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PubMed2002

Smokers--vitamin C--hypercholesterolaemia.

Cigarette smoking is one of the major public health problems of our times. Smokers are damaged by free radicals formed during smoking. The antioxidant capacity of smokers is reduced. Vitamin C (ascorbic acid) deficiency in heavy smokers with a total cholesterol more than 6.7 mmol/l ranges from 35-55%. It is mediated by smoking, by its low dietary intake by preferential high dietary intake of saturated and unsaturated fats. Vitamin C is an important water soluble antioxidant, therefore its intake can at least partially reduce the unfavourable effect of smoking caused by the attack of free radicals on the organism when smokers are unable to quit smoking.

Antioxidants↗
PubMed1968

The effect of scurvy on glycosaminoglycans of granulation tissue and costal cartilage.

1. The effect of ascorbic acid deficiency on glycosaminoglycans of granulation tissue and cartilage of guinea pigs was investigated by determination of the changes in the glucosamine and galactosamine contents 12 days after tendonectomy. 2. In normal granulation tissue, the glucosamine and galactosamine contents rose to a peak at 5 and 10 days respectively, whereas the hydroxyproline and proline contents continued to rise throughout the 20 days after tendonectomy. 3. The galactosamine in scorbutic granulation tissue, but not in that of pair-fed controls, decreased significantly in absolute amount and relatively to glucosamine, which remained practically unchanged; the cartilage galactosamine did not decrease during the 22 days of deficiency owing to the presence of excess of preformed galactosaminoglycans, which masked the small amount of newly formed glycosaminoglycans. 4. The chemical results were confirmed by radioactivity studies in vivo of incorporation of [U-(14)C]glucose into galactosamine and glucosamine of scorbutic granulation tissue and cartilage. The incorporation of (14)C into galactosamine decreased significantly in scurvy in both tissues. 5. The results indicated in both tissues a decreased formation of galactosamine during scurvy, although an increased degradation of polymerized glycosaminoglycans could not be entirely ruled out. It is concluded that, if lack of ascorbic acid causes an impaired galactosamine formation, the most likely position for the block may be in the UDP-N-acetylglucosamine 4-epimerase reaction.

Ascorbic Acid Deficiency↗
PubMed1978

L-Ascorbic acid and lysosomal acid hydrolase activities of guinea pig liver and brain.

The effects of L-ascorbic acid deficiency on guinea pig hepatic and brain lysosomal hydrolases were examined. In general, hepatic beta-N-acetylhexosaminidase, beta-D-glucoronidase, alpha-D-galactosidase, alpha-D-mannosidase, and acid phosphatase were elevated in scorbutic animals. This appears to be independent of the starved state. Brain beta-D-glucoronidase and acid phosphatase followed a similar pattern to that observed with the liver enzymes, but brain beta-N-acetylhexosaminidase was not affected by L-ascorbic acid decreased the activity of hepatic beta-N-acetylhexosaminiadase was unaffected by dietary treatments although the activity of beta-N-acetylhexosaminidase A tended to increase in the scorbutic animals. Subcellular fractions were obtained from the three groups of animals and the recoveries of protein, beta-N-acetylhexosaminidase, and glucose-6-phosphatase estimated.

Acid Phosphatase↗
PubMedDate not supplied

[Effect of amino acid imbalance and ascorbic acid deficit on the carcinogenic effect of N-nitrosopiperidine].

A study was made of the effect of ascorbic acid deficiency and low levels of lysine, methionine and threonine on the cancerogenic effect of nitrosopiperidine which was fed to guinea-pigs with drinking water in a single dose of 4.25 mg/kg bw. Deficiency of the nutrients given alone or especially in combination speeded up the growth tumors induced by the cancerogenic agent. A possibility of inducing esophageal tumors in guinea-pigs has been demonstrated for the first time.

Amino Acids↗
PubMed1995

[Etiology of the cribra orbitalia: effect of amino acid profile in bone collagen and the iron content of bone minerals].

As long as cribra orbitalia manifests itself as an isolated skeletal lesion in excavated human skeletons, it is mostly diagnosed as being of nutritional origin, especially iron deficiency anemia. Since both iron and vitamin C function as cofactors at the hydroxylation of the amino acids proline and lysine in collagen, both amino acid analyses of bone collagen and the determination of bone mineral iron content was carried out at ten medieval skeletons with cribra orbitalia, opposed to ten morphologically healthy individuals from the same skeletal series. The skeletons with cribra orbitalia were significantly depleted with respect to OHpro (the OHpro/Pro-ratio being 16.9% lower than in the control group), but did not differ from the healthy individuals with respect to OHlys and iron content. No correlation was found between proline hydroxylation and age at death or degree of the disease. The data do not support the iron deficiency hypothesis. Most probably, vitamin C deficiency was responsible for the difference between diseased and morphologically healthy individuals. A combination of protein and elemental analysis of excavated bones should thus be suitable for the detection of deficient hydroxylation and its etiology: iron or vitamin C deficiency.

