Greene E L, Paller M S
University of Minnesota, Minneapolis.
Miner Electrolyte Metab. 1991;17(2):124-32.
Renal ischemia injures the renal tubular cell by disrupting the vital cellular metabolic machinery. Further cell damage is caused by restoration of blood flow when oxygen free radicals are produced. Cellular sources of oxygen free radicals include the electron transport chain, the microsomal electron transport chain, oxidant enzymes (xanthine oxidase, cyclo-oxygenase), phagocytes, and cellular auto-oxidation of Fe2+ and epinephrine. Oxygen radicals cause lipid peroxidation of cell and organelle membranes, disrupting the structural integrity and capacity for cell transport and energy production. Studies in models of acute renal failure have yielded convincing evidence that oxygen free radical production occurs during ischemia/reperfusion. More than a dozen reports have demonstrated the ability of exogenous antioxidants to ameliorate renal injury in vivo. Direct demonstration of increased oxygen free radical production during reoxygenation following hypoxia has been shown in cultured renal epithelial cells. Oxygen free radicals also play a role in toxic acute renal failure. The therapeutic usefulness of free radical scavengers remains to be tested.
肾缺血通过破坏重要的细胞代谢机制损伤肾小管细胞。当血流恢复时，氧自由基产生，进而导致进一步的细胞损伤。氧自由基的细胞来源包括电子传递链、微粒体电子传递链、氧化酶（黄嘌呤氧化酶、环氧化酶）、吞噬细胞以及Fe2+和肾上腺素的细胞自氧化。氧自由基导致细胞和细胞器膜的脂质过氧化，破坏细胞运输和能量产生的结构完整性及能力。急性肾衰竭模型研究已产生令人信服的证据，表明缺血/再灌注期间会产生氧自由基。十几份报告已证明外源性抗氧化剂在体内改善肾损伤的能力。在培养的肾上皮细胞中已显示，缺氧后复氧期间氧自由基产生增加的直接证据。氧自由基在中毒性急性肾衰竭中也起作用。自由基清除剂的治疗效用仍有待检验。
