This study was designed to investigate the effect of hyperthyroidism and/or
iron supplementation on cardiac oxidative stress parameters-the lipid pero
xidation end product glutathione (GSH), glutathione peroxidase (GSH-Px), an
d superoxide dismutase (CuZnSOD) - in rats, In plasma, ferritin as an indic
ator of iron status and glutamate oxaloacetate transaminase (GOT) as an ind
icator of damage to the heart tissue were analyzed. Our findings show that
hyperthyroidism increased lipooxidative damage as reflected by higher lipid
peroxidation end product levels and elevated antioxidant defense parameter
s-GSH and GSH-Px. Iron supplementation per se does not affect oxidative str
ess parameters studied in the euthyroid state. Although iron increased lipi
d peroxidation in the hyperthyroid state, this effect was less than that se
en in euthyroidism. Iron supplementation to hyperthyroid rats significantly
lowered plasma ferritin levels, suggesting increased iron elimination with
consequently reduced oxidative stress.