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Beneficial influence of ellagic acid on biochemical indexes associated with experimentally induced colon carcinogenesis

 Department of Biochemistry, Cell Biology Unit, University of Madras, Chennai, Tamil Nadu, India

Correspondence Address:
Sudhandiran Ganapasam,
Department of Biochemistry, University of Madras, Maraimalai Campus (Guindy), Chennai 600 025, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

Objective: To elucidate the key biochemical indexes associated with 1, 2-dimethylhydrazine (DMH)-induced colon carcinogenesis and the modulatory efficacy of a dietary polyphenol, ellagic acid (EA). Materials and Methods: Wistar rats were chosen to study objective, and were divided into 4 groups; Group 1-control rats; Group 2-rats received EA (60 mg/kg body weight/day, orally); rats in Group 3-induced with DMH (20 mg/kg body weight) subcutaneously for 15 weeks; DMH-induced Group 4 rats were initiated with EA treatment. We examined key citric acid cycle enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase and the activities of respiratory chain enzymes NADH dehydrogenase and Cytochrome-C-oxidase and membrane-bound enzyme profiles (Na + /K + ATPase, Ca 2+ ATPase and Mg 2+ ATPase), activities of lysosomal proteases such as b-D-glucuronidase, b-galactosidase and N-acety-b-D-glucosaminidase and cellular thiols (oxidized glutathione, protein thiols , and total thiols). Results: It was found that administration of DMH to rats decreased both mitochondrial and membrane-bound enzymes activities, increased activities of lysosomal enzymes and further modulates cellular thiols levels. Treatment with EA significantly restored the mitochondrial and ATPases levels and further reduced lysosomal enzymes to near normalcy thereby restoring harmful effects induced by DMH. Conclusion: EA treatment was able to effectively restore the detrimental effects induced by DMH, which proves the chemoprotective function of EA against DMH-induced experimental colon carcinogenesis.

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