
Modulating effect of d ‐carvone on 1,2‐dimethylhydrazine‐induced pre‐neoplastic lesions, oxidative stress and biotransforming enzymes, in an experimental model of rat colon carcinogenesis
Author(s) -
Vinothkumar R.,
Sudha M.,
Viswanathan P.,
Kabalimoorthy J.,
Balasubramanian T.,
Nalini N.
Publication year - 2013
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12062
Subject(s) - aberrant crypt foci , 1,2 dimethylhydrazine , oxidative stress , lipid peroxidation , chemistry , carcinogen , pharmacology , enzyme , carvone , antioxidant , biochemistry , endocrinology , carcinogenesis , medicine , food science , colorectal cancer , azoxymethane , cancer , colonic disease , essential oil , limonene , gene
Objectives The present study has aimed to evaluate chemopreventive potential of d ‐carvone on oxidative stress markers, biotransforming enzymes, incidence of colonic polyps and aberrant crypt foci ( ACF ) in 1,2‐dimethylhydrazine ( DMH )‐induced experimental colon carcinogenesis. Materials and Methods Rats were randomly divided into six groups, with group I serving as control. Group II animals received d ‐carvone every day orally (20 mg/kg body weight) for 16 weeks; groups III–VI received subcutaneous injections of DMH (20 mg/kg body weight) once a week, for the first 4 weeks. In addition, groups IV–VI received different doses of d ‐carvone (5, 10 and 20 mg/kg body weight everyday orally) along with DMH injections. Results Our results revealed that supplementation with d ‐carvone significantly reduced incidence of polyps/ ACF and ACF multiplicity in DMH ‐exposed rats compared to DMH ‐alone‐exposed rats. Moreover, our results showed reduced activities of liver and circulatory antioxidants and increased levels of lipid peroxidation by products in DMH ‐exposed animals, which were significantly reversed on supplementation with d ‐carvone. In addition, colonic antioxidants and lipid peroxidation were significantly diminished in DMH ‐exposed rats, which were significantly elevated on supplementation with d ‐carvone. Furthermore, we also determined activities of biotransforming enzymes, which were found to be altered in DMH ‐exposed rats, but reversed on d ‐carvone supplementation. All these observations of changes were supported by histochemical findings. Conclusion Overall, results obtained from this study suggest that d ‐carvone at 10 mg/kg body weight provided optimum protection and could be used as an effective chemopreventive agent against colon carcinogenesis induced by DMH .