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PubMed1975

The collagen content of skin and gingival tissues in ascorbic acid-deficient monkeys.

Five green monkeys were used in this study. Three animals were fed a scorbutigenic diet and the remaining two served as controls. Biopsies were dissected from the vestivular gingiva and dorsal skin and polyvinyl sponges were implanted subcutaneously during 4 week periods throughout the experimental period. The animals were sacrificed after 12 weeks and the periodontal ligament was removed. Collagen extracts were prepared from the gingival and granulation tissues and treated with bacterial collagenase. Following acid hydrolysis the total amount of proline and hydroxyproline was determined in various tissue preparations. In the tissues examined, the content of hydroxyproline decreased in the scorbutic animals throughout the experimental period. The decrease in the hydroxyproline content of the gingiva started within the first 4 weeks and was faster than that of the skin, indicating that the extent of decrease is dependent of the turnover rate of the collagen in the tissues. The synthesis of hydroxyproline was almost totally impaired in the granulation tissue formed in the sponges implanted after the 8th week of experimentation. Collagenase treatment of collagen extracts resulted in a release of proline and hydroxyproline in a higher ratio in extracts from the experimental animals than in extracts from the controls. It is concluded that ascorbic acid is a prerequisite for the maintenance of the collagen pool in the tissues and that lack of this vitamin results in the formation of a collagenase degradable protein fraction with a low hydroxyproline content.

Animals↗
PubMed2005

Spontaneous fractures in the mouse mutant sfx are caused by deletion of the gulonolactone oxidase gene, causing vitamin C deficiency.

UNLABELLED: Using a mouse mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation, reduced bone formation, and development of spontaneous fractures. INTRODUCTION: A major public health problem worldwide, osteoporosis is a disease characterized by inadequate bone mass necessary for mechanical support, resulting in bone fracture. To identify the genetic basis for osteoporotic fractures, we used a mouse model that develops spontaneous fractures (sfx) at a very early age. MATERIALS AND METHODS: Skeletal phenotype of the sfx phenotype was evaluated by DXA using PIXImus instrumentation and by dynamic histomorphometry. The sfx gene was identified using various molecular genetic approaches, including fine mapping and sequencing of candidate genes, whole genome microarray, and PCR amplification of candidate genes using cDNA and genomic DNA as templates. Gene expression of selected candidate genes was performed using real-time PCR analysis. Osteoblast differentiation was measured by bone marrow stromal cell nodule assay. RESULTS: Femur and tibial BMD were reduced by 27% and 36%, respectively, in sfx mice at 5 weeks of age. Histomorphometric analyses of bones from sfx mice revealed that bone formation rate is reduced by >90% and is caused by impairment of differentiated functions of osteoblasts. The sfx gene was fine mapped to a 2 MB region containing approximately 30 genes in chromosome 14. By using various molecular genetic approaches, we identified that deletion of the gulonolactone oxidase (GULO) gene, which is involved in the synthesis of ascorbic acid, is responsible for the sfx phenotype. We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. Treatment of bone marrow stromal cells derived from sfx/sfx mice in vitro with ascorbic acid increased expression levels of type I collagen, alkaline phosphatase, and osteocalcin several-fold. CONCLUSION: The sfx is a mutation of the GULO gene, which leads to ascorbic acid deficiency, impaired osteoblast cell function, and fractures in affected mice. Based on these and other findings, we propose that ascorbic acid is essential for the maintenance of differentiated functions of osteoblasts and other cell types.

Animals↗
PubMed1978

Detection and incidence of B and C vitamin deficiency in alcohol-related illness.

The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness. The incidence of thiamine deficiency was 31% as assessed by the activation of transketolase, and 55% as assessed by the pyruvate tolerance test. The incidence of riboflavin deficiency was 23% and of ascorbic acid deficiency 91%. No cases of pyridoxine deficiency were detected. The pyruvate tolerance test was found to be a more sensitive test of thiamine deficiency than the transketolase activation, and the activation of red blood cell aspartate transaminase was found to be a poor indicator of pyridoxine deficiency. There was a poor correlation of the gamma-glutamyl transferase activity with the degree of vitamin deficiency, suggesting that alcohol exposure is only partly responsible for the observed vitamin deficiency.

Adult↗
PubMed2002

Effect of dietary administration of Lathyrus sativus pulse on intestinal biochemical parameters in normal and scorbutic guinea pigs.

