POLY(ADP-RIBOSE) SYNTHESIS INDUCED BY NITRIC-OXIDE IN A MOUSE BETA-CELL LINE

被引：19

作者：

INADA, C

YAMADA, K

TAKANE, N

NONAKA, K

机构：

[1] Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, Kurume, Fukuoka

来源：

LIFE SCIENCES | 1995年 / 56卷 / 18期

关键词：

NITRIC OXIDE; NICOTINAMIDE ADENINE DINUCLEOTIDE; POLY(ADP-RIBOSE);

D O I：

10.1016/0024-3205(95)00109-J

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

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.

引用

页码：1467 / 1474

页数：8

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