Captopril increased mitochondrial coenzyme Q_{10} level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy
Affiliations: Pharmacobiochemical Laboratory of Medical Faculty, Comenius University, Bratislava, Slovak Republic | Department of Pathophysiology of Medical Faculty, Comenius University, Bratislava, Slovak Republic | Department of Pharmacology and Toxicology of Pharmaceutical Faculty, Comenius University, Bratislava, Slovak Republic
Note: [] Address for correspondence: Dr Anna Gvozdjáková PhD., DSc., Pharmacobiochemical Laboratory of Medical Faculty, Comenius University, Hlboká 7, 81105 Bratislava, Slovak Republic. Tel./Fax: + 421 7 391422.
Abstract: 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 F_{1}‐ATPase protein concentration. Moreover, the level of coenzyme Q_{10} (CoQ_{10}) and coenzyme Q_{9 } were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ_{10} level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F_{1}‐ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.
