Okajima S
Second Department of Surgery, Hokkaido University, School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1990 May;65(3):277-84.
Recently, oxygen free radicals have appeared to play a major role in injury after ischemia, especially that followed by normoxic reperfusion. To clarify the mechanisms of reperfusion injury, the activities of both oxygen radical producing enzymes and radical scavenging enzymes were measured in the ischemic rat kidney followed by reperfusion. All defensive enzymes activities significantly decreased; superoxide dismutase 2.15 +/- 0.14----1.71 +/- 0.11, catalase 186.6 +/- 12.7----116.5 +/- 7.1, glutathione peroxidase 30.0 +/- 2.6----19.1 +/- 2.9, glutathione reductase 118 +/- 5.1----39.9 +/- 6.8 (U/mg protein). Conversion from xanthine dehydrogenase to xanthine oxidase was only 12% of total activity, and all of them were reversible type oxidase. However, it was suggested by the electron spin resonance method that the tissue xanthine oxidase freed of superoxide dismutase could produce oxygen free radicals. In conclusion, reperfusion injury is caused not only by the increase of oxygen free radicals but by the destruction of scavenging systems.
最近，氧自由基似乎在缺血后损伤中起主要作用，尤其是在常氧再灌注后的损伤。为阐明再灌注损伤的机制，我们测定了缺血再灌注大鼠肾脏中氧自由基生成酶和自由基清除酶的活性。所有防御酶活性均显著降低；超氧化物歧化酶从2.15±0.14降至1.71±0.11，过氧化氢酶从186.6±12.7降至116.5±7.1，谷胱甘肽过氧化物酶从30.0±2.6降至19.1±2.9，谷胱甘肽还原酶从118±5.1降至39.9±6.8（U/mg蛋白）。黄嘌呤脱氢酶向黄嘌呤氧化酶的转化仅占总活性的12%，且均为可逆型氧化酶。然而，电子自旋共振法表明，去除超氧化物歧化酶的组织黄嘌呤氧化酶可产生氧自由基。总之，再灌注损伤不仅是由氧自由基增加引起的，也是由清除系统的破坏引起的。
