Captopril as an antioxidant in lead-exposed Fischer 344 rats

被引:43
作者
Gurer, H [1 ]
Neal, R [1 ]
Yang, P [1 ]
Oztezcan, S [1 ]
Ercal, N [1 ]
机构
[1] Univ Missouri, Dept Chem, Rolla, MO 65409 USA
来源
HUMAN & EXPERIMENTAL TOXICOLOGY | 1999年 / 18卷 / 01期
关键词
captopril; antioxidant; lead poisoning; oxidative stress;
D O I
10.1191/096032799678839383
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 [卫生毒理学];
摘要
1 Recent studies suggest that lead induces oxidative stress in various tissues, 2 Captopril ( [2S]-1-[3-mercapto-2-methylpropionyl] -L-proline), an angiotensin-converting enzyme inhibitor, is a well-known antihypertensive agent and is also believed to function as an antioxidant. 3 In the present study the antioxidant effect of captopril on lead-induced oxidative stress was studied in Fischer 344 rats. Their liver, brain and kidneys were assayed for glutathione (GSH), glutathione disulfide (GSSG), malondialdehyde concentrations, and catalase activities. The results from animals treated with captopril were compared to results of control and lead-exposed non-treated groups. 4 The captopril-treated samples showed higher GSH:GSSG ratios in the liver, brain and kidneys, as well as slightly decreased malondialdehyde concentrations. The catalase activity was not significantly affected.
引用
收藏
页码:27 / 32
页数:6
相关论文
共 30 条
[1]
CAPTOPRIL SCAVENGES HYDROGEN-PEROXIDE AND REDUCES, BUT DOES NOT ELIMINATE, OXIDANT-INDUCED CELL INJURY [J].
ANDREOLI, SP .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (01) :F120-F127
[2]
MOBILIZATION OF HEAVY-METALS BY NEWER, THERAPEUTICALLY USEFUL CHELATING-AGENTS [J].
APOSHIAN, HV ;
MAIORINO, RM ;
GONZALEZRAMIREZ, D ;
ZUNIGACHARLES, M ;
XU, ZF ;
HURLBUT, KM ;
JUNCOMUNOZ, P ;
DART, RC ;
APOSHIAN, MM .
TOXICOLOGY, 1995, 97 (1-3) :23-38
[3]
DIRECT SCAVENGING OF FREE-RADICALS BY CAPTOPRIL, AN ANGIOTENSIN CONVERTING ENZYME-INHIBITOR [J].
BAGCHI, D ;
PRASAD, R ;
DAS, DK .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 158 (01) :52-57
[4]
BEERS RF, 1952, J BIOL CHEM, V195, P133
[5]
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[6]
TISSUE GLUTATHIONE, NUTRITION, AND OXIDATIVE STRESS [J].
BRAY, TM ;
TAYLOR, CG .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1993, 71 (09) :746-751
[7]
CHAVEZ E, 1991, J PHARMACOL EXP THER, V256, P385
[8]
BAL, EDTA, DMSA AND DMPS IN THE TREATMENT OF LEAD-POISONING IN CHILDREN [J].
CHISOLM, JJ .
JOURNAL OF TOXICOLOGY-CLINICAL TOXICOLOGY, 1992, 30 (04) :493-504
[9]
SUPEROXIDE-DISMUTASE AND GLUTATHIONE-PEROXIDASE ACTIVITIES ARE INCREASED BY ENALAPRIL AND CAPTOPRIL IN MOUSE-LIVER [J].
DECAVANAGH, EMV ;
INSERRA, F ;
FERDER, L ;
ROMANO, L ;
ERCOLE, L ;
FRAGA, CG .
FEBS LETTERS, 1995, 361 (01) :22-24
[10]
IS LEAD TOXICOSIS A REFLECTION OF ALTERED FATTY-ACID COMPOSITION OF MEMBRANES [J].
DONALDSON, WE ;
KNOWLES, SO .
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY, 1993, 104 (03) :377-379