Vitamin A deficiency caused a marked decrease in the number of goblet cells in the small intestine of the rat but no other morphological changes were revealed by electron microscopy. RNA and protein concentrations remained unaffected. Large polyribosomes could be isolated from the mucosa after the common bile duct was ligated. No differences were found in polyribosome stability or the protein-synthesizing activity of free polyribosomes from mucosa of vitamin A-deficient or pair fed normal rats. Rough endoplasmic reticulum, on the other hand, showed a decrease in uptake of a labeled amino acid into protein (to less than one-half of the normal level) under conditions of vitamin A deficiency. The lesion was located in the pH 5 fraction by crossing-over experiments, that is, by incubating normal rough endoplasmic reticulum with deficient pH 5 fraction and deficient rough endoplasmic reticulum with normal pH 5 fraction. The mucosal lesion occurs at a very early stage of the deficiency, before the weight plateau stage; however, it was not observable in liver. It is concluded that protein synthesis by membrane-bound but not by free polyribosomes of intestinal mucosa is depressed under conditions of vitamin A deficiency and that the vitamin is therefore involved, directly or indirectly, in protein synthesis at the translational level.
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Luca et al. (1969) studied this question.
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