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Background  The development and progression of liver cancer may involve abnormal changes in DNA methylation, which lead to the activation of certain proto-oncogenes, such as  c-myc , as well as the inactivation of certain tumor suppressors, such as  p16 . Betaine, as an active methyl-donor, maintains normal DNA methylation patterns. However, there are few investigations on the protective effect of betaine in hepatocarcinogenesis.    Methods  Four groups of rats were given diethylinitrosamine (DEN) and fed with AIN-93G diets supplemented with 0, 10, 20 or 40 g betaine/kg (model, 1%, 2%, and 4% betaine, respectively), while the control group, received no DEN, fed with AIN-93G diet. Eight or 15 weeks later, the expression of  p16  and  c-myc  mRNA was examined by Real-time PCR (Q-PCR). The DNA methylation status within the  p16  and  c-myc  promoter was analyzed using methylation-specific PCR.    Results  Compared with the model group, numbers and areas of glutathione S-transferase placental form (GST-p)-positive foci were decreased in the livers of the rats treated with betaine ( P < 0.05 ). Although the frequency of  p16  promoter methylation in livers of the four DEN-fed groups appeared to increase, there is no difference among these groups after 8 or 15 weeks ( P > 0.05 ). Betaine supplementation attenuated the down-regulation of  p16  and inhibited the up-regulation of  c-myc  induced by DEN in a dose-dependent manner ( P  < 0.01). Meanwhile, increases in levels of malondialdehyde (MDA) and glutathione S-transferase (GST) in model, 2% and 4% betaine groups were observed ( P < 0.05 ). Finally, enhanced antioxidative capacity (T-AOC) was observed in both the 2% and 4% betaine groups.    Conclusion  Our data suggest that betaine attenuates DEN-induced damage in rat liver and reverses DEN-induced changes in mRNA levels.

Assessment of the effect of betaine on p16 and c-mycDNA methylation and mRNA expression in a chemical induced rat liver cancer model