力竭运动导致大鼠急性肾小管损伤机制的研究

A Research on the Mechaism for the Exhausted Exercise-Induced Acute Renal Tubular Injury in Rats

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。

This research was designed to test and verify the hypothesis that exercise-induced increase in free radical(FR)activity resulted in the ex- tensive damage and injury of the normal structure and function of renal tubular epithelial biomembrane was the major cause of the acute renal tubular injury. Lipid peroxidation levels (LPO)in renal tissues and urinary NAG, r-GT excretion rate increased significantly after exhausted exercise(P < 0.01),but the increase in SOD activity was not significant (P < 0.05). GSH-Px activity decreased apparently (P < 0.05). The rising level of LPO in renal tissues was significantly related with the levelof urinary NAG.r-GT excretion the(r = 0. 89, P < 0.05; r = 0.87,P < 0.05,respec- tively). It indicated that exhausted exercise caused the significant increase in FR activity in renaltissues which resulted in the extensive damage and injury of the normal structure and function of renal tubular epithelial biomembrane and the acute renal tubular injury in rats.