|Marquis, Grace - IOWA STATE UNIVERSITY|
|Kruzich, Laurie - IOWA STATE UNIVERSITY|
|Douglas, Steven - UNIV OF PENNSYLVANIA|
|Wilson, Craig - UNIV OF ALABAMA|
Submitted to: Aids
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 2004
Publication Date: February 1, 2005
Citation: Stephensen, C.B., Marquis, G.S., Kruzich, L., Jacob, R.A., Douglas, S., Wilson, C. 2005. Immune activation and oxidative damage in hiv-positive and hiv-negative adolescents. Journal of Acquired Immune Deficiency Syndrome. 2005. 38(2):180-90. Interpretive Summary: A balanced diet protects against oxidative damage caused by normal metabolic process or inflammation. We examined the relationship of vitamin C intake and plasma vitamin C concentrations to oxidative damage in adolescents and young adults with and without HIV infection. Our principal finding was that vitamin C intake was good in these subjects and that plasma vitamin C was not associated with oxidative damage markers, is might be expected in vitamin C deficiency. In addition, oxidative damage was not found to be greater in the HIV-positive subjects, as compared to the uninfected controls. However, a key antioxidant protection enzyme, glutathione peroxidase, was elevated in HIV infection. This suggests that increased oxidative stress due to HIV infection may induce glutathione peroxidase levels, resulting in increased antioxidant protection. This phenomenon may not be seen in other populations who are older or who have deficiencies in antioxidant micronutrients.
Technical Abstract: Oxidative stress may impair immune function and thus lead to increased HIV replication and accelerated progression of HIV disease. In a cross-sectional study involving subjects from the Reaching for Excellence in Adolescent Health (REACH) cohort, we examined the possible associations between HIV status, disease severity, immune activation and oxidative damage. Subjects were young (14 - 23 y of age), primarily female (75%) and African American (67%). Plasma ascorbic acid, uric acid and total antioxidant status, and whole blood glutathione and glutathione peroxidase, were measured as indicators of antioxidant protection. After correction for demographic, health status, HIV infection, immune activation and dietary variables in multiple regression analysis, glutathione peroxidase concentrations were found to be higher in subjects with HIV infection (p = 0.007). Glutathione peroxidase concentrations were also higher in subjects taking antiretroviral therapy (p = 0.006). Plasma malondialdehyde and protein carbonyls were measured as markers of oxidative damage but were not elevated in HIV infection. However, glutathione peroxidase concentrations (p < 0.001) were positively associated with malondialdehyde concentrations. This correlation suggests that subjects with elevated oxidative stress (and resulting oxidative damage) also have enhanced antioxidant protection due to higher glutathione peroxidase levels. This interpretation suggests that oxidative stress (as indicated by elevated glutathione peroxidase levels) is greater in HIV-infected than uninfected subjects, and is elevated further in subjects taking antiretroviral therapy. Failure to detect oxidative damage in these same subjects may be explained by the effectiveness of inducible antioxidant protection in preventing such damage in these young, relatively healthy subjects.