BS2006038)
关键词
锰
肺脏
睾丸
毒性
脂质过氧化
Manganese
Lung
Testis
Toxicity
Lipid peroxidation