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.