OBJECTIVE: In order to investigate that ascorbic acid deficiency is responsible for lathyrus toxicity, the effect of dietary feeding of lathyrus pulse in normal and scorbutic guinea pigs for 3 months, on intestinal biochemical parameters was undertaken. METHODS: The intestinal brush border membrane (BBM) marker and xenobiotic metabolising enzymes (XME) were assayed. RESULTS: Exposure to 80% lathyrus alone and in scorbutic conditions showed significant inhibition of alkaline phosphatase (28%-30%), sucrase (19%) and gamma-glutamyl transpeptidase (GGT) (15%-27%) enzymes, while Ca(2+)-Mg(2+)-ATPase was significantly inhibited (38%) in scorbutic plus lathyrus treated group. The phase I XME (AHH) remained unchanged while the phase II enzyme glutathione-S-transferase (GST) was significantly decreased (20%-22%) in lathyrus and scorbutic plus lathyrus treated groups. Quinone reductase (QR) activity was found to be significantly decreased in lathyrus exposed group (20%). The intestinal biomarker contents including hexose (25%-34%) and phospholipids (20%-40%) were significantly reduced in lathyrus and scorbutic plus lathyrus exposed animals, while sialic acid showed a significant decrease (28%) in scorbutic plus lathyrus treated group. However, cholesterol levels were significantly enhanced (15%-28%) in lathyrus and scorbutic plus lathyrus treated animals. CONCLUSION: The results indicate that oral feeding of lathyrus pulse to guinea pigs can alter BBM parameters as well as XME, which may result in the intestinal toxicity. Further, ascorbic acid deficiency could be one of the pre-disposing factors of lathyrus toxicity.

Administration, Oral↗
PubMed1998

Impaired expression of noncollagenous bone matrix protein mRNAs during fracture healing in ascorbic acid-deficient rats.

In scorbutic patients, fractures are slow to heal because of impaired collagen synthesis. To investigate the influence of impaired collagen synthesis on the differentiation and proliferation of osteogenic and chondrogenic cells, we examined the expression of genes encoding bone matrix proteins, including osteonectin (ON), osteopontin (OPN), osteocalcin (OC), and matrix Gla protein (MGP), as differentiation markers for osteogenic and chondrogenic cells during fracture healing in Osteogenic Disorder Shionogi (ODS) rats, which have a hereditary defect in the ability to synthesize ascorbic acid (Asc). In ODS rats without Asc supplementation, intramembranous ossification was completely inhibited. Although a few fibroblast-like cells expressing ON mRNA were observed, no OPN mRNA-expressing cells were detected. During endochondral ossification, a small amount of metachromatic staining cartilage appeared at the fracture site, but there was no provisional calcification zone in the cartilage. Chondrocytes expressed ON and MGP mRNAs, but not OPN mRNA. When Asc was given to these rats, callus formation was soon detected around the fracture site, while OPN mRNA was expressed by differentiated osteoblasts and hypertrophic chondrocytes. Our data indicate that impaired collagen synthesis due to Asc deficiency inhibited the increase of ON and MGP mRNA-expressing cells as well as the appearance of OPN mRNA-expressing cells. Since OPN is considered to play an important role in normal and pathological mineralization, lack of OPN mRNA expression accompanying impaired collagen synthesis may have a role in defective mineralization and delayed fracture healing in scurvy.

Animals↗
PubMed1995

Sperm quality and ascorbic acid concentration in rainbow trout semen are affected by dietary vitamin C: an across-season study.

High concentrations of ascorbic acid occur in scurvy-prone, teleost fish plasma. We quantified seasonal relationships between 1) dietary level of vitamin C and level of seminal plasma ascorbic acid, and 2) seminal plasma ascorbic acid concentration and sperm quality, in rainbow trout (Oncorhynchus mykiss). We maintained six groups of 2-yr-old rainbow trout on diets supplemented with 0, 30, 110, 220, 440, and 870 ppm ascorbyl monophosphate beginning in May 1992. Sperm were produced during the end of October 1992 through April 1993; we collected milt 13 times from 3-8 fish per treatment. We quantified ascorbic acid concentration in seminal plasma, and sperm concentration, motility, and weight. Seminal plasma ascorbic acid concentrations were affected directly by the ascorbyl monophosphate level in the diet. Seminal plasma ascorbic acid concentrations also were affected by season. Ascorbic acid deficiency did not influence semen quality (sperm concentration and motility) at the beginning of the spawning season. However, sperm concentration and motility in a group fed an ascorbic acid-free diet declined during the period of study. Ascorbic acid deficiency reduced both sperm concentration and motility, and thus fertility, of rainbow trout. These results indicate that vitamin C is important for male fish reproduction; the dietary requirement for seminal plasma ascorbic acid saturation exceeds that for optimum growth.

