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本文探讨活化氧类在缺血后再灌注时心肌损伤范围扩大方面所起的作用.活化氧类包括超氧阴离子、过氧化氢和羟基.活化氧类通过奇电子可以同所有细胞成份(尤其含巯基的氨基酸和不饱和脂肪酸)起反应,导致蛋白质变性、膜脂质过氧化、趋化因子形成和胶原合成障碍.其结果为酶丧失活力,膜通透性异常,炎症细胞浸润增加.细胞超氧化物歧化酶(SOD)催化超氧化物阴离子成为过氧化氢;细胞浆过氧化氢酶(CAT)和谷胱甘肽过氧化酶催化过氧化氢降解成水和氧,从而防止氧自由基损伤细胞.
This article explores the role of activated oxygen species in expanding the extent of myocardial damage during ischemia-reperfusion injury.Active oxygen species include superoxide anion, hydrogen peroxide and hydroxyl radicals.Active oxygen species can interact with all cellular components Sulfhydryl amino acids and unsaturated fatty acids), resulting in protein denaturation, membrane lipid peroxidation, chemokine formation and collagen synthesis barriers, the result of enzyme loss of vitality, abnormal membrane permeability, increased inflammatory cell infiltration. Oxidative dismutase (SOD) catalyzes the superoxide anion to become hydrogen peroxide; cytoplasmic catalase (CAT) and glutathione peroxidase catalyze the degradation of hydrogen peroxide to water and oxygen, thereby preventing oxygen radical damage cell.