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)

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

The concentration of ascorbic acid (vitamin C) in the adrenal cortex is higher than in any other organ. The role of vitamin C in the adrenal cortex is unknown, but data obtained with bovine adrenocortical cells in vitro favour its role as an antioxidant that especially protects aldosterone synthesis from damaging lipid peroxides. Alternatively, vitamin C could act as part of an auxiliary electron transport system for the last step of aldosterone synthesis. The effects of vitamin C depletion on adrenocortical function cannot be studied in the human for ethical reasons, so we subjected different groups of guinea pigs to vitamin C depletion, sodium depletion and combined vitamin C and sodium depletion. Other groups of animals on normal or vitamin C-deficient diets received high-dose adrenocorticotrophin (ACTH) injections for 3 days before sacrifice. Fifteen days of a vitamin C-free diet led to very low vitamin C levels in adrenals, liver and plasma without clear signs of scurvy. At this time, plasma aldosterone and aldosterone secretion by isolated adrenal cells were stimulated significantly by sodium deficiency. Simultaneous vitamin C depletion completely abolished the rise in aldosterone in vivo and in vitro, significantly reduced the conversion of [3H]deoxycorticosterone to [3H]aldosterone and impaired renal sodium conservation. Plasma renin activity (PRA), plasma ACTH and serum potassium were not different in the sodium-depleted and sodium plus vitamin C-depleted groups. Sodium depletion did not affect cortisol. Vitamin C depletion led to a significant increase in plasma cortisol without an increase in ACTH, while in vitro secretion of cortisol was slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascorbate depletion prevents aldosterone stimulation by sodium deficiency in the guinea pig. 758 76

A child responds to a deficiency of an essential nutrient either by continuing to grow and consuming body stores with eventual reduction in the bodily functions (Type I) or by reducing growth and avidly conserving the nutrient to maintain the concentration of the nutrient in the tissues (Type II). Examples of Type I nutrient deficiency are anemia (iron deficiency), beri-beri (thiamin deficiency), pellagra (niacin or nicotinic acid deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency) and iodine deficiency disorders. Diagnosis is relatively simple via clinical symptoms and measurement of the concentration of the nutrient itself. There are no characteristic symptoms to distinguish which Type II nutrient deficiency an individual has; all deficiencies result in the poor growth, stunting, and wasting generally ascribed to protein-energy malnutrition. In Type II, growth stops, the body starts to conserve the nutrient, and its excretion falls to very low levels. In severe deficiency the body may start to break down its own tissues and the reduction of appetite accompanies this condition. An animal can die from zinc deficiency even though it is has a normal concentration of zinc in its tissues, but it can respond rapidly to small amount of dietary zinc. The mechanisms by which the body stops growing in response to nutritional lack are similar to the hormonal picture seen in endocrine disease (reduction of the production of the hormonal mediators of growth, down-regulation of receptors, and reduction of protein synthesis). Growth failure is the clinical sign characteristic of a diet deficient in protein, zinc, magnesium, phosphorus, and potassium. Wasting may be also ascribed to toxins, infection, worms, or persistent diarrhea. Anorexia is another common response in nutrient deficiency. Only a supplementation diet with a balance of nutrients will promote rapid recovery.
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PMID:Specific deficiencies versus growth failure: type I and type II nutrients. 1234 13