Animals↗
PubMedDate not supplied

Physiological role of dehydroascorbic acid.

Dehydroascorbic acid is present in insignificant amounts in plant and animal tissue but appears in considerable amounts under various physiological and pathological conditions. It is found increased: in blood of patients suffering from infectious diseases; in blood and tissues of thyrotoxic patients; in blood after injection of thyroxin, corticotropin and cortisone. In all the above conditions there is concomitant decrease in L-ascorbic acid and glutathione values of blood and tissues. Dehydroascorbic acid, however, disappears after continued administration of a high dose of ascorbic acid. The accumulation of dehydroascorbic acid seems to be an indication of ascorbic acid deficiency. The extreme sensitivity of the ascorbate system to physiological changes is suggestive of a major biochemical role for this redox system. Accumulated evidences indicate that dehydroascorbic acid possible control cell division.

Animals↗
PubMed1984

A direct correlation between the levels of ascorbic acid and H2O2 in aqueous humor.

There is evidence that H2O2 present in aqueous humor arises from ascorbic acid which is also present in this fluid, but the extent to which peroxide is derived from ascorbic acid is not known. We have measured the concentrations of H2O2 and ascorbic acid normally present in the aqueous humor of various species and also under conditions in which the level of ascorbic acid in the fluid was experimentally altered. In aqueous humor of rabbit and guinea pig the concentration of ascorbic acid was 10 times higher than that present in aqueous of rat and frog. Similarly, the concentration of H2O2 was four to 10 times higher in rabbit and guinea pig aqueous compared to that in rat and frog. Consistent with the higher concentration of ascorbic acid in posterior compared to anterior aqueous humor in the rabbit, the concentration of H2O2 was also significantly higher in the posterior aqueous. When ascorbic acid in rabbit aqueous humor was elevated by intraperitoneal administration of the compound, there was a significant increase in the level of H2O2 in both anterior and posterior aqueous humor. Moreover, when the level of ascorbic acid was lowered experimentally by placing guinea pigs on an ascorbic acid deficient diet, a 10-fold decrease in the level of both ascorbic acid and H2O2 was observed in the aqueous humor. Upon returning the animals to a normal diet, the concentrations of both compounds returned to control values. The direct correlation between the concentrations of ascorbic acid and H2O2 in aqueous humor suggests that ascorbic acid is the primary source of H2O2 in this fluid.

Animals↗
PubMed1980

Leukocyte ascorbic acid and its relationship to coronary artery disease in man.

The ascorbic acid level of the leukocytes in patients with coronary artery disease was compared to the ascorbic acid level of the leukocytes in patients without coronary artery disease as demonstrated by coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary atherosclerosis (P < 0.001). There was also significant difference in the leukocyte ascorbic acid levels among patients with abnormal coronary arteriograms who smoked compared to those who did not. The anatomical changes secondary to atherosclerotic disease, and mainly those changes related to the ground substance, have been shown to be the changes that have been observed in patients with ascorbic acid deficiency. From the present study, with its limitations, it is suggested that ascorbic acid may play a role in the pathogenesis of atherosclerosis, and although not implicated as an etiological factor in coronary artery disease, it suggests that a closer look at its possible role in the pathogenesis and progression of coronary artery disease is warranted.

Adult↗
PubMed1986

Effects of estrogen and progestogen on the ascorbic acid status of female guinea pigs.

