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PubMed1995

Morphological differences in the skull of ascorbic acid-deficient ODS rats.

The physiological importance of ascorbic acid (AsA) in bone formation has been thought to be due mainly to its effects on collagen production and, consequently, matrix formation. However, effects of AsA deficiency on growing animals are poorly understood. The purpose of this experiment was to find how AsA deficiency affects craniofacial growth cephalometrically, and the periodontal ligament and the bone density of alveolar septum histologically. Five-week-old growing male rats with hereditary defects in AsA synthesis (ODS rats) placed on an AsA-deficient or minimally supplemented diet for 4 weeks showed a marked reduction in plasma AsA level and a negative or slight increment in body weight. Cephalometric evaluation revealed that craniofacial growth was influenced by AsA deficiency. Histological observations of periodontal structure and bone density in AsA-deficient animals showed no difference from controls, whereas the periodontal ligament of the upper first molar in the deficient animals was narrower than that of controls. These observations indicate that AsA deficiency reduces craniofacial size and the width of the periodontal ligament significantly in growing rats, whereas bone density is not affected. Thus, AsA, through collagen production, may be important to the increase in size of the craniofacial structures in growing animals.

Alveolar Bone Loss↗
PubMed1988

Effects of methamphetamine on central monoaminergic systems in normal and ascorbic acid-deficient guinea pigs.

Repeated injections (s.c.) of methamphetamine (METH) were administered to normal and ascorbic acid-deficient (scorbutic) guinea pigs to assess a potential role for ascorbic acid in the METH-induced effects in central monoaminergic systems. The ascorbic acid-deficient condition differentially influenced the METH-induced responses of dopaminergic and serotonergic variables in the striatum: drug-induced changes in dopaminergic variables were identical in normal and scorbutic animals; METH-induced decreases in serotonergic variables [tryptophan hydroxylase activity, serotonin (5-HT) and 5-hydroxyindoleacetic acid concentrations], however, were prevented in scorbutic animals. The scorbutic condition did not alter significantly the distribution of METH in the brain, nor were striatal concentrations of dopamine (DA) or 5-HT affected. In vitro, ascorbic acid increased significantly DA-mediated [3H]5-HT release from striatal slices, thus suggesting a potential role for ascorbate in DA-mediated actions of METH on serotonergic systems. Although supplemental ascorbate failed to restore the METH-induced serotonergic effects in scorbutic guinea pigs, these data suggest that, in a normal animal, the effects of multiple injections of METH, on serotonergic systems, involve ascorbic acid.

Amphetamine↗
PubMed1988

Airway responsiveness and prostaglandin generation in scorbutic guinea pigs.

Airway responsiveness to histamine aerosol and lung prostaglandin generation were investigated in normal, partially vitamin C deficient and scorbutic guinea pigs. The ascorbic acid content of the lung expressed as microgram/100 mg wet weight lung parenchyma decreased from 22.1 +/- 1.8 (mean +/- SE) in the control group to 9.0 +/- 1.4 and 1.8 +/- 0.4 in tissues from partially ascorbic acid deficient and scorbutic animals, respectively. Guinea pigs on low and ascorbic acid deficient diets developed significant airway hyperresponsiveness to histamine aerosol after 3 and 4 weeks. Indomethacin (30 mg/Kg, i.p.) further increased the airway hyperresponsiveness in scorbutic animals but was without effect in control animals. Prostaglandin generation from different parts of the lung was significantly changed by the diets. However, airway hyperresponsiveness was not directly attributable to altered prostanoid generation. Scorbutic conditions did not alter the electrophysiological characteristics of airway smooth muscle namely, resting membrane potential and electrogenic sodium pump activity. In summary, ascorbic acid deficiency causes airway hyperresponsiveness to histamine in guinea pigs. This alteration seems not to be related to an altered prostaglandin generation by the lung or to the electrophysiological properties of airway smooth muscle.

Aerosols↗
PubMed1979

Influence of dietary ascorbic acid on plasma lipid levels in the rainbow trout.

Rainbow trout maintained on ascorbic acid deficient and three grades of ascorbic acid supplemented diets (160--1280 mg ascorbic acid pr kg feed) for a period of 53 weeks, were studied for effects on plasma lipid levels. Fish fed the diet with no ascorbic acid manifested lethargy, lordosis, scoliosis, internal hemorrhages and low body weight. With regard to blood properties, ascorbic acid deficient fish had low hematocrit and high plasma levels of triglycerides and cholesterol but low level of free fatty acids. Plasma level of free fatty acids was low also in fish fed the diet containing the highest amount of ascorbic acid.

Administration, Oral↗
PubMed1990

Regulation of procollagen synthesis and processing during ascorbate-induced extracellular matrix accumulation in vitro.

