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大鼠脑缺血及缺血后再灌注期间的谷胱甘肽与抗坏血酸

Glutathione and ascorbate during ischemia and postischemic reperfusion in rat brain.

作者信息

Cooper A J, Pulsinelli W A, Duffy T E

出版信息

J Neurochem. 1980 Nov;35(5):1242-5. doi: 10.1111/j.1471-4159.1980.tb07882.x.

Abstract

Thirty minutes of total cerebral ischemia (decapitation) decreased total glutathione (GSH + GSSG) by 7% but had no detectable effect on the concentration of oxidized glutathione (GSSG), reduced ascorbate, or total ascorbate, In a model of reversible, bilateral hemispheric ischemia (four-vessel occlusion) no changes in glutathione or ascorbate were detected after 30 min of ischemia. During 24 h of reperfusion following such an insult no detectable change in total ascorbate, reduced ascorbate, or oxidized glutathione was noted: however, total brain glutathione declined by 25%. The findings are discussed in relation to the hypothesis that the deleterious effects of ischemia are due to an increase in free radical production which in turn leads to increased lipid peroxidation.

摘要

全脑缺血30分钟(断头)使总谷胱甘肽(GSH + GSSG)降低了7%,但对氧化型谷胱甘肽(GSSG)、还原型抗坏血酸或总抗坏血酸的浓度没有可检测到的影响。在可逆性双侧半球缺血模型(四血管闭塞)中,缺血30分钟后未检测到谷胱甘肽或抗坏血酸的变化。在这种损伤后的24小时再灌注期间,未观察到总抗坏血酸、还原型抗坏血酸或氧化型谷胱甘肽有可检测到的变化;然而,全脑谷胱甘肽下降了25%。结合缺血的有害作用是由于自由基产生增加进而导致脂质过氧化增加这一假说对这些发现进行了讨论。

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