EFFECTS OF IN-VITRO ADDITION OF CAPTOPRIL ON COPPER-INDUCED LOW-DENSITY-LIPOPROTEIN OXIDATION

被引:15
作者
ZIEDEN, B [1 ]
WUTTGE, DM [1 ]
KARLBERG, BE [1 ]
OLSSON, AG [1 ]
机构
[1] LINKOPING UNIV HOSP,FAC HLTH SCI,DEPT INTERNAL MED,S-58185 LINKOPING,SWEDEN
关键词
LOW DENSITY LIPOPROTEIN; OXIDATION; ACE INHIBITORS; CAPTOPRIL; QUINAPRIL; FOSINOPRIL;
D O I
10.1111/j.1365-2125.1995.tb04433.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Low density lipoprotein (LDL) was incubated with 20 mu M of the angiotensin converting enzyme (ACE) inhibitors captopril, fosinopril and quinapril or ethanol. Oxidation of LDL was initiated by addition of CuSO4 and monitored for production of conjugated dienes, thiobarbituric acid reactive substances (TEARS) and lipid peroxides. The inhibition of production of conjugated dienes was expressed as the lag phase in minutes. The lag phase for control samples was 55.2 +/- 6.1 (mean +/- s.e. mean) min and for captopril 86.4 +/- 7.0 min (P = 0.0058). Quinapril had a small but nonsignificant effect, fosinopril and ethanol had no effect. LDL incubated with captopril showed only 13.8% of TEARS and 22.7% of lipid peroxides produced by control (100%) after 1 h. Increasing concentrations of captopril showed a linear increase in the lag phase. We conclude that captopril increases the resistance of LDL to copper-induced oxidation.
引用
收藏
页码:201 / 203
页数:3
相关论文
共 11 条
[1]  
Buege J A, 1978, Methods Enzymol, V52, P302
[2]   ANTIOXIDANT EFFECTS OF ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS - FREE-RADICAL AND OXIDANT SCAVENGING ARE SULFHYDRYL DEPENDENT, BUT LIPID-PEROXIDATION IS INHIBITED BY BOTH SULFHYDRYL-CONTAINING AND NONSULFHYDRYL-CONTAINING ACE INHIBITORS [J].
CHOPRA, M ;
BESWICK, H ;
CLAPPERTON, M ;
DARGIE, HJ ;
SMITH, WE ;
MCMURRAY, J .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1992, 19 (03) :330-340
[3]  
ELSAADANI M, 1989, J LIPID RES, V30, P627
[4]   CONTINUOUS MONITORING OF INVITRO OXIDATION OF HUMAN LOW-DENSITY LIPOPROTEIN [J].
ESTERBAUER, H ;
STRIEGL, G ;
PUHL, H ;
ROTHENEDER, M .
FREE RADICAL RESEARCH COMMUNICATIONS, 1989, 6 (01) :67-75
[5]   DISTRIBUTION AND CHEMICAL COMPOSITION OF ULTRACENTRIFUGALLY SEPARATED LIPOPROTEINS IN HUMAN SERUM [J].
HAVEL, RJ ;
EDER, HA ;
BRAGDON, JH .
JOURNAL OF CLINICAL INVESTIGATION, 1955, 34 (09) :1345-1353
[6]   ANTIATHEROSCLEROTIC EFFECTS OF THE ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS CAPTOPRIL AND FOSINOPRIL IN HYPERCHOLESTEROLEMIC MINIPIGS [J].
JACOBSSON, LS ;
PERSSON, K ;
ABERG, G ;
ANDERSSON, RGG ;
KARLBERG, BE ;
OLSSON, AG .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1994, 24 (04) :670-677
[7]   CAPTOPRIL DOES NOT SCAVENGE SUPEROXIDE - CAPTOPRIL PREVENTS O2 PRODUCTION BY CHELATING COPPER [J].
JAY, D ;
CUELLAR, A ;
ZAMORANO, R ;
MUNOZ, E ;
GLEASON, R .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1991, 290 (02) :463-467
[8]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265
[9]   PHARMACOKINETICS OF CAPTOPRIL AND ITS EFFECTS ON BLOOD-PRESSURE DURING ACUTE AND CHRONIC ADMINISTRATION AND IN RELATION TO FOOD-INTAKE [J].
OHMAN, KP ;
KAGEDAL, B ;
LARSSON, R ;
KARLBERG, BE .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1985, 7 :S20-S24
[10]   EFFECT OF CAPTOPRIL ON MORTALITY AND MORBIDITY IN PATIENTS WITH LEFT-VENTRICULAR DYSFUNCTION AFTER MYOCARDIAL-INFARCTION - RESULTS OF THE SURVIVAL AND VENTRICULAR ENLARGEMENT TRIAL [J].
PFEFFER, MA ;
BRAUNWALD, E ;
MOYE, LA ;
BASTA, L ;
BROWN, EJ ;
CUDDY, TE ;
DAVIS, BR ;
GELTMAN, EM ;
GOLDMAN, S ;
FLAKER, GC ;
KLEIN, M ;
LAMAS, GA ;
PACKER, M ;
ROULEAU, J ;
ROULEAU, JL ;
RUTHERFORD, J ;
WERTHEIMER, JH ;
HAWKINS, CM .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 327 (10) :669-677