Nitric oxide toxicity in islet cells involves poly(ADP-ribose) polymerase activation and concomitant NAD+ depletion.

Abstract:

:Previous studies have shown that DNA strand breaks are an early consequence of nitric oxide toxicity in pancreatic islet cells. We show here that exposure of islet cells to chemical NO donors causes the formation of ADP-ribose polymers in cell nuclei, with concomitant depletion of intracellular NAD+. Islet cell lysis was largely prevented by the ADP-ribosylation inhibitors nicotinamide, 3-aminobenzamide, and 4-amino-1,8-naphthalimide, the latter being a potent new-generation compound with high selectivity for poly(ADP-ribosyl)-ation. These findings indicate a key role of poly(ADP-ribose) polymerase activation in NO toxicity in islet cells.

authors

Radons J,Heller B,Bürkle A,Hartmann B,Rodriguez ML,Kröncke KD,Burkart V,Kolb H

doi

10.1006/bbrc.1994.1368

subject

Has Abstract

pub_date

1994-03-30 00:00:00

pages

1270-7

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(84)71368-4

journal_volume

199

pub_type

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