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以大鼠增负荷力竭性运动为模型，利用低温电子自旋共振（ＳＥＲ）技术，分别于安静时、运动中、运动后即刻、运动后３０ｍｉｎ、２ｈ、４ｈ、８ｈ提取大鼠肾组织，测定氧自由基（ＯＦＲ）信号强度，同时测定ＳＯＤ活力和ＭＤＡ含量，结果表明：①运动后恢复期３０ｍｉｎ，肾脏ＯＦＲ信号强度升高明显，提示运动性肾缺血及恢复期再灌注诱导的黄嘌呤氧化酶机制可能是肾组织ＯＦＲ生成的主要来源；②在运动过程中及恢复期ＯＦＲ改变与ＳＯＤ变化趋势基本吻合，提示肾内源性ＳＯＤ在防止ＯＦＲ损伤中起重要作用；③肾脏ＭＤＡ于运动后２ｈ出现峰值，而ＯＦＲ则于恢复期３０ｍｉｎ升至最高，说明除肾脏自身产生活性氧诱导脂质过氧化以外，其它部位转移的ＭＤＡ也许占很大比重
The rats were subjected to exhaustive exercise with increasing load as model, and the renal tissue was extracted at low temperature by Electron Spin Resonance (SER) technique at rest, during exercise, immediately after exercise, 30min, 2h, 4h, 8h after exercise, OFR signal intensity was measured and SOD activity and MDA content were measured at the same time. The results showed that: (1) After 30min exercise recovery, OFR signal intensity increased significantly, suggesting that renal ischemia and convalescent reperfusion-induced yellow The mechanism of purine oxidase may be the main source of OFR in renal tissue. ② The changes of OFR during exercise and convalescence basically coincide with the changes of SOD, suggesting that endogenous renal SOD plays an important role in preventing OFR injury. Peaked at 2h after exercise, whereas OFR rose to the highest level at 30min after recovery, indicating that the MDA content of other sites may account for a large proportion of all, except that the kidney itself produces reactive oxygen species to induce lipid peroxidation