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Results for “ASCORBIC ACID DEFICIENCY”

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At least 793 records · Page 44Linked to original sources
PubMed1995

Renal handling of carnitine in experimental vitamin C deficiency.

Experimental vitamin C deficiency is associated with carnitine concentrations in blood and some tissues, but is not due to a decreased ability of scorbutic animals to synthesize carnitine. The effect of experimental vitamin C deficiency on urinary carnitine excretion in vivo and carnitine transport into renal cortical brush-border membrane vesicles in vitro was investigated in guinea pigs fed normal and vitamin C-deficient diets for 24 days. Excretion of free and total carnitine was approximately fourfold greater in scorbutic animals as compared with normal guinea pigs during the last 6 days of the experimental regimen. The rate of carnitine transport into renal cortical brush-border membrane vesicles prepared from scorbutic animals was approximately 36% lower than the corresponding rate for vesicles prepared from normal animals. However, this effect was not specific, since rates of sodium gradient-dependent transport of glucose, lysine, and taurine (but not alanine) were also lower in vesicles prepared from scorbutic animals, although the magnitude of the decrease was less than for carnitine. The results are consistent with the hypothesis that carnitine depletion in vitamin C deficiency is due to decreased efficiency of carnitine reabsorption.

Amino Acids↗
PubMed2001

[Vitamin C status of inhabitants of the Gomel region].

The carried out research of vitamin C status of 250 young people 17-20 years old constantly living in region of the periodic radioactive control of the Gomel region of Republic Byelorussia have shown, that in the spring the vitamin C deficiency is observed at more than 55% examined, and autumn this parameter is reduced approximately on 20%. The vitamin C provision of the women is slightly higher, than one of men. The vitaminization of the population within 1 month by polyvitaminic complexes results in twofold reduction of number examined with vitamin deficiency.

Adolescent↗
PubMed1977

Effects of a prolonged vitamin E deficiency in the rat.

Rats fed a vitamin E-deficient diet containing 10% "stripped" corn oil had reduced growth rate and elevated platelet count by 12 weeks of age, and a normocytic anemia with elevated reticulocytes by 16 weeks of age. After 5 months, rats became emaciated and developed kyphoscoliosis. Some rats developed skin ulcers and tremors, and mortality was high. Neuromuscular lesions included a chronic necrotizing myopathy and localized axonal dystrophy. There was also a selective activation of lysosomes in the central nervous system microcirculation. Liver ascorbic acid of deficient rats was the same as in those receiving vitamin E. Urinary excretion of p-hydroxyphenylpyruvate after a tyrosine load was also the same in deficient and control rats. It was concluded that neither vitamin C synthesis or utilization was affected the E-deficient rats.

Age Factors↗
PubMed1983

A histological and biochemical study of the effect of vitamin C-deficiency on induction of amelogenesis in hamster molars in vitro.

Second maxillary molars of hamsters were cultured in the presence or absence of 250 micrograms/ml vitamin C for periods up to 12 days. At various days, cultured explants were studied with histological and biochemical methods to investigate effects of vitamin C-deficiency on matrix production and mineralization in vitro. As biochemical parameters for protein synthesis and mineralization, uptake and incorporation of [3H]-proline, 45Ca and 32PO4 were used. To discriminate between synthesis of collagenous and non-collagenous proteins digestion of the [3H]-proline-labelled material by purified collagenase and its degree of hydroxylation were measured. Histologically, in control explants cultured with vitamin C, normal dentinogenesis, amelogenesis and mineralization in vitro were observed. In the vitamin C-deficient explants, odontoblasts produced an abnormal predentine matrix and de-differentiated. Eventually, this matrix mineralized aspecifically. In the presence of this abnormal matrix, ameloblasts failed to differentiate, which suggests that a cell-matrix type of interaction is involved in the differentiation of the pre-ameloblasts. Biochemically, in the vitamin C-deficient explants protein synthesis and collagen synthesis were reduced by about the same extent; the in-vitro produced collagens appeared under-hydroxylated and could, in degraded form, easily be extracted in formic acid. An increase of [3H]-proline solubility in formic acid in the control explants, however, paralleled enamel matrix production and was attributed to the solubilization of proline-rich enamel matrix proteins. The production of acid insoluble phosphate was not affected by vitamin C-deficiency. The uptakes of 45Ca and 32PO4 were retarded and the molar Ca:PO4 uptake ratio was lower, reflecting the histologically observed aspecific mineralization.

Amelogenesis↗