This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.
Animals ; Glutathione/metabolism ; Human ; Hyperthyroidism/*metabolism ; Iron/*pharmacology ; Lipid Peroxidation/drug effects ; Male ; Muscle, Skeletal/*metabolism ; Oxidative Stress/*drug effects ; Rats ; Rats, Wistar ; Superoxide Dismutase/metabolism ; Thiobarbituric Acid Reactive Substances/metabolism ; Triiodothyronine/blood

This experimental study was designed to investigate the effects of vitamin E supplementation, especially on lipid peroxidation and antioxidant status elements3/4namely, glutathione (GSH), CuZn superoxide dismutase (CuZn SOD), and glutathione peroxidase (GSH Px), both in blood and liver tissues of streptozotocin (STZ) diabetic rats. The extent to which blood can be used to reflect the oxidative stress of the liver is also investigated. In diabetic rats, plasma lipid peroxide values were not significantly different, from control, whereas erythrocyte CuZn SOD (p< 0.01), GSH Px (p< 0.001) activities and plasma vitamin E levels (p< 0.001), were significantly more elevated than controls. Vitamin E supplementation caused significant decreases of erythrocyte GSH level (p< 0.01) in control rats and of erythrocyte GSH Px activity (p< 0.05) in diabetic rats. Liver findings revealed significantly higher lipid peroxide (p< 0.001) and vitamin E (p< 0.01) levels and lower GSH (p< 0.001), CuZn SOD (p< 0.001) and GSH Px (p< 0.01) levels in diabetic rats. A decreased hepatic lipid peroxide level (p< 0.01) and increased vitamin E/lipid peroxide ratio (p< 0.001) were observed in vitamin E supplemented, diabetic rats. A vitamin E supplementation level which did not cause any increase in the concentration of the vitamin in the liver or blood, was sufficient to lower lipid peroxidation in the liver. Vitamin E/lipid peroxide ratio is suggested as an appropriate index to evaluate the efficiency of vitamin E activity, independent of tissue lipid values. Further, the antioxidant components GSH, GSH Px and CuZn SOD and the relationships among them, were affected differently in the liver and blood by diabetes or vitamin E supplementation.
Animals ; Antioxidants/*pharmacology ; Diabetes Mellitus, Experimental/*metabolism ; Glutathione/blood ; Glutathione Peroxidase/blood ; Lipid Peroxidation/drug effects ; Liver/*metabolism ; Male ; Oxidative Stress/*drug effects ; Rats ; Rats, Wistar ; Superoxide Dismutase/blood ; Vitamin E/*pharmacology