| RESEARCH PAPER |
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| Year : 2005 | Volume
: 37
| Issue : 5 | Page : 294-299 |
Influence of DL α-lipoic acid and vitamin-E against doxorubicin-induced biochemical and histological changes in the cardiac tissue of rats
SA Ayaz, U Bhandari, KK Pillai
Department of Pharmacology, Faculty of Pharmacy, Jamia Hamdard (Hamdard University) New Delhi-110 062, India
Correspondence Address:
K K Pillai
Department of Pharmacology, Faculty of Pharmacy, Jamia Hamdard (Hamdard University) New Delhi-110 062
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.16852
Objective: The present study was undertaken to find out the preventive and curative role of lipoic acid (LA) and vitamin E (Vit. E) on doxorubicin (DOX)-induced oxidative stress and to make comparative evaluation between LA and vitamin E in this regard.
Materials and Methods: Wistar albino rats were used in this experiment. DOX was administered intraperitoneally in six equal injections (each containing 2.5 mg/kg DOX at 48 h interval) to a total cumulative dose of 15 mg/kg over a period of 2 weeks to produce cardiotoxicity. Lipoic acid and vitamin E were administered as pretreatment and post-treatment. The biochemical parameters such as tissue glutathione (GSH), malondialdehyde (MDA), lactate dehydrogenase (LDH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-s-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PD) were monitored after 30 days.
Results: Post-treatment with lipoic acid and vitamin E significantly protected the myocardium from the toxic effects of DOX, by reducing the levels of antioxidant enzymes such as CAT, SOD, GPx, GST, and G6PD towards normal and decreased the increased levels of malondialdehyde. It has also reduced the severity of cellular damage of the myocardium. The restoration of the endogenous antioxidant system clearly depicts that lipoic acid and vitamin E have produced their protective effect by scavenging the reactive oxygen species (ROS). Pretreatment with LA did not alter DOX-induced changes of histopathological parameters. Pretreatment with vitamin E has significantly increased the levels of blood and tissue GSH and significantly decreased the levels of MDA as compared to DOX-treated group. Vitamin E has significantly reduced the activities of the antioxidant enzymes except GSHR as compared to the DOX-treated group.
Conclusion: The study strongly supports the use of these antioxidants in the treatment of DOX-induced cardiotoxicity; however, vitamin E is better for both preventive and curative therapy but LA can be used only for curative therapy.
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