Effect of myricetin on 1,2 dimethylhydrazine induced rat colon carcinogenesis.

Colorectal cancer (CRC) is a leading cause of cancer mortality especially in the western world. The incidence of CRC in Asia is now increasing at an alarming rate from the previously negligible levels. The pathogenesis of CRC is a multistep process wherein pre cancer lesions accumulate in the mucosal cells finally resulting in cancer. Diet plays an important role in its aetio-pathogenesis--the high levels of dietary fat correlates to the increased incidence of CRC. This along with hereditary, environmental factors and singular lack of physical exercise provides a potent combination in its pathogenesis. Besides CRC isfrequently associated with persistent oxidative stress which results not only in DNA damage but also in mutation of cancer related genes besides the epigenetic silencing of the tumor suppressor gene. An important approach in the prevention of cancer is chemoprevention. Variety of plant products have been found to be highly effective in retarding the pathogenesis of the colorectal cancer. Myricetin is a well known bioflavonoid that is claimed to have anti cancer action particularly in colorectal cancer. Myricetin not only brought about significant decrease in the incidence of number of tumor bearing rats but also the tumor incidence. Myricetin supplementation significantly reduced liver TBARS. Further the anti oxidant enzymes like Catalase, Glutathione peroxidase and GSH were significantly rejuvenated following myricetin supplementation in a dose dependent manner. The fecal and colonic bacterial enzyme activity was also significantly decreased with the supplementation of myricetin 50 and 100 mg/kg. There was no additional benefit with the supplementation of 200 mg/kg of myricetin.