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Cole SB, Langkamp-Henken B, Uphold CR, Herrlinger-Garcia KA, Bender BS, Findley K, Hoffinger R. Oxidative stress and antioxidant capacity in smoking vs. nonsmoking men with HIV/AIDS. Paper presented at: Federation of American Societies for Experimental Biology Annual Meeting; 2004 Mar 24; Washington, DC.
Oxidative stress increases viral replication by activating NFkB and causes destruction of CD4+ T cells in the HIV/AIDS population. Cigarette smoking also causes oxidative stress. The purpose of this study was to determine whether male smokers with HIV/AIDS had increased levels of oxidative stress (lipid peroxidation, LPO) and decreased antioxidant potential (AOP). Nonsmokers (n = 10) and smokers (n = 10) attending VA infectious disease clinic who were HIV+ and on antiretroviral triple combination therapy with a suppressed viral load were enrolled. Blood samples were analyzed for LPO, AOP, CD4+ cell count and viral load. There were no significant differences in age (46+2 vs 47+2 y, mean + SEM), BMI (26+2 vs 24+1), CD4+ (444+99 vs 534+103/mm3) and viral load (152, < 50-3969 vs < 50, < 50-1754 copies/ml, median, range) between nonsmokers and smokers, respectively. Mean LPO was outside the normal range of 0-1.3 nmol/ml and tended to be higher in smokers (3.3+1.3 vs 4.5+1.5 nmol/ml, p = 0.07) but there was no difference in AOP between nonsmokers and smokers (393, 84-733 vs 340, 135-462 M Uric Acid equiv.). However, AOP measures overall antioxidant potential and is not specific for antioxidants (vitamins E, C, glutathione peroxidase) known to decrease with smoking. These data suggest that cigarette smoking may contribute to increased oxidative stress in men with HIV.
