Mg2+ is an important cation in our body. It is an essential co-factor for many enzymes. Despite many works, nothing is known about the protective effects of MgSO4 against hypoxia-induced lethality and oxidative damage in brain mitochondria. In this study, antihypoxic and antioxidative activities of MgSO4 were evaluated by three experimental models of induced-hypoxia (asphyctic, haemic, and circulatory) in mice. Mitochondria protective effects of MgSO4 were evaluated in mice brain after induction of different models of hypoxia. Antihypoxic activity was especially pronounced in asphyctic hypoxia where MgSO4 at dose 600 mg/kg showed the same activity as phenytoin which used as a positive control (P< 0.001). In the haemic model, MgSO4 at all used doses significantly prolonged latency of death. In circulatory hypoxia, MgSO4 (600 mg/kg) doubles the survival time. MgSO4 significantly decreased Lipid peroxidation, protein carbonyl, and improved mitochondrial function and glutathione content in brain mitochondria compared to control groups. The results obtained in this study showed that MgSO4 administration has protective effects against lethality induced by different models of hypoxia and improves brain mitochondria oxidative damage.

中文翻译：

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硫酸镁减轻不同模型低氧所致小鼠的致死性和氧化损伤

Mg2 +是人体中重要的阳离子。它是许多酶必不可少的辅助因子。尽管有许多工作，关于硫酸镁对脑线粒体中低氧引起的致死性和氧化损伤的保护作用还一无所知。在这项研究中，通过小鼠诱导性缺氧（窒息，血液和循环）的三种实验模型评估了MgSO4的抗缺氧和抗氧化活性。诱导不同的缺氧模型后，在小鼠脑中评估了MgSO4的线粒体保护作用。抗窒息活性在窒息性缺氧中尤为明显，剂量为600 mg / kg的MgSO4与用作阳性对照的苯妥英钠具有相同的活性（P <0.001）。在贫血模型中，所有使用剂量的MgSO4均显着延长了死亡潜伏期。在循环性缺氧中 MgSO4（600 mg / kg）使生存时间加倍。与对照组相比，MgSO4显着降低了脂质过氧化，蛋白质羰基，并改善了脑线粒体中的线粒体功能和谷胱甘肽含量。这项研究获得的结果表明，硫酸镁的施用对不同缺氧模型引起的致死性具有保护作用，并改善了脑线粒体的氧化损伤。