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Results for “ASCORBIC ACID DEFICIENCY”

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At least 397 records · Page 22Linked to original sources
PubMed1997

L-ascorbic acid metabolism in the ascorbate-deficient arabidopsis mutant vtc1.

The biosynthesis of L-ascorbic acid (vitamin C) is not well understood in plants. The ozone-sensitive Arabidopsis thaliana mutant vitamin c-1 (vtc1; formerly known as soz1) is deficient in ascorbic acid, accumulating approximately 30% of wild-type levels. This deficiency could result from elevated catabolism or decreased biosynthesis. No differences that could account for the deficiency were found in the activities of enzymes that catalyze the oxidation or reduction of ascorbic acid. The absolute rate of ascorbic acid turnover is actually less in vtc1 than in wild type; however, the turnover rate relative to the pool of ascorbic acid is not significantly different. The results from [U-14C]Glc labeling experiments suggest that the deficiency is the result of a biosynthetic defect: less L-[14C]ascorbic acid as a percentage of total soluble 14C accumulates in vtc1 than in wild type. The feeding of two putative biosynthetic intermediates, D-glucosone and L-sorbosone, had no positive effect on ascorbic acid levels in either genotype. The vtc1 defect does not appear to be the result of a deficiency in L-galactono-1,4-lactone dehydrogenase, an enzyme able to convert L-galactono-1,4-lactone to ascorbic acid.

Arabidopsis↗
PubMed1980

Effects of dietary ascorbic acid and vitamin E deficiency on rat adrenal cholesterol ester metabolism and corticosteroidgoenesis.

The effect of dietary ascorbic acid (AA) and deficiency of vitamin E, alone and in combination, upon adrenal steroidogenesis in rats have been tested in vivo. High concentrations of AA blocked the normal stress-induced increase in plasma and adrenal corticosteroid concentration. Adrenal cholesterol ester hydrolase activity was also markedly inhibited by the high AA diet, while acylcoenzyme A:cholesterol acyltransferase was significantly increased. Vitamin E deficiency caused generally opposite effect, while simultaneous excess AA and vitamin E deficiency caused these parameters to return toward control values. Thus the role of AA in blocking adrenal steroidogenic response to stress is confirmed. It's mode of action may be at least partly through control of cholesterol availability for steroidogenesis.

Adrenal Glands↗
PubMedDate not supplied

Lack of protection by ascorbic acid from lethality resulting from exposure to 1 atm O2.

The role of ascorbic acid in protecting animals against the toxic effects of exposure to 1 atm. of O2 was examined. The mean time until death resulting from exposure to one atm. O2 was not different in rats treated intraperitoneally 3 times per day with 1.5 g/kg ascorbic acid compared to saline injected controls. Exposure of rats to one atm. O2 for 48 hr did not alter ascorbic acid or non-protein thiol concentration in lung or liver compared to room air controls. Lung ascorbic acid concentration was markedly depressed in guinea pigs fed an ascorbic acid-deficient diet for 6 days prior to O2 exposure. However, the mean time until death of ascorbic acid-deficient guinea pigs did not significantly differ from those fed an ascorbic acid-supplemented diet. Exposure to one atm. O2 of guinea pigs fed an ascorbic acid-deficient diet or an ascorbic acid-supplemented diet failed to decrease the concentration of ascorbic acid or of non-protein thiol in lung. Results from this study do not support an involvement of ascorbic acid in protection from pulmonary oxygen toxicity.

Animals↗
PubMed1986

Antiscorbutic effect of dehydro-L-ascorbic acid in vitamin C-deficient guinea pigs.

The antiscorbutic effect of dehydro-L-ascorbic acid (DAsA) was investigated in vitamin C-deficient guinea pigs. Male guinea pigs were fed vitamin C-deficient diets for 16 days to deplete body L-ascorbic acid (AsA) pools and then fed the deficient diet supplemented with DHA and/or AsA intraperitoneally for 14 days. During the repletion period, most of the animals injected with 0.5 mg DAsA/day developed scurvy, their body weights decreased and their mortality rate was higher than that of the other groups injected with 0.5 mg AsA/day or 5 mg DAsA/day. Injecting animals with 0.5 mg AsA/day resulted in the disappearance of the typical scorbutic symptoms and regaining of body weight. These data indicate that DAsA has considerably less antiscorbutic activity than AsA in vitamin C-deficient guinea pigs.

Adrenal Glands↗
PubMed1985

Elevated levels of dietary ascorbic acid increase immune responses in channel catfish.

