Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003969 (vitamin C deficiency)
 625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In guinea-pigs a diet which was deficient in ascorbic acid provoked neurogenic atrophy of the muscles, degeneration of the anterior horn motor cells and demyelination of the pyramidal tract. Muscles showed a decrease of cytochrome and cytochrome c oxidase. Subcutaneous haemorrhages were also found, particularly around the knee joints. The haemorrhages and the histopathology of the muscles and spinal cord were prevented by a high dosage of ascorbic acid. In animals with an ascorbic acid deficiency, histopathology of muscles and spinal cord were also prevented by L-cysteine, L-methionine and L-hydroxyproline. Subcutaneous haemorrhages were not prevented by these supplements.
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PMID:Experimental amyotrophic lateral sclerosis in the guinea-pig. 398 Dec 16

ABNORMALITIES OF TYROSINE METABOLISM ARE DISCUSSED UNDER FOUR HEADINGS: (1) accumulation of tyrosine and its metabolites secondary to severe liver damage, vitamin C deficiency, etc.; (2) transient neonatal tyrosinemia; (3) hereditary tyrosinosis with hepatorenal dysfunction where elevation of tyrosine and methionine levels in the plasma may be a secondary manifestation of an unknown disease process; and (4) "essential tyrosinemia" or tyrosinosis without hepatorenal dysfunction which may represent a kkrimary fault in the metabolism of tyrosine.A new case of tyrosinosis without hepatorenal dysfunction in a 13-year-old mentally retarded girl is reported. Clinical findings, laboratory investigations and results of dietary management and normalization of the plasma tyrosine level and of urinary metabolites are presented and compared with the features of three similar cases in the liteature. It is suggested that these cases represent "essential tyrosinemia" where there is a primary genetic defect in tyrosine metabolism.
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PMID:Tyrosinosis: a new variant. 468 72

Folate metabolism in the rat was investigated using radiolabelled 5-methyltetrahydropteroylglutamate (5-CH3-H4PteGlu) and its oxidation products. 5-CH3-H4PteGlu is absorbed completely from the intestine, although in some preparations it is an equimolecular mixture of C-6 epimers, only one of which is naturally present in biological systems. The methyl group is incorporated into non-folate compounds, including methionine and creatine. No evidence was observed for the oxidation of the methyl group of 5-CH3-H4PteGlu to form other folate types. The tetrahydrofolate moiety of 5-CH3-H4PteGlu is metabolized in a similar manner to folic acid, forming formyl folates and tissue polyglutamates, and is catabolized by scission. The triazine oxidation product of 5-CH3-H4PteGlu is not metabolized by the rat or its gut microflora. 5-Methyl-5,6-dihydropteroylglutamate, however, is assimilated into the folate pool, but is substantially broken down by passage through the gut. The possible implication of this in scorbutic diets is discussed.
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PMID:The metabolism of 5-methyltetrahydropteroyl-L-glutamic acid and its oxidation products in the rat. 715 Feb 48

A study was made of the effect of ascorbic acid deficiency and low levels of lysine, methionine and threonine on the cancerogenic effect of nitrosopiperidine which was fed to guinea-pigs with drinking water in a single dose of 4.25 mg/kg bw. Deficiency of the nutrients given alone or especially in combination speeded up the growth tumors induced by the cancerogenic agent. A possibility of inducing esophageal tumors in guinea-pigs has been demonstrated for the first time.
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PMID:[Effect of amino acid imbalance and ascorbic acid deficit on the carcinogenic effect of N-nitrosopiperidine]. 724 95

Among nutrients, the role of water-soluble vitamins as genetic expression modulators has not been exhaustively stu-died. Relevant information is shown herein on the present state of the art in this field. For example, vitamin C deficiency leads to a decrease in mRNA levels of apolipoprotein A1 (Apo A1) in liver. Biotin participates in the regulation, both at mRNA and protein level, of the enzymes that participate in its own metabolic cycle and of enzymes that contribute to glucose metabolism. Thiamine regulates the expression of some genes that code for enzymes using thiamine diphosphate as cofactor. Thiamine deficiency diminishes the mRNA levels of transketolase and pyruvate dehydrogenase. It has been shown in riboflavin-deficient rats that FAD regulates some acetyl CoA dehydrogenases, producing a marked increase in mRNA levels. Nicotinamide positively regulates glyceraldehyde-3-phosphate dehydrogenase when NADH is added. Vitamin B6 modulates the expression of a variety of genes that respond to hormones. Vitamin B12 increases concentrations of the enzymatic protein methionine synthetase and doe not affect mRNA levels, which implies that this protein is regulated by its cofactor post-transcriptionally. Most mechanisms involved in these regulation examples are not known, which opens new research areas for the future.
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PMID:[Importance of water-soluble vitamins as regulatory factors of genetic expression]. 1199 11