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)

It was reported previously that dietary ascorbate (ASC) delays the development of galactose-induced cataract in guinea pigs compared to the rate which is observed in ASC-deficient animals. Experiments were conducted to explore the possible mechanism of this phenomenon. Guinea pigs were fed for a period of up to 4 weeks either a normal diet (1 g ASC/kg diet) or a scorbutic diet (< 0.04 g ASC/kg diet) combined with 10% galactose in the drinking water. After 2 weeks, levels of ASC in animals on the scorbutic diet decreased by 95% in the aqueous humor and by 78% in the lens. Slit lamp examination showed that galactose-induced vacuoles in the lens equator formed at a significantly faster rate in the scorbutic animals. However, examination of biochemical parameters in whole lenses of the two groups of animals after 2 weeks showed no significant differences with regard to accumulation of galactose and galactitol, decreases in the levels of myoinositol, taurine and GSH or changes in cation concentrations. In order to examine possible regional changes in the lenses, various parameters were studied in the lens capsule-epithelium. On day 4, the capsule epithelia of scorbutic animals on a galactose diet had a content of galactitol two-and-a-half times higher than that of normal galactose-fed animals. Scorbutic conditions also intensified the loss of Na(+)-K+ ATPase activity in the lens capsule-epithelium caused by galactose feeding. Oxidized glutathione was not detectable in the lens capsule epithelia of any of the animals studied. Hexose monophosphate shunt activity was elevated in lenses of normal galactose-fed animals during the first hour of culture after death whereas lenses of scorbutic galactose-fed animals were not. Consistent with the in vivo findings, galactitol accumulation in dog lens epithelial cells exposed to 30 mM galactose was significantly inhibited by the presence of either ASC or dehydroascorbate (DHA) in the medium. Hexose monophosphate shunt activity in the cells was stimulated to two-and-a-half times its initial level by either 1 mM DHA or 30 mM galactose and slightly more than three-fold by a combination of the two challenges. The results suggest that decreased polyol accumulation in the lens epithelium of the normal galactose-fed guinea pig, which has a high level of ASC in the aqueous humor, accounts for the delay in onset of cataract compared to that for the ASC-deficient animal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A physiological level of ascorbate inhibits galactose cataract in guinea pigs by decreasing polyol accumulation in the lens epithelium: a dehydroascorbate-linked mechanism. 815 13

Previous studies indicate that benzanthrone, an anthraquinone dye intermediate, caused significant depletion of ascorbic acid (AsA). In this investigation the effect of benzanthrone on the status of different forms of AsA and other bio-antioxidants such as glutathione (GSH) was studied. Oral administration of benzanthrone (50, 125 or 250 mg/kg body weight) resulted in a significant increase of urinary AsA levels with a concomitant decrease in the urinary dehydroascorbic acid (DHA) content in both rats and guinea-pigs. Benzanthrone caused a dose-dependent decrease in hepatic, adrenal and serum AsA levels with a subsequent increase in DHA and diketogulonic acid (DKA) levels in both rats and guinea-pigs. Following benzanthrone treatment, rats showed an increase in the scorbutic index (to 1.01-1.21) of the liver, adrenal glands and serum compared to controls (0.12-0.24). The scorbutic indices of liver, adrenal glands and serum were also substantially increased (to 3.61-11.20) in benzanthrone-treated guinea-pigs compared to controls (0.16-0.38). Single oral administration of benzanthrone to guinea-pigs caused a dose-dependent depletion of GSH in liver (15-51%), adrenal glands (27-64%) and serum (32-86%). Furthermore, the depletion of GSH by benzanthrone in rats was of a lesser degree. This suggests that continued exposure of guinea-pigs to benzanthrone may lead to scurvy-type changes in this animal species but not to the same extent in rats, since the latter has the enzymatic capacity to synthesise AsA. Therefore, it can be hypothesised that benzanthrone per se, or its metabolites, interact with reduced GSH thereby causing its depletion. Furthermore, in order to replenish the depleted GSH levels, AsA might be oxidized to DHA and hence the decrease in AsA with the simultaneous increase in DHA was observed.
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PMID:Role of biological antioxidants in benzanthrone toxicity. 1148 20

We examined whether prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or adequate ascorbic acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of ascorbic acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of ascorbic acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.
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PMID:Prolonged marginal ascorbic acid deficiency induces oxidative stress in retina of guinea pigs. 1194 96

Because standard culture media for human aortic endothelial cells (HAEC) do not contain vitamin C, we hypothesized that HAEC may be under significant oxidative insult compared with the situation in vivo. To assess parameters of oxidative stress, intracellular vitamin C, glutathione (GSH), GSH/GSSG, and NAD(P)H/NAD(P)+ ratios, as well as oxidant appearance and oxidative damage, were measured in HAEC with or without vitamin C addition. The effect of vitamin C on eNOS activity was also determined. Results showed that HAEC without vitamin C treatment were essentially scorbutic. On addition of 100 mM vitamin C to the culture media, intracellular vitamin C levels increased and peaked at 6 h. A concomitant increase in the total GSH and the GSH/GSSG ratio was also observed; the NAD(P)H/NAD(P)+ ratio increased more slowly over the 24-h time course. Significantly lower (P <0.05) oxidant appearance and steady-state oxidative damage were also observed following vitamin C repletion. Vitamin C treatment increased eNOS activity by 600%. Thus, HAEC are scorbutic under normal culture conditions and exhibit higher oxidative stress than vitamin C repleted cells. Vitamin C supplementation should be considered when using cultured cells, especially when experimental endpoints are related to cellular redox status and eNOS activity.
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PMID:Vitamin C matters: increased oxidative stress in cultured human aortic endothelial cells without supplemental ascorbic acid. 1203 48