isopropyl-thiogalactoside and zinc-chloride

Toxic effects of nitric oxide (NO) were suggested to be mediated by its metabolite peroxynitrite, a strong oxidizing agent. To determine if antioxidative effects of Bcl-2 protooncogene can prevent NO-mediated apoptosis, we used vaccinia virus recombinants expressing mouse inducible NO-synthase, iNOS, or human bcl-2 genes. Expression of iNOS in HeLa G cells induces apoptosis which can be prevented by co-expression of bcl-2 or by addition of reduced glutathione or N-acetylcysteine. We demonstrate that this NO-induced apoptosis proceeds through the activation of interleukin-1 beta-converting enzyme-like proteases and cleavage of the poly(ADP-ribose) polymerase, an effect which is also prevented by Bcl-2.

Topics: Acetylcysteine; Animals; Apoptosis; Caspase 1; Chlorides; Cysteine Endopeptidases; DNA; Gene Expression; Genes, bcl-2; Genetic Vectors; Glutathione; HeLa Cells; Humans; Isopropyl Thiogalactoside; Lipid Peroxidation; Mice; Nitric Oxide; Nitric Oxide Synthase; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; Thiobarbituric Acid Reactive Substances; Vaccinia virus; Zinc Compounds