Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhesus monkeys fed an ascorbic acid-free, purified liquid diet, developed scurvy in 70 to 105 days as evidenced by loss of weight, anemia, bleeding gums, inflamed palate, diarrhea, and inability to stand. Oral administration of either 10 mg/kg body weight of ascorbic acid or an equimolar amount of the magnesium salt of 1-ascorbic acid phosphate cured all symptoms of scurvy. Similarly, oral administration of 1-ascorbic acid phosphate cured all symptoms of scurvy in the guinea pig and resulted in liver ascorbate levels equal to those of animals feed ascorbic acid. It is concluded that ascorbic acid phosphate is a readily available source of ascorbic acid activity in vivo.
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PMID:Antiscorbutic activity of ascorbic acid phosphate in the rhesus monkey and the guinea pig. 10 21

Fifty percent of the ascorbic acid content of sliced rat lung was released from the tissue to the media within a few minutes by either washing or incubating the slices with Krebs-phosphate solution. Measurement of the lactate dehydrogenase and potassium content of the medium after incubating lung slices for 5 min showed that about 20% of the cells were damaged by slicing. Sephadex chromatography of tissue extracts prepared from washed lung slices showed that none of the ascorbic acid in these slices were bound to protein. Also, metabolic poisons were shown to deplete the ascorbic acid content of washed lung slices. Approx. 57% of the lung ascorbic acid of guinea pigs that had been supplemented with ascorbic acid and 78% of the lung ascorbic acid of ascorbic acid-deficient guinea pigs were found in the medium when lung slices from these animals were incubated with Krebs-phosphate solution. These results were taken to indicate the presence of an extracellular pool of ascorbic acid in lung which is maintained even during scurvy.
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PMID:Extracellular ascorbic acid in lung. 95 21

Vitamin C (VitC) plays a critical role in the maintenance of a normal mature collagen network in humans (anti-scurvy properties) by preventing the auto-inactivation of lysyl and prolyl hyroxylase, two key enzymes in collagen biosynthesis. In this study two in vitro models were designed to evaluate the effects of VitC on collagen biosynthesis and cross-linking at cellular and tissue levels. It was shown that VitC induced a dose-dependent increase in collagen type I deposits by normal human fibroblasts (NHF) cultured in monolayer, and enhanced extracellular matrix contraction by NHF in a lattice model, in a non-cytotoxic range of concentrations (103m, 104m, 105m). Exogenous VitC supply could thus contribute to the maintenance of optimal collagenic density in the dermis and locally strengthen the collagen network. Vitamin C-phosphate (VitC-P) and vitamin C-glucoside (VitC-Glu) (two VitC derivatives presenting higher chemical stability in aqueous solution) were also tested in our two models, and showed similar biological properties, but with different potencies. These two compounds can be considered as pro-vitamins for skin, and could thus advantageously substitute for VitC in VitC-based anti-ageing products, as they allow the development of stable, easy-to-use formulations.
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PMID:Effect of vitamin C and its derivatives on collagen synthesis and cross-linking by normal human fibroblasts. 1850 99