Glutathione regulation during exercise: Effect of fasting-refeeding, glutathione depletion and supplementation
Leeuwenburgh, Christiaan
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https://hdl.handle.net/2142/23109
Description
Title
Glutathione regulation during exercise: Effect of fasting-refeeding, glutathione depletion and supplementation
Author(s)
Leeuwenburgh, Christiaan
Issue Date
1995
Doctoral Committee Chair(s)
Ji, Li Li
Department of Study
Kinesiology and Community Health
Discipline
Kinesiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Health Sciences, Nutrition
Health Sciences, Recreation
Language
eng
Abstract
Glutathione (GSH) is an important intracellular and extracellular antioxidant, critical for the organism's protection against reactive oxygen species. Since prolonged aerobic exercise has shown to increase formation of reactive oxygen species, this thesis investigated the importance of GSH during exhaustive exercise under several conditions: (1) after fasting-refeeding; (2) following drug-induced chronic glutathione depletion; and (3) after GSH and GSH ethyl ester (GSHE) supplementation. The effects of fasting and refeeding were investigated on GSH status, antioxidant enzyme activity, lipid peroxidation and hormonal responses, at rest and after acute exercise in rodents. This study lead us to suggest that (1) refeeding increases liver GSH content and synthesizing activity, possibly mediated by an insulin-stimulated mechanism; (2) hepatic GSH content declines significantly with exercise and this GSH efflux may be regulated by glucagon; and (3) skeletal muscle is under oxidative stress with exhaustive exercise. Also, investigated was the effect of in vivo chronic GSH depletion with buthionine sulfoximine investigated in male Swiss-Webster mice at rest and after an acute bout of exhaustive swim exercise. After 12 days of buthionine sulfoximine treatment concentrations of GSH decreased significantly in the liver, kidney, heart, quadriceps muscle, and plasma. There was no difference in exercise endurance time between the GSH-adequate and GSH-depleted mice. However, exercise in the GSH-depleted state exacerbated GSH deficit in the plasma, muscle, and myocardium, without adequate GSH supply from the liver. Lipid peroxidation in the liver increased significantly in the GSH-adequate and GSH-depleted mice. Next investigated was the efficacy of GSH supplementation in attenuating the exercise-induced decline of GSH in rodent tissues. This study found that: (1) GSH and GSHE supplementation did not increase tissue GSH content and did not attenuate the exercise-induced GSH decline; (2) GSH supplementation disturbed GSH homeostasis in the liver, kidney, heart, quadriceps, and plasma; (3) GSHE caused lipid peroxidation in the myocardium muscle at rest, and in the kidney and heart following exercise; (4) quadriceps muscle was under severe oxidative stress, while GSH and GSHE prevented significant lipid peroxidation. These studies showed that interorgan GSH homeostasis is essential for prooxidant-antioxidant balance during prolonged physical exercise.
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