Amino Acids↗
PubMed1997

[Correlations between cribra orbitalia, archeometric findings on the skeleton and habitat conditions].

The interpretation of cribra orbitalia as an isolated skeletal lesion is mainly based on malnutrition, in particular in terms of iron deficiency or vitamin C deficiency. A chronic iron deficiency anemia should result in both a reduced iron content of the skeleton and an underhydroxylation of the amino acid proline with the consequence of a less stable collagen matrix of the bone. The latter holds also for a vitamin C deficiency. Trace element and amino acid analyses were independently applied to subsamples of two early medieval human skeletal series to test whether a relation between cribra orbitalia and skeletal iron content and amino acid hydroxylation was detectable. For one of these series (Nusplingen, district Balingen, Schwäbische A1b), habitat specific properties have already been assumed to be responsible for an insufficient iron supply of the inhabitants. Both archaeometric approaches led to a verification of the malnutrition hypothesis, but for advanced states of the skeletal lesion only. Less affected individuals did not reveal any of the expected relationships. Possible adaptive subsistence strategies are discussed which might compensate for such unfavourable living conditions.

Amino Acids↗
PubMed1985

Glucose inhibits cellular ascorbic acid uptake by fibroblasts in vitro.

It has been suggested earlier that the local deficiency of ascorbic acid in tissues could be responsible for development of various angiopathies in diabetes. Hyperglycemia is one of the factors which could contribute considerably to the development of local ascorbic acid deficiency. Therefore, the effect of glucose on uptake of L-[1-14C] ascorbic acid by fibroblasts was studied in vitro. The data clearly show that ascorbic acid uptake is inhibited instantly by glucose in a concentration dependent fashion. The results support the contention that local ascorbic acid deficiency in tissues could be a natural consequence of hyperglycemia of whatever cause. The rate of ascorbic acid uptake under various conditions suggests that additional supplements of ascorbic acid might be helpful to individuals in averting deleterious effects of hyperglycemia on tissue ascorbic acid supply.

Animals↗
PubMed1986

Treatment of a metabolic disease, scurvy, by administration of the missing enzyme.

Reaction of immunoprecipitated L-gulonolactone oxidase with glutaraldehyde allows multiple administrations of large amounts of this enzyme extracted from either chicken or rats to guinea pigs. L-Gulonolactone oxidase converts L-gulonolactone to ascorbic acid, and its absence from guinea pigs and primates results in their requirement for this vitamin. By administration of this enzyme guinea pigs are able to survive on an ascorbic-acid-deficient regimen.

Animals↗
PubMed1992

Testosterone production in mature scorbutic mutant rats unable to synthesize ascorbic acid.

The effect of a deficiency of ascorbic acid (AsA) on in-vivo testosterone production in mature male rats was investigated using a mutant strain of rats (ODS rats) unable to synthesize AsA. Male 60-day-old rats were fed AsA-deficient lab chow for 28 days with [ODS(+)] or without [ODS(-)] AsA supply. The AsA levels in the liver of ODS(-) rats were undetectable and those in the testes decreased to about 25% of those in ODS(+) rats by day 28. Plasma LH levels in ODS(-) rats decreased to about 30% of those in ODS(+) rats by day 28. However, there were no significant differences in the plasma levels of testosterone, or in the relative weights of seminal vesicles and ventral prostates between ODS(+) and ODS(-) rats. Plasma levels of testosterone in ODS(-) rats after a single injection of 200 IU hCG changed similarly to that in ODS(+) rats. The metabolic clearance rate of testosterone was also the same at 60 min after an intravenous injection of [3H]testosterone in both groups. These results indicate that AsA-deficiency in adult rats causes no significant change in basal plasma levels of testosterone or in the response to hCG, despite decreased plasma LH levels.

Animals↗
PubMed1991

Vitamin C: newer insights into its biochemical functions.

