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Results for “ASCORBIC ACID DEFICIENCY”

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PubMed1981

Ischaemic heart disease and aged patients: effects of ascorbic acid on lipoproteins.

Aged men and women with ischaemic heart disease had higher total triglyceride levels than controls, and also lower mean percentage cholesterol levels in the high-density lipoprotein fraction. Subnormal levels of leucocyte ascorbic acid were found in 15/25 patients. In men, but not in women, the initial leucocyte ascorbic acid levels were correlated positively with HDL-cholesterol concentrations. After six weeks treatment with ascorbic acid, the mean HDL-cholesterol concentration had increased not only in all men, but also in those women with IHD. Furthermore, total serum cholesterol and LDL-cholesterol concentrations were reduced in men with IHD, but triglyceride levels were not significantly changed; whereas in women with IHD both total serum and VLDL-triglycerides were reduced. Ascorbic acid deficiency appears to contribute to disorders of lipoprotein metabolism in the aged. Latent ascorbic acid deficiency may be one of several preventable 'risk' factors contributing to the present epidemic of IHD in the western world.

Aged↗
PubMed1989

[Vitamin C in children with trisomy 21].

The present study revealed ascorbic acid deficiency in the blood of many children with Down's syndrome. It also revealed a fairly definite connection between Vitamin C deficiency and diet in these patients and a similar link between ascorbic acid deficiency and this incidence of infections. Where necessary the prescription of Vitamin C for the prevention and treatment of recurring infection is therefore recommended, bearing in mind the valuable antioxidant properties of ascorbic acid that can be exploited in combating cell deterioration.

Adolescent↗
PubMed1976

Ascorbic acid and hepatic drug metabolism.

Previous in vivo studies indicate that hepatic microsomal drug metabolism decreases in ascorbic acid deficiency and is augmented when high supplements of the vitamin are given to guinea pigs. Kinetic studies with O-demethylase indicate no significant change in the apparent Km of p-nitroanisole in normal, ascorbic acid-deficient animals, or in animals given high supplements of ascorbic acid. The decrease in drug metabolism activity caused by ascorbic acid deficiency is not due to increased lipid peroxidation, nor was phosphatidyl choline significantly altered quantitatively or qualitatively in microsomes from ascorbic acid-deficient animals. Microsomal cytochrome P-450 prepared from ascorbic acid-deficient livers is less stable to sonication, dialysis and treatment with metal chelators. The decrease in cytochrome P-450 and O-demethylase activity associated with dialysis could be prevented by the addition of ascorbic acid. The molar ratio of microsomal ascorbic acid to cytochrome P-450 (plus P-420) is in the order of 2:1. This ratio is maintained during ascorbic acid deficiency in liver and adrenal tissue, during dialysis, on storage and with a partial purification of the cytochrome, which suggests a close association between ascorbic acid and the cytochrome. In addition, ascorbic acid protects cytochrome P-450 and aniline hydroxy lase activity from inhibition by ferrous iron chelators such as alpha, alpha'-dipyridyl. The chelator binds to cytochrome P-450 and prevents formation of the reduced cytochrome P-450-CO spectrum; it in turn gives a reduced spectrum with the cytochrome at 450 nm. These studies suggest that there is an interaction between ascorbic acid and cytochrome P-450 involving the reduced form of the heme iron.

Animals↗
PubMed1969

The effect of scurvy on hexosamine-containing substances in healing wounds in guinea pigs.

1. Granulation tissue from healing tendonectomy wounds in guinea pigs was analysed and the effects of inanition and ascorbic acid deficiency on this tissue were investigated. 2. Inanition produced no significant effect on either the glucosamine or the galactosamine content of the tissue. Ascorbic acid deficiency decreased the galactosamine content without affecting the glucosamine content. 3. Fractionation of papain-digested granulation tissue gave three major fractions, which behaved respectively as glycopeptide, hyaluronic acid and a sulphated glycosaminoglycan mixture. At least half of the sulphated glycosaminoglycan mixture behaved as dermatan sulphate. 4. Inanition produced no consistent effect on the fractions examined. In ascorbic acid deficiency, a decrease in the sulphated glycosaminoglycan fraction was observed, which accounted for the decreased galactosamine content of the tissue. This was accompanied by a decrease in hyaluronic acid and a slight increase in the glycopeptide fraction.

Animals↗
PubMed2001

Hepatocyte transplantation using biodegradable matrices in ascorbic acid-deficient rats: comparison with heterotopically transplanted liver grafts.

