Role of Selenium and Selenoproteins in mitochondrial function and disease

Abstract

Selenium is a key dietary micronutrient, essential for a wide range of physiological functions. The incorporation of selenium in place of sulphur to form the amino acid selenocysteine is fundamental for the synthesis of selenoproteins and reliant on dietary intake. A significant body of work has identified 25 selenoproteins with important roles in the maintenance of cellular redox homeostasis and regulation of mitochondrial function and biogenesis. The upregulation of selenoproteins have been associated with the prevention of mitochondrial dysfunction and oxidative stress through increased antioxidant function, decreased inflammatory responses and increased respiratory function within the electron transport chain of mitochondria. These mechanisms are important in supporting muscular function, cardiovascular health, reproduction and the prevention of neurological degeneration. This review collates the evidence of interactions between selenoproteins, mitochondrial function and diseases with pathophysiological mechanisms of mitochondrial dysfunction and increased oxidative stress. The beneficial effect of selenium supplementation and selenoprotein upregulation may provide the platform for the development of novel treatments to reduce the burden of diseases characterised by mitochondrial dysfunction and oxidative stress.