Oral carcinoma (OC) remains one of the most difficult malignancies to cure. selenium (Se) is an essential trace mineral for human and animals, but high concentrations of Se induce apoptosis and oxidative effects. Although cell apoptosis has been evidenced as a critical mechanism mediating the anticancer activity of Se, the underlying molecular mechanisms remain elusive. To explore the role of Se in rat OC, we examined the weather the oxidative stress-mediated apoptotic pathway induced by Se was involved in the development of OC. In this study, we successfully constructed the OC rat model by 4-Nitroquinoline-1-oxide (4-NQO) exposure which reflected from histopathological observations. Se-induced the productions of methane dicarboxylic aldehyde (MDA) and reactive oxygen species (ROS), which was accompanied by the inhibition of superoxide dismutase (SOD) both in vivo and vitro. The anti-apoptotic gene (Bcl-2) was down-regulated and pro-apoptosis members (Bax, Bak, Cyt-c, caspase9 and caspase3) were up-regulated by Se in OC cells. Meanwhile, we also found that Se could strongly inhibited the cell proliferation of OC lines in vitro. These results suggested that excessive Se could effectively cause oxidative stress and induce apoptosis in OC cells, as a result the OC was also inhibited to some extent. Therefore, the information presented in this study is believed to be helpful in supplementing data for further therapy of OC.
Keywords: apoptosis; cell proliferation; oral carcinoma; oxidative stress; selenium.