Nitric oxide donor SIN-1 mediated down-regulation of the G-protein alpha-subunit in C6 glioma cells

Life Sci. 1997;60(15):1279-85. doi: 10.1016/s0024-3205(97)00071-4.

Abstract

In C6 glioma cells, the nitric oxide (NO) donor 3-morpholinosynonimine hydrochloride (SIN-1) (0.5 mM) produced a significant decrease in the stimulatory G-protein alpha subunit (G alpha(s)) levels. Northern hydridization did not detect any differences in G alpha(s) mRNA levels after SIN-1 treatment. Furthermore SIN-1 increased endogenous and cholera toxin-catalyzed ADP-ribosylation of G alpha(s). 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) (0.5mM), a NO scavenger, had no effect on endogenous or cholera toxin-catalyzed ADP-ribosylation of G alpha(s), but reversed the increase in endogenous and cholera toxin-catalyzed ADP-ribosylation of G alpha(s) induced by SIN-1. These results suggest that increasing ADP-ribosylation may be involved in SIN-1 mediated G alpha(s) down-regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate Ribose / metabolism
  • Animals
  • Blotting, Northern
  • Cholera Toxin / pharmacology
  • Cyclic N-Oxides / pharmacology
  • Down-Regulation / drug effects*
  • Enzyme Inhibitors / pharmacology*
  • GTP-Binding Proteins / metabolism*
  • Glioma / drug therapy
  • Glioma / metabolism*
  • Glioma / pathology
  • Imidazoles / pharmacology
  • Molsidomine / analogs & derivatives*
  • Molsidomine / pharmacology
  • Nitric Oxide / metabolism*
  • RNA, Messenger / metabolism
  • Rats
  • Tumor Cells, Cultured

Substances

  • Cyclic N-Oxides
  • Enzyme Inhibitors
  • Imidazoles
  • RNA, Messenger
  • 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide
  • Adenosine Diphosphate Ribose
  • Nitric Oxide
  • linsidomine
  • Cholera Toxin
  • Molsidomine
  • GTP-Binding Proteins