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近年来,有关氧自由基在放射、炎症损伤和氧毒性等病理、生理改变过程中的作用的文章不断出现,本文的目的是验证活性氧物质在缺血后再灌注过程中加剧心肌损伤作用的假说。活性氧包括超氧阴离子、过氧化氢和羟自由基等。它们依靠其外层结构不成对电子,与多种细胞成份,尤其是含有-SH基的氨基酸和不饱和脂肪酸等物质产生反应。自由基的连续性的反应可致潜在的并发症,包括蛋白质变性、膜脂质过氧化、趋化因子产生和胶原合成的损害,结果是酶活性丢失、膜通透性紊乱及炎性细胞浸润增加。细胞内对抗氧自由基损害
In recent years, articles on the role of oxygen free radicals in pathology and physiological changes such as radiation, inflammatory injury and oxygen toxicity continue to emerge. The purpose of this paper is to verify the effect of reactive oxygen species on myocardial injury during ischemia-reperfusion hypothesis. Reactive oxygen species include superoxide anion, hydrogen peroxide and hydroxyl radicals. They relied on unpaired electrons in their outer structures to react with a variety of cellular components, especially those containing -SH-based amino acids and unsaturated fatty acids. The reaction of free radical continuity can lead to potential complications including protein denaturation, membrane lipid peroxidation, chemokine production and collagen synthesis, resulting in loss of enzyme activity, membrane permeability disorders and inflammatory cell infiltration increase. Cells against oxygen free radical damage