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Am J Physiol Endocrinol Metab 276: E205-E211, 1999;
0193-1849/99 $5.00
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Vol. 276, Issue 1, E205-E211, January 1999

Erythrocyte glutathione deficiency in symptom-free HIV infection is associated with decreased synthesis rate

Farook Jahoor1, Alan Jackson2, Brian Gazzard3, Gary Philips2, Danny Sharpstone3, Margaret E. Frazer1, and William Heird1

1 United States Department of Agriculture/Agricultural Research Station Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030; 2 Institute of Human Nutrition, University of Southampton, Southampton S016 6YD; and 3 Chelsea and Westminster Hospital, London SW10 9TH, United Kingdom

Although several studies have documented intra- and extracellular glutathione (GSH) deficiency in asymptomatic human immunodeficiency virus (HIV) infection, the mechanisms responsible for the altered GSH homeostasis remain unknown. To determine whether decreased synthesis contributes to this alteration of GSH homeostasis, a primed-constant infusion of [2H2]glycine was used to measure the fractional and absolute rates of synthesis of GSH in five healthy and five symptom-free HIV-infected subjects before and after supplementation for 1 wk with N-acetylcysteine. The erythrocyte GSH concentration of the HIV-infected group was lower (P < 0.01) than that of the control group (1.4 ± 0.16 vs. 2.4 ± 0.08 mmol/l). The smaller erythrocyte GSH pool of the HIV-infected group was associated with a significantly slower (P < 0.01) absolute synthesis rate of GSH (1.15 ± 0.14 vs. 1.71 ± 0.15 mmol · l-1 · day-1) compared with controls. Cysteine supplementation elicited significant increases in both the absolute rate of synthesis and the concentration of erythrocyte GSH. These results suggest that the GSH deficiency of HIV infection is due in part to a reduced synthesis rate secondary to a shortage in cysteine availability.

glutathione synthesis; human immunodeficiency virus infection; N-acetylcysteine; stable isotope


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