Selenium compounds in various forms have been known to be cancer-preventive. Specially, selenomethionine (SeMet), which is known to be a major component of dietary selenium and non-genotoxic to cells, has been shown to modulate the redox (reduction/oxidation) status and the activation of p53 tumor suppressor. The p53 tumor suppressor gene plays a pivotal role in the cellular response to genotoxic stress. Activated wild-type p53, after genotoxic stress, may either trigger the onset of DNA repair, leading to the completion of the cell cycle, or alternatively, induce apoptosis and/or cellular differentiation, leading to exit from the cell cycle. DNA base damage generated by ionizing radiation (IR), simple alkylating agents, as well as endogenous hydrolytic and oxidative processes is corrected by the base excision repair (BER) pathway. In this study, we employed IR as a DNA-damaging agent to confirm that SeMet protects p53 wild-type cells from IR-induced DNA damage. We investigated weather SeMet has a protective effect implicated with p53-mediated DNA repair activity in response to IR. Our results show that p53 wild-type cells with pretreated-SeMet enhance DNA repair activity in response to IR-induced DNA damage.

[Proc Amer Assoc Cancer Res, Volume 47, 2006]