Xiong Yanlian, Xiong Yanlei, Zhou Shuai, Yu Zhenhai, Zhao Dongmei, Wang Zhiqiang, Li Yuling, Yan Jingtong, Cai Yu, Zhang Wenqian
Department of anatomy, School of Basic Medicine, Binzhou Medical University, Yantai, P.R. China.
Cell Physiol Biochem. 2016;40(6):1410-1421. doi: 10.1159/000453193. Epub 2016 Dec 20.
BACKGROUND/AIMS: The main purpose of this study was to investigate the effect of exhaustive exercise on L-cysteine uptake and its effect on erythrocyte glutathione (GSH) synthesis and metabolism.
Rats were divided into three groups: sedentary control (C), exhaustive running exercise (ERE) and moderate running exercise (MRE) (n=12 rats/group). We determined the L-cysteine efflux and influx in vitro in rat erythrocytes and its relationship with GSH synthesis. Total anti-oxidant potential of plasma was measured in terms of the ferric reducing ability of plasma (FRAP) values for each exercise group. In addition, the glucose metabolism enzyme activity of erythrocytes was also measured under in vitro incubation conditions.
Biochemical studies confirmed that exhaustive running exercise significantly increased oxidative damage parameters in thiobarbituric acid reactive substances (TBARS) and methemoglobin levels. Pearson correlation analysis suggested that L-cysteine influx was positively correlated with erythrocyte GSH synthesis and FRAP values in both the control and exercise groups. In vitro oxidation incubation significantly decreased the level of glucose metabolism enzyme activity in the control group.
We presented evidence of the exhaustive exercise-induced inhibition of GSH synthesis due to a dysfunction in L-cysteine transport. In addition, oxidative stress-induced changes in glucose metabolism were the driving force underlying decreased L-cysteine uptake in the exhaustive exercise group.
背景/目的:本研究的主要目的是探讨力竭运动对L-半胱氨酸摄取的影响及其对红细胞谷胱甘肽(GSH)合成与代谢的作用。
将大鼠分为三组:久坐对照组(C)、力竭跑步运动组(ERE)和适度跑步运动组(MRE)(每组12只大鼠)。我们测定了大鼠红细胞体外L-半胱氨酸的流出和流入及其与GSH合成的关系。通过血浆铁还原能力(FRAP)值测定每个运动组血浆的总抗氧化能力。此外,还在体外孵育条件下测定了红细胞的葡萄糖代谢酶活性。
生化研究证实,力竭跑步运动显著增加了硫代巴比妥酸反应物质(TBARS)和高铁血红蛋白水平中的氧化损伤参数。Pearson相关分析表明,对照组和运动组中L-半胱氨酸流入均与红细胞GSH合成和FRAP值呈正相关。体外氧化孵育显著降低了对照组的葡萄糖代谢酶活性水平。
我们提供了证据表明,力竭运动导致L-半胱氨酸转运功能障碍,从而抑制了GSH合成。此外,氧化应激引起的葡萄糖代谢变化是力竭运动组中L-半胱氨酸摄取减少的潜在驱动因素。