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. 2011 Sep;43(5):507-11.
doi: 10.4103/0253-7613.84952.

Cardioprotective effect of ascorbic acid on doxorubicin-induced myocardial toxicity in rats

Affiliations

Cardioprotective effect of ascorbic acid on doxorubicin-induced myocardial toxicity in rats

A H M Viswanatha Swamy et al. Indian J Pharmacol. 2011 Sep.

Abstract

Objective: To investigate the preventive and curative role of ascorbic acid on doxorubicin (dox)-induced myocardial toxicity in rats.

Materials and methods: Animals were divided into five groups of six animals each. Group I served as normal control and received saline 5 ml/kg/day intraperitoneal (i.p.) for a period of 15 days. Group II animals received ascorbic acid 20 mg/kg per oral (p.o.) for 15 days as a pretreatment control (PR). Group III animals received dox 2.5 mg/kg body weight (b.w.), i.p., in six equal injections for two weeks for a total cumulative dose of 15 mg/kg b.w. Group IV animals received ascorbic acid 20 mg/kg p.o. for 15 days as a pretreatment followed by dox 2.5 mg/kg b.w., i.p., in six equal injections for two weeks for a total cumulative dose of 15 mg/kg body weight. Group V animals received dox 2.5 mg/kg b.w., i.p., in six equal injections for two weeks for a total cumulative dose of 15 mg/kg b.w. followed by ascorbic acid 20 mg/kg p.o for 15 days as post-treatment control (CR). The biochemical parameters such as tissue glutathione (GSH), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD), and enzyme biomarkers such as creatine phosphokinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were monitored.

Results: Pretreatment with ascorbic acid (20 mg/kg p.o.) significantly protected the myocardium from the toxic effect of dox (PR), by increasing the levels of antioxidant enzymes such as GSH, SOD, and CAT toward normal and decreased the levels of MDA, CPK, LDH, AST, and ALT as compared with dox-treated rats. Post-treatment with ascorbic acid to dox-treated group (CR) significantly increased the levels of tissue GSH, SOD, CAT and significantly decreased the level of MDA as compared with dox-treated group. It also reduced the severity of cellular damage of the myocardium as confirmed by histopathology. The restoration of the endogenous antioxidant system clearly depicts that ascorbic acid produced its protective effect by scavenging the reactive oxygen species.

Conclusion: The results obtained in this study provide evidence for the usefulness of the ascorbic acid as a cardioprotective agent.

Keywords: Ascorbic acid; cardiotoxicity; doxorubicin; free radicals.

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Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1a
Figure 1a
Photomicrograph of rat heart of normal showing regular morphology
Figure 1b
Figure 1b
Photomicrograph of rat heart treated with doxorubicin showing extensive vacuolization and myofi bril loss
Figure 1c
Figure 1c
Photomicrograph of rat heart treated with ascorbic acid + doxorubicin (PR) showing less extensive vacuolization and no myofi bril loss
Figure 1d
Figure 1d
Photomicrograph of rat heart treated with doxorubicin + ascorbic acid (CR) showing less extensive vacuolization and myofi bril loss as compared with doxorubicin treated rats

References

    1. Singal PK, Segstro RJ, Singh RP, Kutryk MJ. Changes in lysosomal morphology and enzyme morphology and enzyme activities during the development of Adriamycin induced cardiomyopathy. Can J Cardiol. 1985;1:139–47. - PubMed
    1. Bristow MR, Sageman WS, Scott RH, Billingham ME, Bowden RE, Kernoff RS, et al. Acute and chronic cardiovascular effect of doxorubicin in dog. J Cardiovasc Phamacol. 1980;2:487–515. - PubMed
    1. Wold LE, Aberle NS, 2nd, Ren J. Doxorubicin induces cardiomyocytes dysfunction via P38 MAP kinase dependant oxidative stress mechanism. Cancer Detect Prev. 2005;29:294–9. - PubMed
    1. Hanna HA, Fatima M, Gamal AE, Senot HD. Cardioprotective activities on doxorubicin induced cardiotoxicity. Bioorg Med Chem. 2005;13:1847–57. - PubMed
    1. Premkumar K, Bowlus CL. Ascorbic acid does not increase the oxidative stress induced by dietary iron in C3H mice. J Nutr. 2004;134:435–8. - PubMed