Dietary Fish Oil Modulates the Effect of Dimethylhydrazine-Induced Colon Cancer in Rats

Rasmy, G. E., W. K. B. Khalil, S. A. Moharib, A. A. Kawkab, and E. W. Jwanny, "Dietary Fish Oil Modulates the Effect of Dimethylhydrazine-Induced Colon Cancer in Rats", grasas y aceites, vol. 62, issue 3, pp. 253-267, 2011.


This study was conducted to examine the efficacy of fish oil supplementation in male wistar rat colon carcinogenesis.In order to induce colon cancer, the rats were given a weekly subcutaneous injection of 1,2-Dimethyl hydrazine (DMH) at a dose of 20 mg/kg b.w. for five weeks. Afterwards, some of the rats ingested fish oil for either 4 weeks (DMH-FO4 group), or 17 weeks (DMH-FO17 group). The remaining rats continued without any supplementation for the same 4 weeks (DMH4 group), or 17 weeks (DMH17 group). Another two groups of rats did not receive the DMH and were given fish oil (FO17 group) or a normal diet only and considered as the control group (CN group). At the end of the experiment, the rats were sacrificed; and were subsequently subjected to biochemical and molecular biological analyses as well as histopathological examinations. The results showed increased levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and alkaline phoshatase (ALP) activities in the DMH rats compared to the control. The liver and colonic changes that were induced by DMH were significantly improved through fish oil supplementation in the DMH-FO17 group. The molecular analysis revealed that DMH treatment induced the expression alterations of genes p53, p27 and p21 and increased DNA band patterns related to cancer, while both FO17 and DMH-FO17 groups showed much better results. A histopathological examination of the DMH17 group revealed colon adenocarcinoma and several lesions in rat liver tissues. An improvement in the histopathological picture was seen in the livers and colons of groups DMH- FO17. In conclusion, the present results demonstrated the anti-carciongenic effect of herring fish oil against DMH induced colon carcinogenesis in rats. The inhibitory effect ofFO was due to the modulation of elevated biochemical parameters, DNA damage and histopathological lesions caused by DMH.



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