ABSTRACT
Selenium (Se) is required for many essential enzymes, and provides protection against various diseases (Pickering et al. 2011). Several studies have shown a significant inverse relationship between cancer prevalence and Se levels in diet (the unholy-cross) (Glattre et al. 1989, Dreher et al. 1996). Serum Se levels have been observed to be lower in variety of cancer cases compared to controls (Ujie et al. 1998, Helzsouer et al. 1989). Several intervention studies have demonstrated the link between Se and incidence of various cancers (Yu et al. 1997). The role of Se in cancers is considered to be due to its effect in cell cycle and maintenance of homoeostasis (Huawei 2009, Ip et al. 2001). Studies have shown the up-regulation effect of selenite and SeMet on cell-cycle-related genes (Zeng et al. 2009). A cytokine, Cyclin d4 (cdk4) that controls cell cycle progression responds to mitogenic stimuli of G1 phase of cell cycle by phosphorylation of tumor suppressor protein pRb (Gille et al. 1999). Furthermore, others have suggested that Se anticancer properties be due to enhanced expression of humoral genes (A2M) and tumor suppressor gene-IGFBP3, HHIP (Huawei. 2009). L-Methionine-gamma-lyase in tumor cells converts SeMet into methylselenol, which activates caspase cascade and apoptosis in cancer cells (Miki et al. 2001). Both selenite (inorganic Se) and organic Se induce anti-cancer effects through different pathways (Huawei 2009). The evidence available shows that the inorganic Se induces anti-cancer effects (genotoxicity) by inducing DNA single strand breaks, which affects cell cycle at S-phase, while organic Se in turn exerts its genotoxicity effects at G1 phase of cell cycle.
