Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet monoamine oxidase (MAO) activity was found to be significantly reduced in human alcoholics as compared to matched controls. A probable transitory increase in activity was observed during the abstinence phase. The low platelet MAO activity was not due to iron deficiency or to the presence of acetaldehyde. Since we have previously found a lowered MAO activity in the brains of suicide victims, especially in those with a previous history of alcohol abuse, we suggest that low platelet MAO activity reflects a primarily "weak" monoaminergic system in the CNS which causes an increased vulnerability to alcohol abuse and suicidal behaviour.
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PMID:Low platelet monoamine oxidase activity in human alcoholics. 89 16

Cultures of Streptomyces griseus grown under phosphate-limiting conditions produced a complex of green products. Three of these were separated from the mixture and characterized. One was identified as viridomycin A, the ferrous chelate of 4-hydroxy-3-nitrosobenzaldehyde; the second (actinoviridin A) was the corresponding carboxylic acid chelate and the third (viridomycin E) was a hybrid chelate containing both the aldehyde and acid ligands. Only two out of nine strains of S. griseus examined produced viridomycins and the ligands were biosynthesized only in media from which phosphate had been exhausted. Optimization of the production medium showed that fructose and alanine were the most favorable carbon and nitrogen sources and that relatively high concentrations of ferrous ions were necessary. The results suggest that viridomycins are not produced by S. griseus as iron scavengers in response to iron deficiency but as secondary metabolites that are stabilized adventitiously in the broth by metal ion chelation.
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PMID:Characterization of new viridomycins and requirements for production in cultures of Streptomyces griseus. 368 25

n-Pentylamine enters into intermediary metabolism by the action of monoamine oxidase. [1-(14)C] Pentylamine injected into rats is rapidly converted to (14)CO(2). The rate of catabolism decreases progressively in the course of nutritional iron deficiency, reaching about 60 percent of control values in 3 weeks. Feeding with iron yields control levels within 6 days. The catabolism of amyl alcohol, which shares a common pathway with n-pentylamine by way of valeric aldehyde, is not significantly affected by the deficiency. The results demonstrate that the maintenance of normal monoamine oxidase activity in vivo depends upon an adequate supply of dietary iron.
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PMID:Iron- and riboflavin-dependent metabolism of a monamine in the rat in vivo. 511 26