小鼠氧化乐果急性中毒后心肌组织ATP酶及自由基代谢的变化

ATPase Activities and Metabolism of Free Radical of Cardiac Muscle Tissue in Mice with Acute Oxide Dimethoate Poisoning

目的观察小鼠氧化乐果急性中毒后心肌组织ATP酶活性水平和自由基的代谢,探讨氧化乐果急性中毒后心肌损害的发生机制。方法20只健康小鼠随机分为对照组和氧化乐果染毒组,每组10只。染毒组按25 mg/kg腹腔注射氧化乐果,对照组注射生理盐水。30 m in后处死,分别测定两组小鼠心肌组织Na+-K+-ATP酶、Mg2+-ATP酶和Ca2+-ATP酶活性,丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)含量并进行比较。结果染毒组小鼠心肌组织Na+-K+-ATP酶、Mg2+-ATP酶和Ca2+-ATP酶活性均明显低于对照组(6.48±2.64 vs 17.96±2.07、9.48±2.93 vs 21.18±3.10、10.06±2.43 vs 18.29±2.13)(均P<0.05),染毒组小鼠心肌组织SOD、GSH-Px含量明显低于对照组(5.21±1.59 vs 6.85±1.43、8.12±3.73 vs11.96±3.98)(均P<0.05),而MDA含量高于对照组(4.98±1.76 vs 2.74±1.82)(P<0.05),上述差异均具有统计学意义。结论氧化乐果可影响心肌组织能量代谢和抗自由基水平,损害心肌;其机制可能与自由基引起的肌细胞脂质过氧化有关。

Objective To investigate the mechanism of cardiac muscle injury by oxide dimethoate through observing the ATPase activities and metabolism of free radical of cardiac muscle tissue in mice with organophosphorus poisoning. Methods 20 healthy mice were randomly divided into control and poisoning groups. Oxide dimetboate was given intraperitoneally into mice of poisoning groups and the physiological saline were injected into control mice. The activities of Na ^＋ - K ^＋ - ATPase, Mg^2＋ - ATPase, Ca^2＋ - ATPase and the contents of MDA, SOD and GSH - Px of cardiac muscle tissue were measured after 30 min. Results The activities of Na^＋ - K ^＋- ATPase, Mg^2 ＋ - ATPase and Ca^2 ＋ - ATPase in poisoning groups decreased much more signifeantly than those in control （6. 48 ± 2.64 vs 17.96 ±2.07 ;9.48 ±2.93 vs 21.18 ±3.10 ; 10. 06 ± 2.43 vs 18.29 ±2. 13 ） （ P 〈 0. 05 ）. The contents of SOD and GSH - Px in poisoning groups were obviously lower than those in eantrol （5.21 ±1.59 vs 6. 85 ±1.43 ; 8. 12 ±3.73 vs 11.96 ±3.98 ） （ P 〈 0. 05 ） , but the content of MDA was higher than that in control（4. 98 ±1.76 vs 2.74 ±1.82） （ P 〈 0. 05 ）. Conclusion Oxide dimetboate can impact energy metabolism and anti - free radical and damage myocardial, its mechanism might be related to lipid peroxidation of cardiac musele cell caused by free radical.