Captopril increased mitochondrial coenzyme Q10 level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy

The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 mi...

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Bibliographic Details
Published inBioFactors (Oxford) Vol. 10; no. 1; pp. 61 - 65
Main Authors Gvozdjáková, A, Simko, F, Kucharská, J, Braunová, Z, Psenek, P, Kyselovic, J
Format Journal Article
LanguageEnglish
Published Amsterdam IOS Press 1999
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Summary:The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial F1‐ATPase protein concentration. Moreover, the level of coenzyme Q10 (CoQ10) and coenzyme Q9 were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ10 level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F1‐ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.
Bibliography:istex:50587795AE90EA0F56BDD9BAE80B2432138D6D7C
ark:/67375/WNG-QH6J3C0F-3
ArticleID:BIOF5520100107
ISSN:0951-6433
1872-8081
DOI:10.1002/biof.5520100107