Poly(ADP-ribose) synthesis induced by nitric oxide in a mouse beta-cell line.
Nitric oxide (NO) has been implicated as an immunological effector molecule that mediates beta-cell dysfunction associated with Type 1 diabetes. To assess whether NO induces poly(ADP-ribose) synthesis in islet cells, we examined the effect of nitroprusside on islet cells. The exposure of mouse islet cells and a beta-cell line (beta TC1) to 0.05-0.2 mM nitroprusside resulted in the reduction of intracellular nicotinamide adenine dinucleotide (NAD) levels. Nitroprusside stimulated poly(ADP-ribose) synthetase activity in beta TC1 cells. An inhibitor of poly(ADP-ribose) synthetase, 3-aminobenzamide, prevented both NAD decrease and poly ADP-ribosylation. These observations suggest that NO-induced pancreatic beta-cell damage may be ascribable to the activation of poly(ADP-ribose) synthetase that results in the decrease of NAD content.
Inada
C
C
Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Yamada
K
K
Takane
N
N
Nonaka
K
K
D000818:Animals; D002460:Cell Line; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism*; D051379:Mice; D009243:NAD / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism / Q000494:pharmacology*; D009599:Nitroprusside / Q000378:metabolism / Q000494:pharmacology; D011064:Poly Adenosine Diphosphate Ribose / Q000096:biosynthesis*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism
D009243:NAD; D009599:Nitroprusside; D011064:Poly Adenosine Diphosphate Ribose; D009569:Nitric Oxide; D011065:Poly(ADP-ribose) Polymerases