The effects of supplemental selenium intake have been evaluated in multiple chronic and acute diseases, including cancer, cardiovascular disease, and inflammatory conditions such as sepsis, trauma, and burns (Clark et al. 1996; Mark et al. 2000; Nomura et al. 2000; Brown & Arthur 2001; Angstwurm & Gaertner 2006; Angstwurm et al. 2007). In many studies, selenium has demonstrated beneficial properties but the results of the Selenium and Vitamin E Trial (SELECT) do not support the utility of supplemental selenomethionine in prostate cancer prevention (Lippman et al. 2009). The mechanism by which selenium exerts its effects during disease conditions is not completely understood; however, it has been hypothesized to be due to the antioxidant activity of selenoproteins (Diwadkar-Navsariwala & Diamond 2004; Irons et al. 2006). These proteins contain selenium incorporated as the amino acid selenocysteine during translation of the protein (Tujebajeva et al. 2000; Small-Howard et al. 2006; Howard et al. 2007). Adequate selenium intake is important in maintaining proper translation and function of the selenoproteins (Bermano et al. 1996; Wingler & Brigelius-Flohe 1999). Therefore, maintenance of selenoprotein function may be
