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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Neuroprotective effect of cobalt chloride on hypobaric hypoxia-induced oxidative stress.
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Neuroprotective effect of cobalt chloride on hypobaric hypoxia-induced oxidative stress.

机译：氯化钴对低压缺氧诱导的氧化应激的神经保护作用。

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Hypobaric hypoxia, characteristic of high altitude is known to increase the formation of reactive oxygen and nitrogen species (RONS), and decrease effectiveness of antioxidant enzymes. RONS are involved and may even play a causative role in high altitude related ailments. Brain is highly susceptible to hypoxic stress and is involved in physiological responses that follow. Exposure of rats to hypobaric hypoxia (7619 m) resulted in increased oxidation of lipids and proteins due to increased RONS and decreased reduced to oxidized glutathione (GSH/GSSG) ratio. Further, there was a significant increase in superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) levels. Increase in heme oxygenase 1 (HO-1) and heat shock protein 70 (HSP70) was also noticed along with metallothionein (MT) II and III. Administration of cobalt appreciably attenuated the RONS generation, oxidation of lipids and proteins and maintained GSH/GSSH ratio similar to that of control cells via induction of HO-1 and MT offering efficient neuroprotection. It can be concluded that cobalt reduces hypoxia oxidative stress by maintaining higher cellular HO-1 and MT levels via hypoxia inducible factor 1alpha (HIF-1alpha) signaling mechanisms. These findings provide a basis for possible use of cobalt for prevention of hypoxia-induced oxidative stress.
机译：低压缺氧是高海拔地区的特征，已知会增加活性氧和氮物质（RONS）的形成，并降低抗氧化酶的有效性。 RONS参与其中，甚至可能在与高海拔有关的疾病中起致病作用。大脑对低氧应激高度敏感，并参与随后的生理反应。大鼠暴露于低压缺氧（7619 m）导致脂质和蛋白质的氧化增加，这是由于RONS的增加和氧化谷胱甘肽（GSH / GSSG）的降低所致。此外，超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和谷胱甘肽S-转移酶（GST）含量也显着增加。还观察到血红素加氧酶1（HO-1）和热休克蛋白70（HSP70）的增加以及金属硫蛋白（MT）II和III。通过诱导HO-1和MT提供有效的神经保护作用，钴的施用显着减弱了RONS的产生，脂质和蛋白质的氧化，并维持了与对照细胞相似的GSH / GSSH比。可以得出结论，钴通过缺氧诱导因子1α（HIF-1alpha）信号传导机制维持较高的细胞HO-1和MT水平，从而降低了缺氧的氧化应激。这些发现为钴可能用于预防缺氧诱导的氧化应激提供了基础。

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