Objective: Oxidative stress is developing by disequilibrium between antioxidative and oxidative mechanisms. In these conditions dysfunction of thyroid gland (TG) has been reported. It is related with deranged biosynthesis of thyroid hormones, in particular, with the absorption of iodine in thyrocytes. The objective of our investigation was to study the impact of oxidative stress on autoimmune diseases (AD) of TG.
Methods: 38 patients [group 1 - with diffuse-toxic goiter (DTG, n=19), and group 2 with chronic autoimmune thyroiditis (ChAT, n=19)] have been investigated. 10 healthy subjects serve as controls. The investigation was approved by the local ethics committees. The parameters of blood redox-system were investigated by electron-paramagnetic resonance. The AD was diagnosed by ultrasonography, function of TG and thyroid autoantibodies.
Results: Ceruloplasmin in group 1 was significantly higher than in controls (18.6±1.3 vs. 16.0±1.1 mm/mg, P<0.001) and lower than in group 2 (18.6±1.3 vs. 20.0±2.0 mm/mg, P=0.015). Fe3+-transferrin in group 1 and 2 was significantly lower than in controls (19.2±1.2 and 18.5±1.3 vs. 22.0±0.9 mm/mg; P<0.001 in both cases). The difference between nitric oxide EPR-signals in groups was not significant. EPR-signals of Mn2+, methemoglobin and lipid peroxyradical ions were appeared in investigated groups. Ceruloplasmin EPR-signals significantly inversely correlated with plasma thyroxine levels in main group and thyroid volume.
Conclusions: The results of our investigation suggest that oxidative stress occurs at AD of TG and expressed: a) by increase of blood ceruloplasmin levels; b) by decrease of blood Fe3+-transferrin levels; c) by appearance of Mn2+, methemoglobin and lipid peroxyradical ions in blood. These changes demonstrate possible association between AD of TG and REDOX-system.