Abstract

Conditions interfering with the translational facility of liver ribosomes to synthesize protein have been associated with decreased ability of rats to synthesize, store and excrete L-ascorbic acid. Hypophysectomized rats whose hepatic ribosomes fail to incorporate amino acids into protein at a normal rate (1, 2), also show a substantial diminution in rate of biosynthesis, body pool size and urinary excretion of L-ascorbic acid (3). Growth hormone administration, which has been shown to restore the amino acid incorporating function of ribosomes from hypophysectomized animals (4), has been found to enhance the biosynthesis, storage and excretion of ascorbate (3). This enhancing effect on ascorbate production appears to depend primarily on an induced increase in the activity of gulonolactone hydrolase (EC3.1.1.18) (5), an enzyme in the biosynthetic pathway between D-glucuronic acid and L-ascorbic acid specifically diminished by hypophysectomy and apparently the rate-limiting enzyme in ascorbate synthesis in ...

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