Abstract
One of the more widely recognized signs of vitamin A deficiency is the depression of growth. Even though numerous factors can affect growth, sufficient evidence is accumulating to suggest that vitamin A plays a direct role in this process (1). The exact mechanisms by which vitamin A affects growth are not known but recent findings suggest that it may be by regulating or controlling protein synthesis. For instance, DeLuca et al. (2) have reported that protein synthesis by the intestinal mucosa is decreased in the deficiency state, while Tryfiates and Krause (3) have demonstrated the opposite effect in liver. Both of these studies have examined protein synthesis in deficient animals at the translational level.
With the discovery of methylated bases as a minor constituent of transfer RNA (tRNA) (4), Borek has suggested that modification of preformed tRNA might serve a regulatory function in protein synthesis (5). Since methylation of tRNA is accomplished by the addition of methyl groups to a preformed tRNA by the methylase enzymes located in the soluble portion of the cell (6), it seems appropriate to use tRNA methylase activity as an indicator of this modification process.
Bradford et al. (7) have reported that both the rate and the extent of methylation of tRNA decreased in extracts of vitamin Adeficient bone.
The purpose of this investigation was to determine if there was a change in tRNA methylase activity accompanying the stimulation in liver protein synthesis previously observed in vitamin A deficiency.
Materials and Methods, Animals. Weanling male albino Wistar rats were made vitamin Adeficient as previously described by Krause et al. (8). Rats were judged to be deficient when their weight plateaued and no vitamin A could be detected in either their serum or liver.
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