Glutathione supplementation and training increases myocardial resistance to ischemia-reperfusion in vivo
The present study examined the effects of oral reduced glutathione (GSH) supplementation in conjunction with endurance training on contractile function, antioxidant defense, and oxidative damage in response to ischemia-reperfusion (I/R) in rat hearts.
Myocardial superoxide dismutase, GSH peroxidase, glutathione reductase, and γ-glutamyl transpeptidase activities were increased with treadmill training in both GSH-S and C rats. I/R induced myocardial lipid peroxidation and lactate dehydrogenase release were attenuated with T/GSH-S treatment.
The present data indicate that training in conjunction with dietary GSH supplementation can increase myocardial GSH content and antioxidant defense capacity, thereby protecting the intact heart against oxidative damage and functional retardation caused by I/R. [Source]
Effects of Oral Glutathione Supplementation on Systemic Oxidative Stress Biomarkers in Human Volunteers
The tripeptide glutathione (GSH) is the most abundant free radical scavenger synthesized endogenously in humans. [Source]
Exercise-induced oxidative stress: glutathione supplementation and deficiency
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. [Source]
Reversal of age-associated decline in immune responsiveness by dietary glutathione supplementation in mice
The potential of dietary glutathione to alter immune response in aging mice was studied. Four (young), 17 (mature) and 24 (old) month old C57BL/6Nia male mice were fed semi-purified, nutritionally adequate diets containing 0 (control) to 1.0% of reduced glutathione (GSH) for 4 weeks. Concanavalin A (Con A) stimulated proliferation of splenocytes was assessed by [3H]thymidine incorporation. Delayed-type hypersensitivity (DTH) to dinitrofluorobenzene (DNFB) was measured by a radioisotopic method. Spleen GSH and splenocyte thiol (−SH) levels were determined by HPLC and binding, respectively.
In the control fed group, mature and old mice showed 67% and 72% reductions (P < 0.05) in Con A stimulated [3H]thymidine incorporation compared to young mice. Dietary GSH supplementation partially, but significantly (P < 0.05) reversed this age-associated decline in mature and old mice. DTH assays revealed that the in vivo T-cell-mediated immune function is depressed with age and that dietary GSH supplementation reverses this depression. Spleens from control-fed mature and old mice contained 12 and 19% less GSH, respectively, than young mice (). This decline was also reversed () by dietary GSH supplementation. Splenocyte −SH content after incubation with Con A and responsiveness to this mitogen were positively correlated in old mice and were greater () in GSH supplemented animals.
Thus, dietary GSH supplementation improves the splenic status of this tripeptide and enhances T-cell mediated immune responses in aging mice. [Source]