Female, adult guinea pigs were fed a low ascorbic acid diet ad libitum. Oral administrations of either estinyl (5 micrograms) or progestogen (250 micrograms) in combination with 5 mg of ascorbic acid (minimum requirement) daily for 21 d, resulted in significantly lower (P less than 0.05) concentrations of ascorbic acid in plasma, liver, adrenals and urine than in animals receiving only 5 mg of the vitamin. None of these animals showed any clinical signs of ascorbic acid deficiency. Clinical manifestations of scurvy were exhibited, however, when animals receiving no ascorbic acid supplement were treated with the steroid hormones for 7 d. All of these animals died by d 10. On the other hand, the animals receiving neither ascorbic acid nor the steroids remained free from any signs of scurvy, except one (out of six), which died by d 12. In vitro studies revealed a markedly higher rate of oxidation of ascorbic acid in the presence of either estinyl or progestogen than in untreated controls. These results were further supported by a higher level of plasma ceruloplasmin in animals receiving a combination of estrogen and progestogen than in animals receiving no hormones. An in vivo dose-related effect of ascorbic acid indicated that the steroid-mediated lowering effect of the vitamin status could be counteracted by increasing the dose of ascorbic acid from 5 to 10 mg/d for 2 wk. These results suggest that the interactions between oral contraceptive hormones and ascorbic acid may be of clinical importance only in the case of borderline intake of the vitamin.

Adrenal Glands↗
PubMed1992

Dietary ascorbic acid depresses plasma and low density lipoprotein lipid peroxidation in genetically scorbutic rats.

The effects of dietary ascorbic acid on plasma lipoprotein and liver lipid peroxide concentrations were examined using ODS od/od rats with a genetic defect in the ability to synthesize ascorbic acid. ODS od/od rats were fed purified diets supplemented with 0 to 300 mg ascorbic acid/kg diet for 21 d. An ascorbic acid-free diet induced body weight loss, depleted ascorbic acid in the plasma and increased thiobarbituric acid-reactive substances in the plasma and liver as compared with rats fed ascorbic acid supplemented diets and with normal ODS +/+ rats fed the ascorbic acid-free diet. Increasing ascorbic acid concentration in the diet inhibited the development of these ascorbic acid deficiency symptoms in a dose-dependent manner. The dietary requirement of ascorbic acid to maintain normal body weight gain and plasma lipid peroxide concentrations was approximately 150 mg ascorbic acid/kg diet. On the other hand, even 300 mg ascorbic acid/kg diet was insufficient to maintain a hepatic concentration of ascorbic acid comparable to that in the liver of ODS +/+ rats. The lipid peroxide concentration in plasma LDL and liver was significantly elevated in ODS od/od rats fed the ascorbic acid-free diet. Supplementing the diet with 300 mg ascorbic acid/kg kept those concentrations within the normal ranges seen in the ODS +/+ rats.

Animals↗
PubMed1959

Studies on the formation of collagen. IV. Effect of vitamin C deficiency on the neutral salt-extractible collagen of skin.

The skin of severely scorbutic guinea pigs which were losing weight contained no detectible neutral salt-extractible collagen. Conditions of growth (weight gain) which actively induced the formation of neutral salt-extractible collagen in the skin of normal guinea pigs failed to do so in the animal with ascorbic acid deficiency. No excess of non-collagenous proline was found in neutral salt extracts of scorbutic skin as compared with normal. Fractionation of these extracts failed to reveal the presence of significant amounts of a soluble component containing unusual proportions of glycine and proline relative to hydroxyproline. It is concluded that deficiency of ascorbic acid either interferes with the synthesis of new collagen in intact skin or causes its destruction and removal as rapidly as it is produced.

Animals↗
PubMed1976

The effect of certain vitamin deficiencies on hepatic drug metabolism.

