Abstract
The aim of the study was to evaluate the effect of resveratrol in doxorubicin-induced cardiac and hepatic toxicity. Doxorubicin was administered once a week throughout the period of 7 weeks with 1.0 or 2.0 mg/kg body weight or concomitantly with resveratrol (20 mg/kg of feed). Heart and liver toxicity was histologically and biochemically evaluated. Resveratrol protected from the heart lipid peroxidation caused by 1 mg doxorubicin and it sharply diminished superoxide dismutase activity. An insignificant effect of resveratrol on the lipid peroxidation level and the superoxide dismutase activity was observed in the hearts of rats administered a higher dose of doxorubicin. However, resveratrol attenuate necrosis and other cardiac histopathological changes were induced by a high dose of doxorubicin. Interestingly, it slightly intensified adverse cardiac histological changes in rats receiving a lower dose of doxorubicin. Resveratrol did not have any protective effect on the hepatic oxidative stress, while exerting a mild beneficial effect on the morphological changes caused by doxorubicin. All in all, this study has shown different effects of resveratrol on dose-related doxorubicin-induced heart and liver toxicity. Resveratrol may modulate the hepatic and cardiac effect of doxorubicin, depending on the drug dose.
Highlights
Drug-drug and drug-food interactions are specially important in the anticancer therapy because of the very narrow therapeutic index of these chemotherapeutics
Alanine aminotransferase (ALT) activity was increased in animals exposed to both resveratrol and a low dose of doxorubicin but decreased among the rats treated with resveratrol and a high dose of the drug
A statistically significant decrease of lactate dehydrogenase (LDH) activity was noted in the groups exposed to a high dose of doxorubicin with or without resveratrol
Summary
Drug-drug and drug-food interactions are specially important in the anticancer therapy because of the very narrow therapeutic index of these chemotherapeutics. Many patients suffering from cancer in the terminal state decide to take unconventional agent, very frequently beyond of a doctor knowledge. Doxorubicin (DOX) is a very efficient antitumor drug, but its administration is limited by a dose-dependent, irreversible, and progressive cardiomyopathy, which may become evident years after completion of the therapy [1,2,3,4,5]. The pathomechanism of DOX-related late cardiotoxicity is multifactorial [6, 7], but the prevalent hypothesis ascribes the dominant role to oxidative stress linked to redoxcycling of the drug [8, 9].
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