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局部肠道缺血再灌注后超氧化物歧化酶对脂质过氧化的抑制作用。

Inhibition of lipid peroxidation by superoxide dismutase following regional intestinal ischemia and reperfusion.

作者信息

Younes M, Mohr A, Schoenberg M H, Schildberg F W

出版信息

Res Exp Med (Berl). 1987;187(1):9-17. doi: 10.1007/BF01854963.

Abstract

In a feline model of regional intestinal ischemia, reoxygenation resulted in a rise in the concentration of oxidized glutathione, from 2.3 +/- 0.7 to 4.1 +/- 0.5% of the total glutathione. Also conjugated diene as an indirect measurement for lipid peroxidation increased after reperfusion from 2.5 +/- 0.5 mumol/g to 5.5 +/- 1.2 micrograms mol/g tissue. These results are in line with the hypothesis that ischemia results in an accumulation of hypoxanthine and a conversion of xanthine dehydrogenase into its O2-dependent form. Upon reoxygenation, hypoxanthine can be oxidized giving yield to a burst of O2-. and its interconversion products. These may initiate peroxidative tissue damage. Pretreatment of the cats with superoxide dismutase inhibited the biochemical alterations and protected the tissue from peroxidation damage.

摘要

在猫的局部肠道缺血模型中,再灌注导致氧化型谷胱甘肽浓度升高,从总谷胱甘肽的2.3±0.7%升至4.1±0.5%。作为脂质过氧化间接测量指标的共轭二烯在再灌注后也从2.5±0.5μmol/g增加到5.5±1.2μmol/g组织。这些结果与以下假设一致,即缺血导致次黄嘌呤积累以及黄嘌呤脱氢酶转化为其O₂依赖形式。再灌注时,次黄嘌呤可被氧化产生一阵超氧阴离子(O₂⁻)及其相互转化产物。这些可能引发过氧化组织损伤。用超氧化物歧化酶对猫进行预处理可抑制生化改变并保护组织免受过氧化损伤。

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