ATTENUATION OF DAUNORUBICIN-AUGMENTED MICROSOMAL LIPID-PEROXIDATION AND OXYGEN-CONSUMPTION BY CALCIUM-CHANNEL ANTAGONISTS

被引：15

作者：

ENGINEER, FN

SRIDHAR, R

机构：

[1] HOWARD UNIV HOSP,DEPT RADIAT THERAPY,WASHINGTON,DC 20060

[2] HOWARD UNIV HOSP,CTR CANC,WASHINGTON,DC 20060

[3] UNIV S CAROLINA,COLL PHARM,COLUMBIA,SC 29208

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1991年 / 179卷 / 02期

关键词：

D O I：

10.1016/0006-291X(91)91933-4

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：

Daunorubicin (20 μM) stimulated NADPH-dependent microsomal lipid peroxidation about 2-fold over control values and enhanced the rate of oxygen utilization by microsomes. The calcium channel blockers tested inhibited daunorubicin-augmented lipid peroxidation and O2 consumption to varying degrees. Inhibition of daunorubicin-stimulated lipid peroxidation was found to be dose dependent; the IC50 (drug concentration producing 50% inhibition of lipid peroxidation) values for verapamil, nifedipine and diltiazem were approximately 150 μM, 200 μM, and 600 μM respectively. Our in vitro studies suggest that calcium channel antagonists may modulate the free radical-mediated, cardiotoxic effects of daunorubicin. © 1991.

引用

页码：1101 / 1106

页数：6

共 20 条

[11] GENERATION OF HYDROXYL RADICAL BY ANTI-CANCER QUINONE DRUGS, CARBAZILQUINONE, MITOMYCIN-C, ACLACINOMYCIN-A AND ADRIAMYCIN, IN THE PRESENCE OF NADPH-CYTOCHROME-P-450 REDUCTASE [J].