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 decrease of tyrosine hydroxylase activity in adrenal homogenate in scurvy was recovered after the administration of ascorbic acid. The causes of the increase in the enzyme activity after the administration of ascorbic acid have been studied. 1. No significant elevation in the enzyme activity was observed after the administration of reserpine to the scortutic guinea pig. 2. A dose of metal chelating agent, alpha, alpha'-dipyridyl, prevented the ascorbic acid-induced or reserpine-induced increase in enzyme activity in the scorbutic and the non-scorbutic guinea pigs, respectively. 3. Tyrosine hydroxylase activity was partially recovered by the administration of FeSO4 to the scorbutic guinea pig. From these results, it became clear that the induction of tyrosine hydroxylase which was not observed in scurvy was due to the deficiency of Fe2+. These results suggested that ascorbic acid affected the induction of this enzyme via Fe2+.
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PMID:Role of ascorbic acid on tyrosine hydroxylase activity in the adrenal gland of guinea pig. 1 71

Ascorbic acid exists in high intracellular concentrations in fetal rat brain. In mesencephalic cultures the cellular ascorbic acid content drops sharply to undetectable levels when no ascorbic acid is added to the medium, thus creating a model of scorbutic neuronal tissue and affording the study of ascorbic acid's effects on mesencephalic cell development and function. Cultures treated with 0.2 mM ascorbic acid were compared with controls (scorbutic cultures) by using morphological and biochemical indices. Ascorbic acid cultures at 7 and 14 days in vitro showed a marked increase in glial proliferation on glial fibrillary acidic protein staining and increased neurite growth and number on tyrosine hydroxylase staining. Significantly higher dopamine uptake and levels of dopamine and 3,4-dihydroxyphenylacetic acid were also observed after 7 and 14 days of ascorbic acid treatment. The capacity to accumulate ascorbic acid and the ability to retain the intracellular ascorbic acid developed gradually as the cultures matured. Ascorbic acid reached the embryonal levels by day 14 in vitro. We conclude that although neuronal cultures can survive and grow in the absence of detectable levels of ascorbic acid, its presence exerts a broad effect on dopamine neuron morphology and biochemical functioning either directly or through increased glial proliferation, or possibly both.
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PMID:Ascorbic acid in mesencephalic cultures: effects on dopaminergic neuron development. 207 96

The effect of ascorbic acid depletion on the 1-methyl-4-phenylpyridinium ion (MPP+)-induced neurotoxicity in the dopaminergic system has been tested in guinea-pig striatal slices. Guinea-pigs were divided into three groups and fed on a control diet, ascorbic acid-free diet and ascorbic acid-supplemented diet, respectively. Diets were maintained during 30 days. Striatal slices from ascorbic acid-deficient animals showed the highest levels of dopamine following 25 microM MPP+ treatment; the results from animals under this treatment condition were statistically different from both control and ascorbic acid-supplemented animals under identical experimental conditions. In addition, neurochemical analysis demonstrated that the levels of ascorbic acid and dehydroascorbic acid were highly reduced in striatal tissue from ascorbic acid-deficient animals, thus proving scorbutic conditions in our experimental animals. In view of the higher resistance of the ascorbic acid-deficient animals to the neurotoxicity elicited by MPP+, additional dopaminergic parameters were also measured in striatal tissue from ascorbic acid-deficient animals in the absence of MPP+, including levels of dopamine and its metabolites, tyrosine hydroxylase activity and dopamine uptake, with the aim of finding an explanation for this unexpected result. While dopamine levels and tyrosine hydroxylase activity remained close to control levels, dopamine uptake was significantly reduced in striatal synaptosomes from ascorbic acid-deficient animals as compared with control animals. Since MPP+ is actively accumulated into dopaminergic nerve terminals via the high-affinity dopamine uptake system, this finding could explain the higher resistance of ascorbic acid-deficient animals to the dopamine-depleting effect induced by MPP+ toxicity assayed in striatal slices.
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PMID:Less induced 1-methyl-4-phenylpyridinium ion neurotoxicity on striatal slices from guinea-pigs fed with a vitamin C-deficient diet. 904 84