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Increased levels of oxidized glutathione in CD4+ lymphocytes associated
with disturbed intracellular redox balance in human immunodeficiency virus
type 1 infection
P Aukrust, AM Svardal, F Muller, B Lunden, RK Berge, PM Ueland and SS Froland
Medical Department A, University of Oslo, National Hospital, Norway.
We investigated the intracellular glutathione redox status in isolated
lymphocyte subpopulations and monocytes in patients with human
immunodeficiency virus type 1 (HIV-1) infection and in healthy controls.
CD4+ lymphocytes from HIV-1-infected patients were primarily characterized
by a substantial increase in oxidized glutathione levels and a considerable
decrease in the ratio of reduced to total glutathione, in most cases below
0.5 in patients with symptomatic HIV-1 infection, rather than decreased
levels of reduced glutathione. The increase in oxidized glutathione was
strongly correlated with low numbers of CD4+ lymphocytes in peripheral
blood and impaired stimulated interleukin-2 production and proliferation in
peripheral blood mononuclear cells, which is compatible with an
immunopathogenic role for these redox disturbances. The HIV-1-infected
patients with the most advanced clinical and immunologic disease were also
characterized by an increase in levels of reduced glutathione in monocytes,
suggesting that the glutathione redox cycle may be differentially regulated
in CD4+ lymphocytes and monocytes. We could not confirm previous reports
suggesting cysteine deficiency as a major cause of disturbed glutathione
homeostasis during HIV-1 infection. The demonstrated glutathione
abnormalities were correlated with raised serum levels of tumor necrosis
factor alpha. These findings suggest that a therapeutical approach, which
can restore the glutathione redox dysbalance in CD4+ lymphocytes and
decrease the inflammatory stress, may be worthwhile exploring in HIV-1
infection.
Volume 86,
Issue 1,
pp. 258-267,
07/01/1995
Copyright © 1995 by The American Society of Hematology
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