Abstract
IN THE search for an explanation of how thyroxine acts to increase the rate of oxygen consumption of various tissues of the body, many workers have examined enzyme effects (1). Considering that the activity of several enzyme systems, such as succinoxidase, cytochrome C and cytochrome oxidase, is appropriately increased in hyperthyroidism, it is logical to attempt to demonstrate direct hormonal effects on these. In general, Smith and Williams-Ashman (2) and others found no consistent stimulation. This may well be due to the fact that enzyme studies are carried out under conditions so chosen as to yield maximal activities. With less favorable conditions, thyroxine might act to prevent denaturation of specific proteins, to stabilize oxidation-reduction potentials, etc. Such an action may not even remotely be related to the in vivo effect of the hormone. Thus, the thyroxine potentiation of the ascorbic acid oxidase system, pointed out by Gemmill (3), was shown by Frieden (4) to be a protective action
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