Channel catfish fingerlings were fed purified diets containing 0 to 3000 mg/kg of ascorbic acid until external signs of scurvy were seen in the fish fed the ascorbic acid-deficient diet. At this time, resistance to bacterial infection, antibody production, complement activity and phagocytic activity were assessed for fish from the various dietary treatments. Mortality rates of fish experimentally infected with Edwardsiella ictaluri, the bacterium causing enteric septicemia in channel catfish, decreased with increases in dietary ascorbic acid doses, ranging from 100% for fish fed the ascorbic acid-deficient diet to 15% for fish fed 300 mg ascorbic acid per kilogram diet and 0 for fish fed 3000 mg ascorbic acid per kilogram diet. Antibody response to E. ictaluri antigen, hemolysis of sensitized sheep erythrocytes by complement activity and phagocytic engulfment of E. ictaluri by peripheral phagocytes were each impaired in fish fed the diet without supplemental ascorbic acid; intracellular bactericidal activity of the phagocytes was not affected by ascorbic acid deficiency. There were no differences in antibody production, complement activity, or phagocytic activities among fish fed diets containing 30-300 mg ascorbic acid/kg of diet. However, the dose level of 3000 mg ascorbic acid/kg significantly enhanced antibody production and complement activity.

Animal Nutritional Physiological Phenomena↗
PubMed2003

Impaired adrenal catecholamine system function in mice with deficiency of the ascorbic acid transporter (SVCT2).

Ascorbic acid (vitamin C) is a cofactor required in catecholamine synthesis for conversion of dopamine to norepinephrine by dopamine beta-hydroxylase. Mutant mice lacking the plasma membrane ascorbic acid transporter (SVCT2) have severely reduced tissue levels of ascorbic acid and die after birth. We therefore investigated whether these mice might have impaired synthesis of catecholamines. Levels of catecholamines in brain were unaffected by SVCT2 deficiency. In heart, the only evidence for impaired dopamine beta-hydroxylase activity was a twofold increase in tissue dopamine. An influence of the deficiency on tissue catecholamines was most prominent in the adrenals where norepinephrine was decreased by 50% and epinephrine, by 81%. On the ultrastructural level, adrenal chromaffin cells in SVCT2 null mice showed depletion of catecholamine storage vesicles, increased amounts of rough endoplasmic reticulum, signs of apoptosis, and increased glycogen storage. Decreased plasma levels of corticosterone indicated additional effects of the deficiency on adrenal cortical function. These data show that deranged catecholamine system function in SVCT2 null mice is largely restricted to the adrenal medulla and cannot account for the lethality in these animals. The data, however, establish a crucial role for ascorbic acid in adrenal chromaffin cell function.

Adrenal Glands↗
PubMed1987

Modulation of the flavin-containing monooxygenase in guinea pigs by ascorbic acid and food restriction.

Modulation of the flavin-containing monooxygenase (FMO) by varying the ascorbic acid and food intake was investigated. Hepatic activity of the FMO in ascorbic acid-deficient guinea pigs fed a restricted amount of diet which resulted in a 10-15% body weight loss, was 17% of that in animals fed restricted amounts of the adequate diet. FMO hepatic activity in ascorbic acid-supplemented guinea pigs on a food-restricted regimen was 176% of that found in animals fed the adequate diet ad libitum. This increase in activity was not related to stress. Alteration in the activity of this important drug-metabolizing enzyme system by a combination of ascorbic acid deficiency and reduced food intake could potentially alter the rate of metabolism of a great variety of pharmaceutical drugs and environmental chemicals.

Animals↗
PubMed1997

Functional assessment of proliferating hepatocytes stimulated by hepatic stimulatory substance in ascorbic acid biosynthetic enzyme-deficient rats.

The functional ability of hepatic stimulatory substance (HSS)-stimulated proliferating hepatocytes was investigated by intrasplenic and/or intraportal transplantation in ascorbic acid (AsA) biosynthetic enzyme-deficient (ODS-od/od) rats that die of osteogenic disorders unless there is AsA supplementation. HSS was extracted from regenerating porcine livers. Hepatocytes isolated from the livers of congeneic ODS-+/+ rats that are capable of synthesizing AsA were transplanted into the spleen (Sp-HTx) and/or the portal vein (Pv-HTx) of ODS-od/od rats. The recipients were divided into eight groups as follows: HSS-untreated groups [group Ia, sham-operated, HTx(-); group IIa, Sp-HTx; group IIIa, Pv-HTx; and group IVa, Sp- and Pv-HTx], HSS-treated groups [group Ib, HSS only; group IIb, Sp-HTx + HSS; group IIIb, Pv-HTx + HSS; and group IVb, Sp- and Pv-HTx + HSS]. The recipients were given a diet and water containing AsA for 6 weeks after HTx, and AsA supplementation was then halted. The average bromodeoxyuridine (BrdU) labeling index (LI) and hepatocyte-occupied ratio in the spleen (H/S ratio) of HSS-treated rats were significantly higher than those of HSS-untreated rats. All the rats in HSS-untreated groups and group Ib died by 8 weeks after the cessation of AsA. In HSS-treated groups IIb, IIIb, and IVb, the survival rates were 60%, 50%, and 80%, respectively, at 16 weeks after HTx. The average serum AsA level of the surviving rats in groups IIb, IIIb, and IVb was significantly higher than that in HSS-untreated groups. These results indicate that HSS treatment induced rapid proliferation of transplanted hepatocytes in the spleen and the portal vein, and that these proliferating hepatocytes synthesized AsA and improved the survival rate of ODS-od/ od rats.

Animals↗