2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide and Glioma

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.

Topics: Adenosine Diphosphate Ribose; Animals; Blotting, Northern; Cholera Toxin; Cyclic N-Oxides; Down-Regulation; Enzyme Inhibitors; Glioma; GTP-Binding Proteins; Imidazoles; Molsidomine; Nitric Oxide; Rats; RNA, Messenger; Tumor Cells, Cultured