Role of thyroid gland in oxygen toxicity.
The effects of hyperoxia at ambient pressure on thyroid function and thyroid hormone metabolism have been assessed. Thyroidal activity was depressed in mice and rats by exposure to hyperoxia, due at least in part to a decrease in the rate of secretion of pituitary thyrotropin. The effects of hyperoxia on the peripheral deiodination of thyroxine (T4) were dependent on the concentration of oxygen employed and/or the duration of exposure; exposure to 40--80% oxygen for 96 h resulted in decreases in the rate of deiodination and in the deiodinative clearance of [125I]T4. Hyperoxia also resulted in a marked fall in the serum concentration of endogenous T4 and a decrease in T4-binding activity in serum. Many of these effects of hyperoxia were prevented by the concomitanat administration of large amounts of vitamin E (alpha-tocopherol acetate). These decreases in thyroid function and T4 metabolism were associated with a decrease in the rate of whole body oxygen consumption. Thus, the deleterious effects of oxygen in the rat were not due, even in part, to an oxygen-induced hyperthyroid state in the peripheral tissues.
D000818:Animals; D007455:Iodine / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000506:poisoning*; D010101:Oxygen Consumption; D051381:Rats; D013961:Thyroid Gland / Q000378:metabolism*; D013974:Thyroxine / Q000378:metabolism*; D014810:Vitamin E / Q000494:pharmacology
D014810:Vitamin E; D007455:Iodine; D013974:Thyroxine; D010100:Oxygen