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 hypophysectomized rats (6). The specific induction of gulonolactone hydrolase by growth hormone in hypophysectomized rats has been shown to be inhibited by administration of the metabolic inhibitor of protein synthesis, puromycin (7).
The decreased ribosomal function after hypophysectomy bears resemblance to decreased translational function of liver ribosomes in conditions of starvation and protein deficiency (8–11), conditions like hypophysectomy associated with decreased biosynthesis, tissue accumulation and excretion of L-ascorbic acid (12). Since hepatic enzymes are dependent on ribosomal protein synthesis, as are other proteins of liver, it is possible that the changes in ascorbate metabolism in these conditions are the result of decreased production of an enzyme or enzymes acting within the biosynthetic pathway to L-ascorbic acid. Unfortunately, the effects of starvation or protein deficiency on specific enzymes in the biosynthesis of L-ascorbic acid from D-glucuconic acid have not been clear.
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