Dehydroascorbic acid adrenal gland

The oxidative product of ascorbic acid, dehydroascorbic acid, is the preferred form of the vitamin for uptake by neutrophils, erythrocytes, and lymphocytes (27). Once within the erythrocyte, dehydroascorbic acid is reduced to ascorbic acid by a glutathione-dependent, dehydro-ascorbic-acid-reducing enzyme (20,28). However, the reduced form of ascorbic acid is found in most other tissues, that is, liver, lungs, kidneys, skin, and pituitary and adrenal glands (20,29). From these studies, ascorbic acid is taken up by several tissues by an energy-dependent and Na -sensitive process, but the transport of the oxidized vitamin form follows the principles of diflFusion. 

The adrenal gland does not synthesize ascorbic acid but merely concentrates it to a high level in common with a number of other tissues. The ascorbic acid lost from the adrenal under the influence of ACTH leaves as dehydroascorbic acid, which is the more diffusible, neutral form. The mechanism of the prompt oxidation under the influence of ACTH is unknown (S3, S4). 

Dopamine -hydroxylase catalyzes the side-chain hydrox-ylation of dopamine and other phenylethylamine derivatives. Ascorbic acid serves as a specific electron-donating cofactor. The enzyme from bovine adrenal glands contains and a smaller amount of Cu. When the enzyme oxidizes ascorbate to dehydroascorbate, most of the is reduced to Cu Added substrate is hydroxylated, and Cu is reoxidized to Cu This indicates that most of the protein-bound Cu undergoes cyclic reduction and oxidation during hydroxyhtion. The results also rule out an oxygen-carrier function for ascorbate. The possibility that a p-substituted hydroperoxide of the substrate is formed as an intermediate in the reaction has been examined with the use of 13,13 -tritium-labelled substrate. The results indicate that such an intermediate is unlikely. 

Ascorbate and Hormone Balance. The highest concentrations of ascorbate are found in the adrenal and pituitary glands, and the terminal stages of scurvy are just preceded by complete depletion of adrenal ascorbate, leading, it has been frequently stated, to scurvy death from adrenocortical failure. This has caused many to suggest that the ascorbic acid-dehydroascorbic acid system plays an important role in the synthesis and release of hormones of the adrenopituitary axis. The evidence for this is both conflicting and confusing (13, 72, 73,102, 277, 278). 

When an in vitro ascorbic-acid oxidase system is incubated in the presence of added GSH, none of the ascorbic acid is oxidized until all of the reduced GSH disappears (152). Since this system did not oxidize GSH when vitamin C was absent, the added GSH presumably protects the ascorbic acid by reducing the dehydroascorbic acid formed. The changes in GSH in the adrenal gland could, therefore, be a secondary result of the interaction of GSH and dehydroascorbic acid. 

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