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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 observe the ATPase activity and free radical metabolism of myocardial tissue after acute poisoning of omethoate in mice and explore the mechanism of myocardial damage after acute poisoning of omethoate. Methods Twenty healthy mice were randomly divided into control group and omethoate group, with 10 mice in each group. In the exposure group, omethoate was injected intraperitoneally at 25 mg / kg, and saline was injected in the control group. After 30 m in, they were sacrificed and the activities of Na + -K + -ATPase, Mg2 + -ATPase and Ca2 + -ATPase, malondialdehyde (MDA), superoxide dismutase (SOD) Glycopeptide peroxidase (GSH-Px) content and compared. Results The activities of Na + -K + -ATPase, Mg2 + -ATPase and Ca2 + -ATPase in the myocardial tissue of the exposed mice were significantly lower than those of the control group (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) (all P <0.05). The contents of SOD and GSH-Px in the myocardium of the treated mice were significantly lower than those of the control group (5.21 ± 1.59 vs 6.85 ± 1.43, 8.12 ± 3.73 vs 11.96 ± 3.98) All P <0.05), but the content of MDA was higher than that of the control group (4.98 ± 1.76 vs 2.74 ± 1.82, P <0.05). All these differences were statistically significant. Conclusion Omethoate can affect myocardial energy metabolism and anti-free radical levels and damage myocardium. Its mechanism may be related to lipid peroxidation induced by free radicals.