Endocrine Abstracts

Oxidative processes are of special significance in the thyroid gland, as they are indispensable for thyroid hormone synthesis. It is estimated that huge amount of reactive oxygen species, especially of hydrogen peroxide (H₂O₂), are formed in the thyroid under physiological conditions. Also iron, present in thyroperoxidase, is required for thyroid hormone synthesis. Both, H₂O₂ and iron, constitute substrates of the most basic reaction of oxidative stress, i.e. Fenton reaction (Fe²⁺+H₂O₂→Fe³⁺+^•OH+OH⁻). Another element indispensable for thyroid hormone synthesis is iodine, concentrated in the thyroid in high amounts. This trace element is known to affect red-ox balance, revealing either spectacular antioxidative or prooxidative effects. Thus, favourable conditions for oxidative damage to macromolecules are potentially created in the thyroid, justifying the statement that the thyroid gland is an organ of ‘oxidative nature’. Effective protective mechanisms, comprising antioxidative molecules and the process of compartmentalization of potentially toxic molecules, must have been developed in the thyroid to maintain the balance between generation and detoxification of free radicals. However, with additional oxidative abuse caused by exogenous or endogenous prooxidants, increased damage to macromolecules may occur, potentially contributing to different thyroid diseases, cancer included. Therefore, experimental models should be elaborated to characterise most dangerous conditions leading to enhanced oxidative damage in the thyroid and to develop effective protective tools against such conditions. Fenton reaction substrates, potassium bromate, nitrobenzene, GH, IGF1, iodine, and also depletion of antioxidative mechanisms, are among factors, which were up to now documented in experimental models to reveal proxidative and/or antioxidative effects in the thyroid gland. In turn, malignant thyroid cells are characterised by increased oxidative damage to macromolecules.

The increased oxidative damage to macromolecules in the thyroid may occur in response to different exogenous/endogenous prooxidants. The contribution of this oxidative damage to thyroid diseases, cancer included, should be considered.