CHAPTER 30: Selenium and the Heart

Selenoproteins, in which selenium is directly incorpotated as the unique amino acid selenocysteine, serve important regulatory functions in relation to redox balance. Since oxidative stress is implicated in the pathogenesis and progression of cardiovascular diseases, the role of selenium deficiency as a risk factor, and of selenium supplementation as a therapy, have been explored in preclinical studies. Preclinical studies have demonstrated that selenium deficiency is associated with increased oxidant stress and worse damage in the heart. Studies using supplemental levels of selenium have yielded conflicting results on its benefit in myocardial dysfunction due to oxidant stress. Recent clinical trials showing deleterious cardiometabolic effects of supplemental selenium demonstrate that the in vivo effects of selenium are complex. In fact, studies from our laboratories suggest that both selenium deficiency and selenium supplementation lead to adverse effects in the heart as a result of altered collagen metabolism. The complex effects of selenium are derived in part due to the effects of selenium on multiple biological processes such as redox balance and methylation. Recent studies from our laboratories suggest that addressing these concomitant effects on redox–methylation balance is crucial to understanding the role of selenium in cardiovascular disease.