Ever since the discovery of vitamin C (ascorbic acid), scientists have been intrigued as to how ascorbic acid deficiency can lead to the diverse symptoms exhibited in scurvy. Only in recent years has it been appreciated that ascorbic acid has important functions in many cellular reactions and processes in addition to its role in collagen synthesis. The few such reactions that are understood at the molecular level make it apparent that ascorbic acid does not directly participate in enzyme-catalyzed conversion of substrate to product. Instead, the vitamin regenerates prosthetic metal ions in these enzymes in their required reduced forms. This is in agreement with other antioxidant functions of vitamin C, e.g., scavenging of free radicals. Ascorbate and other antioxidant nutrients are presumed to play a pivotal role in minimizing the damage from oxidative products, including free radicals. This protective function is twofold: the already-oxidized groups in prosthetic centers of enzymes are reduced and the oxidants and free radicals are removed.

Animals↗
PubMed1997

Less induced 1-methyl-4-phenylpyridinium ion neurotoxicity on striatal slices from guinea-pigs fed with a vitamin C-deficient diet.

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.

1-Methyl-4-phenylpyridinium↗
PubMed2002

Differences in the accumulation of ascorbic acid in normal, myeloperoxidase deficient and NADPH-oxidase deficient granulocytes.

Granulocytes contain large quantities of ascorbic acid (AA). The uptake mechanism is mainly restricted to the accumulation of the oxidized form, dehydroascorbate (DHA). We investigated the uptake of ascorbic acid and dehydroascorbate of normal, myeloperoxidase (MPO)-deficient, and NADPH-oxidase-deficient granulocytes. The accumulation of ascorbic acid was increased in all types of granulocytes after stimulation with phorbol-myristate-acetate, whereas the NADPH-oxidase-deficient cells showed a decreased uptake compared to normal and MPO-deficient cells. The intracellular concentration of ascorbic acid was further enhanced after incubation of granulocytes with DHA, most prominently in NADPH-oxidase-deficient granulocytes. MPO-deficient granulocytes are not able to produce HOCl after activation. The granulocytes of one individual with total MPO deficiency accumulated ascorbate in higher concentrations than did cells with partial MPO deficiency, indicating that HOCl is of minor importance for the oxidation of ascorbate. Since the ability of MPO-deficient cells to kill microorganisms is pronounced in contrast to NADPH-oxidase-deficient cells, effective mechanisms of compensating for the absence of HOCl must exist. We hypothesize that the enhanced uptake of ascorbic acid combined with an enhanced superoxide anion production may favor the generation of OH radicals via the Fenton reaction.

Antioxidants↗
PubMed1982

Ascorbic acid in lymphocytes: cell preparation and liquid-chromatographic assay.

Measurements of ascorbic acid concentration in leukocytes by "high-performance" liquid chromatography (HPLC) provides better nutritional assessment, leading to better management, particularly of presymptomatic and critically ill patients. This procedure includes a simple, reproducible cell-separation technique that requires no more than 2 mL of whole blood. Cell populations are separable with greater than 95% purity and greater than 99% viability. Ascorbic acid is assayed by HPLC. The vitamin can be reproducibly quantified in concentrations as low as 0.1 microgram/mL of cell extract. The chromatographic procedure is very rapid, analysis being completed within 15 min after specimen preparation. The assay is suitable also for urine and protein-free filtrates of plasma and of other biological materials. Reference intervals for plasma, mononuclear leukocytes, and polymorphonuclear leukocytes were established. A preliminary clinical evaluation revealed that hospital patients were at a greater risk of ascorbic acid deficiency than expected.

Ascorbic Acid↗
PubMed1975

Alleviating mortality associated with a vitamin E-selenium deficiency by dietary ascorbic acid.

Adding ascorbic acid to a practical ration deficient in vitamin E and selenium for the growing duck substantially reduced associated mortality. The continued appearance of various myopathies but absence of vascular faults supported implication of a reduced de novo ascorbate synthesis as part of the syndrome. Presumably, alleviation of this induced secondary inadequacy with its more lethal pathology was the primary reason for the lower death rate.

Animal Feed↗
PubMed1990

Role of the liver in carnitine metabolism: the mechanism of development of carnitine-deficient status in guinea-pigs.

It was shown that carnitine deficiency and an impairment of the conversion of butyrobetaine into carnitine develops not only in ascorbic acid-deficient guinea-pigs but also in partially starved animals. We propose that the same mechanism, an absolute or relative ascorbic acid deficiency, is operating in both nutritional states. An increased urinary excretion greatly contributes to the development of carnitine deficiency in guinea-pigs, both in ascorbic acid deficiency and starvation. With respect to the greatly increased excretion, guinea-pig carnitine deficiency resembles the human disorder and may serve as model for it.

Animals↗