Procollagen biosynthesis and matrix deposition were studied in long-term human skin fibroblast cultures exposed to ascorbic acid. Ascorbic acid specifically stimulated types I and III collagen synthesis, reaching a maximum at day 2 and maintaining a specific high rate of production until day 10 of ascorbate exposure, after which collagen production declined. The increased level of collagen synthesis after different exposure times could also be achieved by only brief treatment (10 h) of parallel scorbutic (ascorbic-acid-deficient) cultures with ascorbic acid. This brief exposure did not result in increased collagen mRNA, thus demonstrating that the ascorbate-induced increase in collagen synthesis at all stages of ascorbic acid exposure was due to post-transcriptional mechanisms, most likely a rapid increase in type 1 collagen mRNA translational efficiency. This mechanism, rather than the transcriptional activation, was the primary response and is adequate to explain the ascorbate-induced increase in collagen synthesis. These data also demonstrate that the presence of a collagenous extracellular matrix was not involved in this collagen biosynthetic regulation. During long-term exposure (18 days) to ascorbic acid, a substantial cross-linked collagenous matrix formed, following an approximately sigmoidal time course. The most rapid matrix deposition occurred during the later days of exposure when the rate of collagen synthesis was decreasing, suggesting that the presence of a pre-existing matrix is important for further collagen accumulation. Procollagen was also efficiently processed to collagen during this phase, demonstrating that efficient procollagen processing is an important regulatory event in collagen matrix deposition.

Ascorbic Acid↗
PubMed1974

Are recommended daily allowances for vitamin C adequate?

Recommended daily allowances, U.S.A., for ascorbic acid are several times the minimum daily requirement of about 10 mg to prevent clinical symptoms in adults. The recommended daily allowances reflect the levels of ascorbic acid required to produce tissue saturation in human beings, so that higher doses are promptly excreted in the urine. In various investigations, responses to ascorbic acid were not obtained under conditions where the intake was considerably lower than the recommended daily allowances, but higher than the level needed to prevent clinical symptoms of ascorbic acid deficiency. The human ascorbic acid requirement cannot be calculated by a linear extrapolation from guinea pigs per kg of body weight because guinea pigs are much smaller than human beings and, hence, their metabolism is more rapid per unit of body weight. Evolutionary loss of ascorbic-acid-synthesizing ability may be a neutral change that was incorporated by genetic drift.

Ascorbic Acid↗
PubMed1980

Activity of microsomal heme oxygenase in liver and spleen of ascorbic acid-deficient guinea pigs.

Hepatic heme oxygenase activity was significantly altered in vitamin C-deficient guinea pigs. It was increased two-fold after 14 days and was decreased by 20% after 21 days of deprivation of the vitamin (always in comparison with the control value). The apparent Km of the enzyme was also altered in the course of ascorbic acid deficiency. The data of hepatic heme oxygenase activity correspond to previous results on the metabolism of hepatic cytochrome P-450 in different stages of ascorbic acid deprivation. Splenic heme oxygenase activity decreased progressively arriving at 50% of the control value after 21 days of vitamin C omission, its apparent Km remained unaltered.

Animals↗
PubMed1990

Marked nitrosation by stimulation with lipopolysaccharide in ascorbic acid-deficient rats.

Marked formation of N-nitrosothioproline (N-nitrosothiazolidine-4-carboxylic acid) by stimulation with Escherichia coli lipopolysaccharide (LPS) was demonstrated in ascorbic acid-deficient mutant rats (osteogenic disorder syndrome rats; ODS rats) unable to synthesize ascorbic acid. The amounts of urinary nitrate and N-nitrosothioproline excretion after thioproline administration was measured in ODS rats with and without ascorbic acid supplement before and after the injection of LPS. LPS caused marked increase of urinary nitrate excretion in both groups. Urinary N-nitrosothioproline excretion increased 6-fold after LPS injection in ODS rats not supplied with ascorbic acid, but supplement with ascorbic acid markedly decreased the excretion of N-nitrosothioproline.

Adrenal Glands↗
PubMed1985

Experimental amyotrophic lateral sclerosis in the guinea-pig.

In guinea-pigs a diet which was deficient in ascorbic acid provoked neurogenic atrophy of the muscles, degeneration of the anterior horn motor cells and demyelination of the pyramidal tract. Muscles showed a decrease of cytochrome and cytochrome c oxidase. Subcutaneous haemorrhages were also found, particularly around the knee joints. The haemorrhages and the histopathology of the muscles and spinal cord were prevented by a high dosage of ascorbic acid. In animals with an ascorbic acid deficiency, histopathology of muscles and spinal cord were also prevented by L-cysteine, L-methionine and L-hydroxyproline. Subcutaneous haemorrhages were not prevented by these supplements.

Amyotrophic Lateral Sclerosis↗
PubMed2000

Identification of ascorbic acid-deficient Arabidopsis thaliana mutants.

