Cause of pituitary-adrenal failure in the riboflavin-deficient rat.

The discharge of cholesterol, ascorbic acid, and histologically demonstrable lipides from the adrenal glands is generally regarded as evidence of increased activity of these glands during stress (l-5). These changes were also produced upon injection of purified corticotropin (6). However, in the detailed study of Fortier et al. (7) it was shown that corticotropin (ACTH) alone cannot account for adrenal response during stress. Repeated injection of this hormone over a period of 2 days did not result in depletion of sudanophilic material, whereas stress produced an intense discharge of this substance. On the other hand, if ACTH injection was continued for a longer period, during the first 8 days the ketosteroids were replenished above normal, but by 12 days depletion recurred (8). In riboflavin-deficient rats and dogs a condition resembling hypocortical activity has been reported (9, 10) which was preceded by a hypercortical condition (11). To elucidate further the state of function of the pituitaryadrenal cortex cycle in riboflavin-deficient rats, the effect of anoxic anoxia, of corticotropin, and of epinephrine was examined. In addition, as a test of pituitary function, the regeneration of an enucleated adrenal gland in the riboflavin-deficient rat was investigated.