|Marquis, G - NUTR.DEPT.IOWA STATE UNIV|
|Douglas, S - CHILD.HOSPIT.PENNSLYVANIA|
|Kruzich, L - NUTR.DEPT.IOWA STATE UNIV|
|Wilson, C - PEDIATRICS, UN ALABAMA|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 17, 2006
Publication Date: March 20, 2007
Citation: Stephensen, C.B., Marquis, G.S., Douglas, S.D., Kruzich, L.A., Wilson, C.M. 2007. GLUTATHIONE, GLUTATHIONE PEROXIDASE AND SELENIUM STATUS IN HIV-POSITIVE AND HIV-NEGATIVE ADOLESCENTS. American Journal of Clinical Nutrition. 85:173-181. Interpretive Summary: Selenium deficiency has been associated with increased cancer risk and increased risk of complications or death from certain infectious diseases. These risks derive from the fact that selenium is a necessary component of the antioxidant enzyme glutathione peroxidase. Thus selenium deficiency increases risk of oxidative damage to cells that can promote damaging inflammation that may hasten the development of cancer or exacerbate the severity of a chronic infectious disease, such as that caused by HIV. In this study we found that a group of adolescents and young adults with HIV who were primarily African American and female had adequate selenium status, rather than the deficiency that has been previously reported from subjects with HIV. In addition, the subjects with HIV had higher glutathione peroxidase levels in the blood than did uninfected subjects, suggesting that these relatively young subjects with good selenium status may responded to the oxidative stress of chronic infection by increasing levels of glutathione peroxidase as a protective mechanism.
Technical Abstract: In a cross-sectional study of HIV-positive and HIV-negative subjects from the Reaching for Excellence in Adolescent Health (REACH) cohort we examined the relationship of plasma selenium, whole blood glutathione and whole blood glutathione peroxidase to HIV status, disease severity, use of antiretroviral therapy, immune activation and oxidative damage. Glutathione peroxidase levels were significantly higher in HIV-positive subjects than in HIV-negative subjects. In addition, HIV-positive subjects taking antiretroviral therapy had higher glutathione peroxidase levels than did HIV-positive subjects not taking antiretroviral therapy. Furthermore, glutathione peroxidase levels correlated positively with malondialdehyde concentrations (a measure of oxidative damage), which were also elevated in subjects taking antiretroviral therapy. Selenium concentrations did not differ significantly by HIV status and were comparable to US population reference standards, suggesting that selenium status was adequate in both HIV-positive and HIV-negative subjects. Glutathione levels were lower in HIV-positive females than in HIV-negative females. These data are consistent with the conclusion that REACH subjects have elevated glutathione peroxidase levels in response to the increased oxidative stress of HIV infection. Glutathione peroxidase levels may be further increased by the apparent additional oxidative stress associated with antiretroviral therapy. Such increases may not be seen in subjects with HIV infection with underlying selenium deficiency, which can depress glutathione peroxidase activity. Monitoring glutathione peroxidase and other antioxidant enzyme activities may be useful for monitoring oxidative stress during HIV infection.