Is euthyroid sick syndrome a defensive mechanism against oxidative stress?

The body has a hierarchy of defence strategies to deal with oxidative stress. Among these arrays of defence mechanisms, the over expression and increased activity of glutathione peroxidases has been suggested as the first line of defence. The two main cofactors required for glutathione peroxidase activity are selenium and reduced glutathione. These two factors have been shown to be required for the deiodinase activity also. In vitro and in vivo studies have shown that oxidative stress decreases the activity of deiodinase. Thus, a decrease in deiodinase activity would facilitate the use of these cofactors by glutathione peroxidase in combating oxidative stress. Lowering of serum T3 is generally regarded as a valuable calorie-sparing economy. A decreased metabolic state of the cells as found in euthyroid sick syndrome indicates a decreased free radical generation from the mitochondria. For this reason, euthyroid sick syndrome could be considered as a physiological mechanism activated in response to oxidative stress.