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Cardiovascular Research 2000 46(3):523-530; doi:10.1016/S0008-6363(00)00039-0
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Effects of probucol on changes of antioxidant enzymes in adriamycin-induced cardiomyopathy in rats

Timao Lia,b, Igor Danelisena,b, Adriane Belló-Kleina,b and Pawan K. Singala,b,*

aInstitute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, R2H 2A6, Canada
bDepartment of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, R2H 2A6, Canada

* Corresponding author. Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Room R3022, 351 Tache Avenue, Winnipeg, Manitoba, R2H 2A6, Canada. Tel.: +1-204-235-3416; fax: +1-204-233-6723 psingal{at}sbrc.umanitoba.ca

Objective: The clinical usefulness of doxorubicin (adriamycin, ADR) is restricted by the risk of developing congestive heart failure. Probucol has been reported to completely prevent ADR cardiomyopathy without interfering with its antitumor effects. The current study investigated the effects of ADR and probucol on antioxidant enzyme gene expression during adriamycin-induced cardiomyopathy in a rat model. Methods: The mRNA abundance by Northern and immunoreactive protein levels by Western blotting of myocardial antioxidant enzymes, glutathione peroxidase (GSHPx), manganese superoxide dismutase (MnSOD) and catalase (CAT) were examined in relation to the enzyme activities in hemodynamically assessed control and treated animals. Results: At 3 weeks post-treatment duration, ADR caused heart failure which was prevented by probucol. MnSOD mRNA abundance as well as protein levels were depressed by ADR treatment by 45% and 20%, respectively, and this change was prevented by probucol. However, the mRNA and protein levels of GSHPx and CAT were not significantly changed by ADR or probucol. ADR had no effect on SOD activity but this enzyme activity was increased by probucol and probucol plus ADR. GSHPx enzyme activity was decreased and oxidative stress as indicated by TBARS was increased by ADR and these changes were also modulated by probucol. Conclusion: An increase in oxidative stress, GSHPx inactivation and MnSOD downregulation during ADR cardiomyopathy were prevented by probucol treatment.

KEYWORDS Cardiomyopathy; Free radicals; Gene expression; Heart failure; Enzyme (kinetics)


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