N-acetylcysteine inhibits apoptosis and decreases viral particles in HIV-chronically infected U937 cells.
Apoptosis or programmed cell death (PCD) is a type of death occurring in various physiological processes. Several data suggest that: (1) apoptosis may play a critical role in AIDS pathogenesis; (2) an increase of endocellular free radical levels can be associated with activation of previously latent HIV virus. Tumor necrosis factor (TNF), a cytokine capable of inducing oxygen free radicals and apoptosis, appears also to be involved in HIV activation. The present findings, which elucidate a relationship between the percentage of apoptotic cells, reduced glutathione (GSH) depletion and an increase of p24 antigenemia, suggest that pretreatment with N-acetylcysteine (NAC) is capable of decreasing the above-mentioned phenomena in HIV-infected U937 cells.
Malorni
W
W
Department of Ultrastructures, Istituto Superiore di Sanità, Rome, Italy.
Rivabene
R
R
Santini
M T
MT
Donelli
G
G
D000111:Acetylcysteine / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D006690:Bisbenzimidazole; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line; D004249:DNA Damage / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D016655:HIV Core Protein p24 / Q000378:metabolism; D015497:HIV-1 / Q000187:drug effects* / Q000254:growth & development; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000382:microbiology; D008856:Microscopy, Fluorescence; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D016655:HIV Core Protein p24; D014409:Tumor Necrosis Factor-alpha; D005978:Glutathione; D006690:Bisbenzimidazole; D000111:Acetylcysteine