Vitamin Chondroitin sulfate

The urinary excretion of glycosaminoglycans by juvenile cases of vitamin A deficiency and of protein-calorie malnutrition (kwashiorkor) is less than normal (M41). The predominant differences are the absence of hyaluronic acid and the presence of chondroitin sulfate of low sulfate content (C12). Treatment of the cases with vitamin A deficiency restored the glycosaminoglycan spectrum to normal. Decreased urinary glycosaminoglycan levels have also been noted in primary hepatoma (K6). It has been suggested that the urinary excretion pattern of individual glycosaminoglycans is pathognomic of certain hereditary bone diseases (T3). 

Fell and his collaborators studied the effect of excess vitamin A on the development of explants on undifferentiated chick embryo bones and on cultures of undifferentiated embryonic chick ectoderm. Histological examination of the embryonic bones exposed to the excess vitamin suggested that chondroitin sulfate disappears under the influence of the vitamin. As for the ectodermic cells, instead of developing into a squamous epithelium topped by a keratinizing layer, they became a mucus-secreting epithelium. 

These effects of excess vitamin A are opposite from those observed in vitamin deficiency, and the changes induced in vitro by the addition of the vitamin mimic hypervitaminosis in vivo. On the basis of these observations made in cultures, it seems safe to conclude that the effects of vitamin A on the metabolism of chondroitin sulfate and on the formation of mucus are direct and do not result from the stimulation of hormonal secretion by the vitamin. The effects of vitamin A on bone and epithelium suggest that the vitamin in some way affects the biosynthesis of mucopolysaccharides, yet the effect on the bone is opposite to that on the epithelium whereas excess vitamin A accelerates the dissolution of chondroitin sulfate, it enhances mucus synthesis. 

The effect of ascorbic acid on the production of proteoglycans is rather controversial. Edward and Oliver (1983) found that both hyaluronate and sulfated gly-cosaminoglycan synthesis by human skin fibroblasts was affected by vitamin C. Kao and coworkers (1990) found that ascorbic acid stimulates the production of glycosaminoglycans in cultured fibroblasts, whereas Pacifici (1990) observed that in chick chondrocyte cultures the secretion of keratin sulfate and chondroitin sulfate-containing proteoglycans was not affected by ascorbic acid in the culture medium. 

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