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

The effects of ascorbic acid deficiency on growth and calcification of bone were studied in whole 18-day fetal rat radii and ulnae cultured in a chemically defined medium. Ascorbic acid deficiency decreased the formation of labeled hydroxyporline from labeled proline in both bone shafts and cartilage ends while incorporation of tryptophan was maintained. Dry weights and collagen content of bone and cartilage were decreased, but calcification was not affected. The optimun initial concentration of ascorbic acid for collagen synthesis was 200 mug/ml. The effect of ascorbic acid was not antagonized by glucoascorbic acid or replaced by dithiothreitol. Decreased collagen synthesis in ascorbic acid deficiency could not be ascribed to loss of available peptidyl proline hydorxylase. Formation of underhydroxylated collagen and its release into the medium accounted for much of the decrease in hydroxylated collagen in ascorbic acid deficient bones. Nevertheless, the total newly synthesized collagen, as measured by collagenase digestion, was still decreased. Similar effects were exerted by alpha, alpha'-dipyridyl which also inhibited general protein synthesis. Ascorbic acid did not stimulate proline incorporation into collagen in the presence of alpha, alpha'-dipyridyl.
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PMID:The effects of ascorbic acid deficiency on calcium and collagen metabolism in cultured fetal rat bones. 16 34

Micronutrient deficiencies occur frequently in refugee and displaced populations. These deficiency diseases include, in addition to the most common Fe and vitamin A deficiencies, scurvy (vitamin C deficiency), pellagra (niacin and/or tryptophan deficiency) and beriberi (thiamin deficiency), which are not seen frequently in non-emergency-affected populations. The main causes of the outbreaks have been inadequate food rations given to populations dependent on food aid. There is no universal solution to the problem of micronutrient deficiencies, and not all interventions to prevent the deficiency diseases are feasible in every emergency setting. The preferred way of preventing these micronutrient deficiencies would be by securing dietary diversification through the provision of vegetables, fruit and pulses, which may not be a feasible strategy, especially in the initial phase of a relief operation. The one basic emergency strategy has been to include a fortified blended cereal in the ration of all food-aid-dependent populations (United Nations High Commissioner for Refugees/World Food Programme, 1997). In situations where the emergency-affected population has access to markets, recommendations have been to increase the general ration to encourage the sale and/or barter of a portion of the ration in exchange for locally-available fruit and vegetables (World Health Organization, 1999a,b, 2000). Promotion of home gardens as well as promotion of local trading are recommended longer-term options aiming at the self-sufficiency of emergency-affected households. The provision of fortified blended foods in the general ration has successfully prevented and controlled micronutrient deficiencies in various emergency settings. However, the strategy of relying only on fortified blended foods to prevent micronutrient deficiencies should be reviewed in the light of recurring evidence that provision of adequate supplies of these foods is often problematic. Donor policies on the bartering or exchange of food aid should also be clarified. Furthermore, the establishment of micronutrient surveillance systems, including standardized micronutrient deficiency diagnostic criteria, are vital for the control of micronutrient deficiency diseases.
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PMID:Meeting the challenges of micronutrient deficiencies in emergency-affected populations. 1213 7

In this report, we present data to indicate that NADPH-cytochrome P450 reductase/cytochrome P450 system is present in the nuclear membrane. The reactive oxygen species generated in this free metal ion-independent P450 system oxidatively modifies and degrades the membrane proteins. The oxidative modification is evidenced by the formation of carbonyl, bityrosine and tryptophan loss. The degradation of membrane proteins is manifested using fluorescamine reactivity and SDS-PAGE. Ascorbic acid exclusively prevents the oxidative modification and degradation of the membrane proteins. Other antioxidants, such as superoxide dismutase, catalase, glutathione, alpha-tocopherol, probucol, beta-carotene, mannitol, histidine and thiourea are found to be ineffective. The observation assumes significance, particularly in subclinical ascorbic acid deficiency, where oxidative damage of the nuclear membrane would occur. This, in turn, would affect the traffic of cytoplasmic enzymes and proteins required for DNA replication and repair, transcription and RNA processing, ultimately leading to disruption of gene regulation of the cell.
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PMID:Cytochrome P450-mediated oxidative damage of nuclear membrane proteins and its prevention by vitamin C. 2290 Mar 24