TodayIt is well known that oxidative stress (OS), defined as an imbalance between radicals and antioxidant defense, is implicated as a pathophysiological mechanism of different diseases and is a topic of growing interest. Cell injury is a consequence of OS; recognized targets are DNA, lipids and proteins, which react with hydroxyl radicals to form specific products. Especially in the field of cardiovascular diseases, the role of OS has been revaluated, even if the therapeutic aftermath is still debated. Antioxidant defenses include enzymatic and non-enzymatic molecules and they are modulated by hormones, which regulate their synthesis and turnover.
Both hypothyroidism and hyperthyroidism can be associated with OS, moreover thyroid hormone (TH)-induced oxidative damage could be a factor responsible for the progression of heart failure, as suggested by the benefit of T3 administration on antioxidant systems in rat heart after pharmacological-induced hypothyroidism. However, few data exist on the possible diagnostic role of antioxidant measurements; in this review we examine thyroid regulation of antioxidants and OS in cardiac physiology and disease; then we speculate on the situation of low-T3 syndrome (also called “non-thyroidal illness”, NTIS), a condition present in chronic disease. This hormonal situation reflects a compensatory mechanism, but the need of replacement therapy is matter of discussion. Therefore the evaluation of OS parameters could represent a further insight into the pathophysiology of NTIS