GLUTATHIONE-DEPENDENT MODULATION OF EXHAUSTING EXERCISE-INDUCED CHANGES IN NEUTROPHIL FUNCTION OF RATS

Reduced glutathione (GSH) plays a central role in maintaining an effec tive synergism between various physiological and exogenous antioxidant s, We tested the effects of GSH and N-acetylcysteine (NAC, a pro-GSH c linical drug), intraperitoneal (i.p.) supplementation and GSH deficien cy on exercise-induced leucocyte margination and neutrophil oxidative burst activity. GSH, NAC 1g . kg(-1)) or placebo saline was i.p. injec ted (one or eight times) to male rats (n greater than or equal to seve n per group). The GSH-deficient rats were prepared by i.p. injections of L-buthionine-[SR]-sulphoximine (BSO, 6 mmol . l(-1). kg(-1)) twice daily for 4 days. Exercised animals were subjected to treadmill run to exhaustion. Exhausting treadmill exercise significantly decreased per ipheral blood leucocyte count in the controls (P < 0.001). Such exerci se-associated leucocyte margination was prevented by GSH supplementati on. Peripheral blood neutrophil counts were significantly higher (P < 0.02) in the GSH-supplemented groups compared to the placebo control g roups. Exercise-induced increase in peripheral blood neutrophil oxidat ive burst activity as measured by luminol-enhanced chemiluminescence p er volume of blood tended to be higher in the GSH-supplemented group ( P < 0.10), and lower in the GSH-deficient rats (P < 0.02). In these ex periments, for the first time we have shown that GSH supplementation c an induce neutrophil mobilization and decrease exercise-induced leucoc yte margination, and that exogenous and endogenous GSH can regulate ex ercise-induced stimulation of the neutrophil oxidative burst.