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通过测定力竭运动后大鼠肾脏组织脂质过氧化水平（ＬＯＰ）、超氧化物歧化酶活性（ＳＯＤ）和谷胱甘肽过氧化物酶活性（ＧＳＨ－Ｐｘ）的变化，以及大鼠尿液中ｒ－谷氨酸转肽酶（ｒ－ＧＴ）和Ｎ－乙酰－β－Ｄ－氨基葡萄糖苷酶（ＮＡＧ）排出率的变化及其相互关系，来研究力竭运动导致大鼠急性肾小管损伤的机制。结果表明：大鼠肾组织ＬＰＯ水平显著升高，Ｐ＜０．０５，ＳＯＤ活性无明显变化（Ｐ＞０．０５），ＧＳＨ－Ｐｘ显著性下降（Ｐ＜０．０５）。尿液中ｒ－ＧＴ及ＮＡＧ含量都显著增加。ＬＰＯ水平升高与ｒ－ＧＴ和ＮＡＧ增加之间有显著相关性（Ｐ＜０．０５）。说明一次性力竭运动导致大鼠肾脏组织自由基水平显著升高，而自由基与肾小管上皮细胞膜性结构中的不饱和脂肪酸发生强烈的过氧化反应，从而导致肾小管上皮细胞膜性结构的完整性丧失和损害以及正常生理功能受到破坏，造成肾小管的急性损伤。
The changes of LOP, SOD and GSH-Px in rat kidney after exhaustive exercise were measured, and the changes of rat urine Fluid r-glutamic acid peptidase (r-GT) and N-acetyl-β-D-glucosaminidase (NAG) changes and their relationship to study exhaustive exercise lead to acute kidney in rats Tubule damage mechanism. The results showed that the level of LPO in rat kidney increased significantly (P <0.05), the activity of SOD did not change significantly (P> 0.05) and the level of GSH-Px decreased significantly (P <0.05). Urine r-GT and NAG levels were significantly increased. There was a significant correlation between LPO level and the increase of r-GT and NAG (P <0.05). This shows that the one-time exhaustive exercise leads to a significant increase in free radical levels in rat kidney tissues, whereas the free radicals undergo a strong peroxidation reaction with unsaturated fatty acids in the membranous structure of renal tubular epithelial cells, resulting in the integrity of the membranous structure of renal tubular epithelial cells Sexual loss and damage as well as normal physiological function is destroyed, resulting in acute tubular damage.