Protective effect of Kalpaamruthaa in combating the oxidative stress posed by aflatoxin B1-induced hepatocellular carcinoma with special reference to flavonoid structure–activity relationship

Authors

  • Mohanasundaram Umarani,

    1. Department of Medical Biochemistry, Dr A. L. Mudaliar Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India
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  • Palanivelu Shanthi,

    1. Department of Pathology, Dr A. L. Mudaliar Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India
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  • Panchanadham Sachdanandam

    1. Department of Medical Biochemistry, Dr A. L. Mudaliar Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India
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Correspondence
Panchanadham Sachdanandam, Department of Medical Biochemistry, Dr A. L. Mudaliar Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, India
Tel: +91 44 24541767
Fax: +91 44 24540709
e-mail: psachdanandam2000@yahoo.co.in

Abstract

Aims/Background: Aflatoxin B1 (AFB1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. It has been postulated to play a major role in the aetiology of primary human liver cancer. Lipid peroxidation (LPO) is one of the main manifestations of oxidative damage and has been found to play an important role in the toxicity and carcinogenesis of many carcinogens. The present investigation aimed at assessing the effect of Kalpaamruthaa (KA), a modified Siddha preparation, on AFB1-mediated hepatocellular carcinoma (HCC). Methods: The drug was administered orally (300 mg/kg body weight/day) for 28 days to HCC-bearing rats. The level of lipid peroxides, antioxidant enzymes, glutathione and glutathione-metabolizing enzyme activity were determined in the plasma, haemolysate and liver homogenate of control and experimental rats. Results: Rats subjected to AFB1 showed a decline in the thiol capacity of the cell, accompanied by high malondialdehyde levels along with lowered activities of enzymic and non-enzymic antioxidant and glutathione-metabolizing enzyme levels. KA treatment restored the deranged LPO and enzyme activities almost to control levels, thereby suggesting hepatoprotection. Conclusion: This study highlighted the beneficial effect of KA in reversing the damage posed by AFB1 and thereby bringing about an improvement in the antioxidant status to combat the oxidative stress.

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