Amplification of superoxide anion generation in phagocytic cells by HIV-1 infection.
Amplification of superoxide (O2-) generation by HIV-1 infection was examined in two human myeloid-monocytic cell lines. The level of O2- generation in HL-60 after infection became significantly higher than that of the steady-state. A similar phenomenon was also shown in U937, but only after acquisition of O2- generation ability by differentiation to macrophages. By means of the NADPH oxidase-coupled responses in infected cells, we reconstituted the O2(-)-generating machinery in cell-free system. The results suggested that cytosolic factor(s) exerted by infection might be responsible for the amplification of O2- generation. Thus, HIV-1 infection could elevate the level of oxidative stress in macrophages which might play an important role in disease progression.
Section of Serology, Hokkaido University, Sapporo, Japan.
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Kimura
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Kameoka
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Ikuta
D000838:Anions; D002454:Cell Differentiation; D006098:Granulocytes / Q000378:metabolism / Q000382:microbiology; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D007700:Kinetics; D009000:Monocytes / Q000378:metabolism / Q000382:microbiology; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D019255:NADPH Oxidases; D010586:Phagocytes / Q000378:metabolism* / Q000382:microbiology*; D013481:Superoxides / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D000838:Anions; D013481:Superoxides; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; D013755:Tetradecanoylphorbol Acetate