7,12-Dimethylbenz(a)anthracene (DMBA)-induced hamster buccal pouch carcinogenesis is widely preferred to assess the tumor-inhibiting efficacy of the medicinal plants or their constituents. The present study explores the tumor-inhibiting potential of esculetin by utilizing the status of lipid peroxidation by products (thiobarbituric acid reactive substances), antioxidants (vitamin E, reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase), and phase I and phase II detoxification agents as biochemical end points and by using histopathological studies as well in DMBA-induced hamster buccal pouch carcinogenesis. Oral tumors developed in the buccal pouch were subjected to histopathological studies, and were confirmed as oral squamous cell carcinoma. Hamsters treated with DMBA alone showed an abnormal pattern of lipid peroxidation, antioxidants, and detoxification agents as compared to control hamsters. The status of the above-mentioned biochemical markers and histopathological abnormalities were found to be reversed in DMBA + esculetin-treated hamsters. The result of the present study thus indicates the tumor preventive potential of esculetin in DMBA-induced oral carcinogenesis.

Background: Cell-cycle disruption is the major characteristic features of neoplastic transformation and the status of cell-cycle regulators can thus be utilized to assess the prognostic significance in patients with cancer. The PCNA, cyclin D1, CDK4, CDK6 and survivin expression in the buccal mucosa was utilized to evaluate the Emodin efficacy on abnormal cell proliferation during 7,12-dimethylbenz(a)anthracene (DMBA) induced oral carcinogenesis in golden Syrian hamsters. Materials and methods: Topical application of DMBA, three times a week for 14 weeks, on the hamsters' buccal pouches developed well differentiated squamous cell carcinoma. Results: Cyclin D1 and PCNA over-expression and up-regulation of CDK4, CDK6 and survivin were noticed in the buccal mucosa of hamsters treated with DMBA alone. Emodin administration (50mg/kg b.w) orally to hamsters treated with DMBA down-regulated the expression of cell proliferation markers in the buccal mucosa. Conclusions:The anti-cell proliferative role of Emodin is owing to its modulating efficacy on cell-cycle markers towards the tumor suppression during DMBA induced oral carcinogenesis.

Apoptotic avoidance is one of the foremost characteristic features of tumour cells. Apoptotic induction in cancer cells could thus help to identify new anticancer agents from the natural products. The present study has taken an effort to investigate the apoptotic efficacy of myrtenal, a monoterpene, in 7,12-dimethylbenz(a)anthracene (DMBA) induced oral carcinoma in male golden Syrian hamsters. The present study used the potent carcinogen, 7,12- dimethylbenz(a)anthracene, to develop oral tumours in the buccal pouches of the golden Syrian hamsters. Topical application of the above said carcinogen on the buccal mucosa (3 times a week for 14 weeks) resulted in well differentiated oral squamous cell carcinoma. The apoptotic potential of myrtenal was investigated using a spectrum of apoptotic markers, including pro-apoptotic and anti-apoptotic markers. Oral tumours developed in the buccal mucosa of hamsters showed higher expression of mutant p53 protein, Bcl-2 and lowered expression of Bax, Bad, Bid, caspase 3 and caspase 9. Myrtenal treatment at a dose of 230mg/kg bw orally to the hamsters treated with DMBA modulated the above said apoptotic markers towards tumour suppression or inhibition. The present findings thus suggests that the tumour preventive effect of myrtenal could partly be ascribed to its apoptotic induction potential during DMBA induced oral carcinogenesis.

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