摘要
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。
Taking incremental exercise to exhaustion as the experimental model and using low temperature electron spin resonance(ESR) technique as the determining method,we sampled rats kidney tissue at rest,druing exercise and post exercise at 0,30,120,240 and 480 min., respectively.the signal strength of OFR species,SOD activity and MDA content were measured.The results showed that:1.The signal strength of OFR species increased apparently at 30 min. post exercise. It indicated that ischemia_reperfusion mechanism might be the major resource of OFR.2.The changes of OFR species coincided with SOD during exercise and recovery,which suggested that SOD might play an important role in protecting kidney from OFR damage.3.MDA content increased to the highest level at 2h post exercise,while the signal strength of OFR reached peak level at 30 min.post exercise,which showed that MDA transferring from other organs might be of a large portion besides kidney produced OFR and induced lipid peroxidation itself.
出处
《中国运动医学杂志》
CAS
CSCD
北大核心
1999年第1期31-33,共3页
Chinese Journal of Sports Medicine
关键词
运动
氧自由基
LPO
SOD
肾脏
递增负荷运动
electron spin resonance(ESR),oxidative free radical(OFR),lipid peroxidation(LPO),superoxide dismutase(SOD),kidney