There is increasing evidence that the liver microsomal drug metabolizing system is affected by various vitamins such as ascorbic acid, riboflavin, and alpha-tocopherol. In regard to ascorbic acid deficiency there is a decrease in the quantity of hepatic microsomal electron transport components such as cytochrome P-450 and NADPH-cytochrome P-450 reductase, as well as decreases in a variety of drug enzyme reactions such as N-demethylation, O-demethylation, and steroid hydroxylation. In addition, young animals given high supplements of vitamin C have increased quantities of electron transport components and overall drug metabolism activities. Kinetic studies indicate no change in the apparent Km of N-demethylase, O-demethylase or hydroxylase for drug substrates in animals depleted or given high amounts of the vitamin. However, there are qualitative changes in both type I and II substrate-cytochrome P-450 binding. Ascorbic acid is not involved in microsomal lipid peroxidation or in any qualitative or quantitative change in phosphatidylcholine. Replenishing vitamin C-deficient animals with ascorbic acid required 3 to 7 days for the electron transport components and drug metabolism activities to return to normal levels. Induction with phenobarbital and 3-methylcholanthrene is not impaired in the deficient animal since drug metabolism activities are induced to the same extent as normal controls; however, the administration of delta-aminolevulinic acid, a precursor of heme synthesis, to deficient animals caused an increase in the quantity of cytochrome P-450. The effects of riboflavin deficiency on electron transport components and drug metabolism activities have been noted only in adult animals after prolonged periods of deficiency. Decreases in drug metabolism activities occur with both type I (aminopyrine and ethylmorphine) and type II (aniline) substrates. As was found with ascorbic acid deficiency, drug enzyme induction occurred to the same extent with phenobarbital in deficient and normal animals. In addition, it required from 10 to 15 days for the drug metabolism activities to return to normal levels when deficient animals were replenished with riboflavin. The effect of vitamin E on drug metabolism is specific in N-demethylase activities decrease while O-demethylase activities are not affected in the deficient state. This vitamin differs from ascorbic acid and riboflavin in that several laboratories have reported no quantitative decrease in cytochrome P-450, although there are some reports that it and delta-aminolevulinic acid dehydratase are lowered quantity of cytochrome in E-deficient animals. The effect of vitamin E, if any, on the P-450 is unresolved; an important question that requires further clarification. As with ascorbic acid there is no difference in the apparent Km of N-demethylase enzymes for varous substrates and the protective effect of vitamin E does not appear to be one of an antioxidant inhibiting microsomal lipid peroxidation.

Animals↗
PubMed1985

Macrophage functions in aging: effects of vitamin C deficiency.

Groups of young adult and senescent guinea pigs were fed normal and vitamin C deficient diets for 4 weeks and tested for their peritoneal macrophage functions. Serum levels of vitamin C in deficient animals indicated a progressive state of ascorbic acid deficiency and correlated well with the clinical signs and symptoms of scurvy. Fewer macrophages were obtained from the peritoneal cavities of deficient animals and morphologically they were smaller in size. Adverse effects of vitamin C deficiency were enhanced in aged animals. Significantly greater number of aged animals died by 4 weeks of deficiency. Deficient senescent animals had greater decline in macrophage random migration and bactericidal capacity. Following phagocytic stimuli, superoxide anion generation also significantly decreased. Data suggest that vitamin C deficiency might affect macrophage functions in the aged more profoundly and could compromise parameters of host defenses effective against microbial infections.

Aging↗
PubMed1976

Macrophage function in vitamin C-deficient guinea pigs.

Guinea pigs were fed a vitamin C-deficient diet and at various time periods thereafter their peritoneal cells were tested for biological activity. The serum levels of vitamin C in the deficient animals indicated a progressive state of ascorbic acid deficiency with time and this correlated well with clinical signs and symptoms of scurvy. Fewer macrophages were obtained from the peritoneal cavities of deficient animals and in structural appearance under the phase contrast and light microscope they were smaller in size. They showed no significant impairment in phagocytosis of bacterial cells. The macrophages, however, exhibited significantly reduced migration on glass as compared to the normal cells. In vitro addition of vitamin C partially reversed this reduced migration.

Animals↗
PubMed1992

Cellular ascorbate depletion in healthy men.

To clarify the relationship of plasma ascorbic acid to cellular ascorbic acid levels, we determined plasma, lymphocyte, buccal cell and semen ascorbic acid in eight healthy men consuming controlled ascorbic acid intakes of 5, 10, 20, 60 or 250 mg/d over 13 wk while living in a metabolic unit. Levels of ascorbic acid in all four specimen types were significantly lower during the three lowest intakes (5, 10, or 20 mg/d) compared with the 60 or 250 mg/d intakes, but only plasma and lymphocyte ascorbic acid levels discriminated between these intakes unequivocally and with no overlap. Priority for maintenance of intracellular lymphocyte ascorbic acid was indicated by rapid repletion of lymphocytes compared with plasma and semen at 60 mg/d intake. Strong correlations of plasma with lymphocyte ascorbic acid within individuals indicated that plasma levels would reliably reflect low lymphocyte levels in nutrition monitoring surveys. Buccal cell ascorbic acid may be useful as a noninvasive screening test for ascorbic acid deficiency. Semen and sperm qualities were unchanged despite an average decline in semen ascorbic acid to 24% of baseline. Short-term ascorbic acid depletion in healthy men did not adversely affect sperm qualities related to fertility nor did moderate supplementation improve them.

Adult↗