N-acetylcysteine inhibits apoptosis and decreases viral particles in HIV-chronically infected U937 cells

FEBS Lett. 1993 Jul 19;327(1):75-8. doi: 10.1016/0014-5793(93)81043-y.

Abstract

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.

MeSH terms

  • Acetylcysteine / pharmacology*
  • Apoptosis / drug effects*
  • Bisbenzimidazole
  • Cell Death / drug effects
  • Cell Line
  • DNA Damage / drug effects
  • Glutathione / metabolism
  • HIV Core Protein p24 / metabolism
  • HIV-1 / drug effects*
  • HIV-1 / growth & development
  • Humans
  • Leukocytes, Mononuclear / microbiology
  • Microscopy, Fluorescence
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • HIV Core Protein p24
  • Tumor Necrosis Factor-alpha
  • Glutathione
  • Bisbenzimidazole
  • Acetylcysteine