ROLE OF CA2+ IN ALLOXAN-INDUCED PANCREATIC BETA-CELL DAMAGE

被引:53
作者
KIM, HR [1 ]
RHO, HW [1 ]
PARK, BH [1 ]
PARK, JW [1 ]
KIM, JS [1 ]
KIM, UH [1 ]
CHUNG, MY [1 ]
机构
[1] CHONNAM NATL UNIV,SCH MED,DEPT INTERNAL MED,KWANGJU,SOUTH KOREA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 1994年 / 1227卷 / 1-2期
关键词
ALLOXAN; CALCIUM; DIABETES MELLITUS; HYDROGEN PEROXIDE; VERAPAMIL;
D O I
10.1016/0925-4439(94)90111-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pretreatment of rats with verapamil, a Ca2+-antagonist, completely prevented alloxan-induced hyperglycemia. Verapamil also abolished the inhibition of insulin secretion by alloxan and H2O2 in isolated rat pancreatic islets. H2O2 generation from alloxan was not affected by verapamil, but alloxan- and H2O2-induced DNA strand breaks were completely prevented. Treatment of beta-cells with alloxan and H2O2 caused elevation of cytosolic free Ca2+, and this increase of Ca2+ was also abolished by verapamil. These results suggest that alloxan-derived oxygen radicals may disturb intracellular Ca2+ homeostasis by increasing Ca2+ influx, which results in secondary reactions ultimately leading to DNA strand breaks and cytotoxicity of beta-cells.
引用
收藏
页码:87 / 91
页数:5
相关论文
共 31 条