Vitamin C (l-ascorbic acid) is a potent antioxidant and cellular reductant present at millimolar concentrations in plants. This small molecule has roles in the reduction of prosthetic metal ions, cell wall expansion, cell division, and in the detoxification of reactive oxygen generated by photosynthesis and adverse environmental conditions. However, unlike in animals, the biosynthesis of ascorbic acid (AsA) in plants is only beginning to be unraveled. The previously described AsA-deficient Arabidopsis mutant vtc1 (vitamin c-1) was recently shown to have a defect in GDP-mannose pyrophosphorylase, providing strong evidence for the recently proposed role of GDP-mannose in AsA biosynthesis. To genetically define other AsA biosynthetic loci, we have used a novel AsA assay to isolate four vtc mutants that define three additional VTC loci. We have also isolated a second mutant allele of VTC1. The four loci represented by the vtc mutant collection have been genetically characterized and mapped onto the Arabidopsis genome. The vtc mutants have differing ozone sensitivities. In addition, two of the mutants, vtc2-1 and vtc2-2, have unusually low levels of AsA in the leaf tissue of mature plants.

Arabidopsis↗
PubMed1979

Bile acid metabolism in ascorbic acid-deficient guinea pigs.

Sterol balance techniques have been used to determine the effect of short-term ascorbic acid (AA) deprivation on bile acid excretion in the guinea pig. The effects of a brief (2-week) AA deficiency on bile acid pool sizes and the activity of the rate controlling enzyme in bile acid biosynthesis have been determined. It was found that, while food intake and body weight were not affected by the short-term AA deficiency, liver AA levels had fallen to 25% of control levels. At the same time, the rate of excretion of bile acids and the size of the bile acid pool were both reduced by about 50% in guinea pigs deficient in AA. These results were supported by a decrease in the activity of cholesterol 7 alpha-hydroxylase in the deficient animals. It is concluded that an AA deficiency will significantly impair bile acid metabolism independent of any side effects of clinical scurvy.

Animals↗
PubMed1969

Studies in vivo on the biosynthesis of collagen and elastin in ascorbic acid-deficient guinea pigs.

1. After the administration of labelled proline to guinea pigs deprived of ascorbic acid for 15 days, the dorsal skin was examined 5 days later in an attempt to detect the presence of hydroxyproline-deficient collagen (protocollagen). The extent of incorporation of proline into skin collagens indicated a severe impairment of collagen synthesis. 2. A comparison of proline and hydroxyproline specific radioactivities in diffusible peptides obtained by treatment with collagenase of either purified skin collagens or direct hot-trichloroacetic acid extracts of skin failed to indicate the presence of protocollagen. Possible reasons for this are discussed. 3. The incorporation results did not indicate an inability of normal collagen, i.e. collagen hydroxylated to the normal degree, to cross-link in scurvy. 4. Incorporation of labelled proline into aortic elastin isolated from the same animals did not indicate a decrease in elastin biosynthesis in ascorbic acid deficiency, beyond that attributable to the inanition accompanying the vitamin deficiency. The proline/hydroxyproline specific-radioactivity ratio in elastin from scorbutic guinea pigs was about 6:1 in contrast with the 1:1 ratio in control groups. It is concluded that the formation of elastin hydroxyproline was ascorbate-dependent and that a hydroxyproline-deficient elastin is formed and retained in scurvy. The formation of desmosines was unimpaired in scorbutic animals. 5. Studies with chick embryos confirmed the formation of elastin hydroxyproline from free proline. Incorporation of free hydroxyproline into elastin hydroxyproline was negligible. 6. Digestion of solubilized samples with collagenase indicated that the hydroxyproline in guinea-pig aortic elastin preparations was not derived from contamination by collagen. It is suggested that most if not all of the hydroxyproline in the guinea pig elastin preparations investigated can be considered an integral part of the elastin molecule.

Animals↗
PubMed1994

Absorption of nonheme iron in ascorbic acid-deficient rats.

Prior studies have shown that the absorption of dietary nonheme iron in rats is much higher and less responsive to dietary variables than in human subjects. The aim of the present study was to determine whether this dissimilarity is explained by species differences in ascorbic acid status or metabolism. Iron absorption studies were performed with normal rats and with a genetic strain that lacks the ability to synthesize the vitamin. Ascorbic acid deficiency was produced in these animals by removing supplemental vitamin C from the diet for a brief period before the study. Iron absorption was measured from meals tagged extrinsically with 59Fe and measured by whole-body counting. We studied the effect on iron absorption of adding meat, ascorbic acid, soybean, tea, or bran to the test meal. A significant but modest effect of bran on iron absorption was observed in normal rats and of ascorbic acid and tea in ascorbate-depleted animals. However, the overall sensitivity of rats to dietary facilitators or inhibitors of nonheme iron absorption was not altered dramatically by ascorbic acid depletion. The relative insensitivity of rats to dietary factors affecting nonheme iron absorption in humans is not explained by differences in ascorbic acid metabolism between rats and humans.

Administration, Oral↗