Decreased antioxidant defence in individuals infected by the human immunodeficiency virus

Background The oxidative stress associated with HIV infection may be important for the progression of the disease because reactive oxygen species activate the nuclear transcription factor NF‐κB, which is obligatory for HIV replication. Patients and methods The activities of the antioxidant enzymes s...

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Veröffentlicht in:European journal of clinical investigation 2000-05, Vol.30 (5), p.454-459
Hauptverfasser: TREITINGER, A, SPADA, C, VERDI, J. C, MIRANDA, A. F. B, OLIVEIRA, O. V, SILVEIRA, M. V. S, MORIEL, P, ABDALLA, D. S. P
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Sprache:eng
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Zusammenfassung:Background The oxidative stress associated with HIV infection may be important for the progression of the disease because reactive oxygen species activate the nuclear transcription factor NF‐κB, which is obligatory for HIV replication. Patients and methods The activities of the antioxidant enzymes superoxide dismutase (SOD, EC 1.15.1.1) and glutathione peroxidase (GPx, EC 1.11.1.9) of blood plasma and peripheral blood mononuclear cells, as well as the plasma levels of ascorbate, α‐tocopherol and β‐carotene, were measured in 75 subjects with HIV infection and in 26 controls. The HIV‐infected patients were classified according to the Walter Reed Army Institute criteria. Results The extracellular SOD (EC‐SOD) of blood plasma activity was decreased in HIV‐infected patients compared to controls, while the SOD activity of mononuclear cells decreased with the HIV‐associated disease progression. GPx activities and α‐tocopherol concentration of HIV‐infected patients neither differed as compared to controls nor in relation to disease progression. Lower concentrations of ascorbate and β‐carotene were found in HIV‐infected patients than in controls. A positive correlation between CD4 lymphocyte counts and the SOD activities of plasma and mononuclear cells was found. Conclusion These results suggest that abnormalities of antioxidant defence, mainly of SOD activity, are related to the progression of the HIV infection.
ISSN:0014-2972
1365-2362
DOI:10.1046/j.1365-2362.2000.00642.x