Abstract

Selenium is an essential nutritional element to mammalians necessary for the active function of different oxidant enzymes, as glutathione peroxidase (GPx), thioredoxin reductases (TrxR), and iodothyronine deiodinases (IDD). The anti-oxidative effect of selenium is pivotal for the human physiology. Oxidative stress is associated with various diseases, such as cardiovascular disease, diabetes mellitus or cancer, and is also associated with the majority of surgical procedures. Particularly, the use of cardiopulmonary bypass for open cardiac surgery with aortic clamping is always related to oxidative stress due to ischemia and reperfusion. Whereas myocardial protection with different temperatures and cardioplegic solutions has become more efficient, reperfusion is often followed by the activation of an injurious oxidative cascade. The pathogenesis of ischemia/reperfusion injury depends on many factors, among them, reactive nitrogen species (RNS) and reactive oxygen species (ROS) are considered as initiators of the injury. ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. ROS production is physiologically controlled by free radical scavengers such as GPx and TrxR, and superoxide dismutase systems. GPx and TrxR are seleno-cysteine dependent enzymes, and their activity is known to be related to selenium availability. Furthermore, selenium has been reported to regulate gene expression of these selenoproteins as a cofactor and there is some evidence that selenium supplementation can attenuate the oxidative stress and decrease the complications after cardiac surgery. However, other clinical studies failed to demonstrate an association between selenium deficiency and cardiovascular outcomes. The aim of our review is to summarize the experimental and clinical evidence of preoperative selenium supplementation and therapy after cardiac surgery, focusing on the pathophysiology of oxidative stress and the clinical usage of selenium.