Sen C K, Atalay M, Hänninen O
Department of Physiology, Faculty of Medicine, University of Kuopio, Finland.
J Appl Physiol (1985). 1994 Nov;77(5):2177-87. doi: 10.1152/jappl.1994.77.5.2177.
Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80-90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.
谷胱甘肽（GSH）在协调不同脂相和水相抗氧化剂之间的协同作用中起着核心作用。我们记录了：1）外源性谷胱甘肽（GSH）和N-乙酰半胱氨酸（NAC）如何影响力竭运动诱导的组织谷胱甘肽状态、脂质过氧化物[硫代巴比妥酸反应性物质（TBARS）]的变化以及耐力；2）通过使用谷胱甘肽缺乏[经L-丁硫氨酸-（S，R）-亚砜亚胺（BSO）处理]的大鼠，内源性谷胱甘肽在规避运动诱导的氧化应激中的相对作用。腹腔注射谷胱甘肽可显著增加血浆谷胱甘肽；外源性谷胱甘肽本身是一种将谷胱甘肽递送至组织的无效载体。重复给予谷胱甘肽（每天1次，共3天）可增加血液和肾脏中的总谷胱甘肽[TGSH；谷胱甘肽+氧化型谷胱甘肽（GSSG）]。谷胱甘肽和NAC均不影响力竭耐力。NAC可减少运动诱导的肺和血液中谷胱甘肽的氧化。BSO使肝脏、肺、血液和血浆中的TGSH池减少约50%，使骨骼肌和心脏中的TGSH池减少80 - 90%。与对照组相比，静息状态下谷胱甘肽缺乏的大鼠肝脏、红色腓肠肌、心脏和血液中的GSSG较低；肝脏、心脏、肺、血液和血浆中的GSSG/TGSH比值相似；骨骼肌中的GSSG/TGSH比值较高；骨骼肌、心脏和血浆中的TBARS较多。与对照组相反，谷胱甘肽缺乏的大鼠进行力竭运动后，肝脏、肌肉或心脏中的TGSH并未减少，血浆中的TGSH也未增加；肌肉、血液或血浆中的GSSG未增加；血浆或肌肉中的TBARS也未增加。谷胱甘肽缺乏的大鼠耐力降低约50%，这表明内源性谷胱甘肽在规避运动诱导的氧化应激以及作为运动表现的决定因素方面起着关键作用。