BACKGROUND: Hepatocyte transplantation using polymeric matrices is under investigation as an alternative therapy for metabolic liver diseases. Long-term engraftment of hepatocytes in polymers has been demonstrated. However, the metabolic activity of hepatocytes in such devices has never been assessed in direct comparison with liver grafts. METHODS: Hepatocyte and partial liver transplantation were evaluated in the scurvy-prone osteogenic disorder Shionogi rat model. Biodegradable poly glycolic acid matrices seeded with hepatocytes equivalent to 20% of the recipient's liver mass, or 20% liver grafts were heterotopically transplanted into ascorbic acid- (AsA) deficient recipients. Recipients of cell-free matrices or AsA-deficient liver grafts served as controls. Recipients were set on AsA-free diet after transplantation. Plasma AsA levels, AsA concentrations in liver and adrenal gland tissue, and body weight ratios were assessed and H&E histology was performed. RESULTS: Recipients from the control groups showed symptoms of scurvy at 1 month after cessation of AsA supply. Hepatocyte transplantation and auxiliary liver transplantation prevented symptoms of scurvy and increased plasma and tissue AsA levels and body weight ratios. AsA levels in recipients of 20% liver grafts were comparable to normal control animals. CONCLUSIONS: Hepatocytes transplanted in polymeric matrices are able to compensate for liver-based metabolic deficiencies. Hepatocyte transplantation improves plasma AsA levels in AsA-deficient recipients. However, auxiliary liver grafts are superior to hepatocyte grafts in improving metabolic parameters. Further research work is needed to increase the efficiency of liver cell transplantation with regard to a clinical application.

Animals↗
PubMed1980

Vitamin C deficiency.

In a case of ascorbic acid deficiency, recognition of the characteristic cutaneous manifestations of this entity is often the first step in making a diagnosis. These features are perifollicular hemorrhages, intrafollicular keratosis and numerous coiled hairs. Treatment of the condition requires a thorough understanding of the precipitating medical and socioeconomic factors of the patient.

Ascorbic Acid Deficiency↗
PubMed1988

Deficiency of ascorbic acid in experimental diabetes. Relationship with collagen and polyol pathway abnormalities.

The plasma and tissue concentration of ascorbic acid (AA) is reduced in diabetes. This study was designed to investigate the mechanism and significance of this phenomenon. The low plasma AA concentration of diabetic rats can be normalized by dietary AA supplement (20-40 mg/day), a dosage approximately equal to the maximal synthetic rate of this substance in the rats. Treatment of diabetic rats with this regime prevented the decrease in activity of granulation tissue prolyl hydroxylase (PRLase), an AA-dependent enzyme required for maintaining the normal properties of collagen. The decreased plasma AA concentration and granulation tissue PRLase activity in diabetes can also be normalized by the aldose reductase inhibitor tolrestat. We conclude that in diabetic animals there is a true deficiency of AA that may be responsible for some of the changes of collagen observed in diabetes. Treatment with AA or an aldose reductase inhibitor may prevent some of the diabetic complications with underlying collagen abnormalities.

Aldehyde Reductase↗
PubMed2001

Generation and properties of ascorbic acid-deficient transgenic tobacco cells expressing antisense RNA for L-galactono-1,4-lactone dehydrogenase.

In higher plants, the terminal step of L-ascorbic acid (AsA) biosynthesis is catalyzed by the enzyme L-galactono-1,4-lactone dehydrogenase (EC 1.3.2.3, GalLDH). We generated AsA-deficient transgenic tobacco BY-2 cell lines by antisense expression of the GalLDH cDNA that was amplified from BY-2 cells using PCR. Two transgenic cell-lines, AS1-1 and AS2-2, having a marked expression of antisense RNA were analyzed. Antisense suppression of GalLDH mRNA led to a significant decline in the GalLDH activity. The AsA levels in the transgenic cell lines were found to be 30% lower than the wild-type BY-2 cells. In synchronous cultures, division of AS1-1 and AS2-2 cells was restrained with a concomitant decrease in mitotic index that was probably due to a decline in AsA levels. The rate of cell growth was also found to be less than that of the wild-type cells. Interestingly, there was a significant phenotypic difference between the transgenic and wild-type cells. The calli of AS1-1 and AS2-2 appeared to be sticky and soft. Back extrusion method also showed that AsA-deficient BY-2 callus was rheologically soft. Furthermore, microscopic analysis revealed that AS1-1 and AS2-2 cells were abnormally slender, suggesting a potential for a significant and a uni-axial elongation. Thus, we observed that decline in the AsA levels has an adverse effect on the division, growth and structure of a plant cell.

Ascorbic Acid↗
PubMed1980

Status of ascorbic acid in iron deficiency anaemia and thalassaemia.

The status of ascorbic acid was studied at the levels of platelet and leucocyte in 32 cases of iron deficiency anaemia, 35 cases of thalassaemia and 18 normal subjects. It was found that in iron deficiency anaemia, platelet ascorbic acid was significantly higher than normal values indicating tissue excess and came down sharply after treatment with iron. In thalassaemia, associated presumably with iron overload, ascorbic acid status of platelets was definitely lower than normal indicating tissue deficiency. Leucocytic level of ascorbic acid was not as good an index of ascorbic acid status as the platelet level.

Anemia, Hypochromic↗