Lipid peroxidation levels in rat cardiac muscle are affected by age and thyroid status

Free radicals, hydroxyperoxides and H2O2 are all known to damage cell compo nents. This study was designed to compare the concentrations of hydroxypero xide and free radical scavengers in the cardiac muscles of old rats in the hyper- or hypothyroid condition, to determine whether rates of peroxidation would differ with age, thyroid status, or both. Rats were rendered hyper- or hypothyroid by administration of L-thyroxine o r methimazole for 4 weeks. Among the old rats, the lipid peroxide (LPO) con centrations, measured as thiobarbituric acid (TBA) reactants, were signific antly greater in the hyperthyroid than in the euthyroid state and the LPO c oncentrations measured as TBA+Fe3+ reactants, which may he precursors of LP O, were significantly greater in the hyperthyroid state, whereas in young r ats, the LPO concentrations measured by TEA or TBA+Fe3+ methods did not dif fer significantly in the hyperthyroid state. In the euthyroid state, the co ncentration of LPO measured as TBA+Fe3+ reactants was significantly reduced with age. Xanthine oxidase (XOD) activity also was markedly increased with age, being more pronounced in the hyperthyroid than in the euthyroid state . The Mn and Cu/Zn superoxide dismutase activities were greater in the hype rthyroid than in the euthyroid state. Glutathione peroxidase activity decre ased with age in the euthyroid and, particularly, in the hyperthyroid state . Catalase activity was not affected in the old rats. Concentrations of alp ha-tocopherol in the old rats were high in the hyperthyroid state and low i n the hypothyroid state, whereas the levels of beta- and gamma-tocopherols in these rats were unchanged in both conditions as compared with the euthyr oid state findings. Data suggest that the site of free radical generation differs in older rats , with additional shifts in the location of intracellular Lipid peroxidatio n being noted during hyperthyroidism. Thus, as rats age, the reduction of t he free radical scavenger system and the increase in LPO and XOD activities might induce myocardial dysfunction.