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PubMedDate not supplied

Biological function of ascorbic acid and the pathogenesis of scurvy: a working hypothesis.

This communication advances the proposal that all the diverse manifestations of scurvy can be attributed to depolymerisation of ground substance glycosaminoglycans brought about by exposure to uninhibited cellular hyaluronidase. It suggests that ascorbic acid exerts its prime biological function indirectly by incorporation into a glycosaminoglycan residue to form the physiological hyaluronidase inhibitor. The therapeutic implications of this working hypothesis are briefly discussed.

Ascorbic Acid↗
PubMed1981

Vitamin C, titrating to bowel tolerance, anascorbemia, and acute induced scurvy.

A method of utilizing vitamin C in amounts just short of the doses which produce diarrhea is described (TITRATING TO BOWEL TOLERANCE). The amount of oral ascorbic acid tolerated by a patient without producing diarrhea increase somewhat proportionately to the stress or toxicity of his disease. Bowel tolerance doses of ascorbic acid ameliorate the acute symptoms of many diseases. Lesser doses often have little effect on acute symptoms but assist the body in handling the stress of disease and may reduce the morbidity of the disease. However, if doses of ascorbate are not provided to satisfy this potential draw on the nutrient, first local tissues involved in the disease, then the blood, and then the body in general becomes deplete of ascorbate (ANASCORBEMIA and ACUTE INDUCED SCURVY). The patient is thereby put at risk for complications of metabolic processes known to be dependent upon ascorbate.

Administration, Oral↗
PubMed1996

Scurvy results in decreased collagen synthesis and bone density in the guinea pig animal model.

The effect of severe ascorbic acid deficiency on bone remodeling and collagen synthesis was evaluated in a 21 day experiment, using the scorbutic guinea pig model. Animals (n = 6-7/group) were assigned to one of three groups: scorbutic, pair-fed ascorbic acid-replete, or ad libitum ascorbic acid-replete groups. After 2 weeks, scorbutic animals started voluntarily decreasing food intake and losing weight. By day 19-21, at which time bone and tissue samples were collected and analyzed, scorbutic animals decreased food intake to 46% of usual and lost 9% body weight. Serum 25OHD3, 1,25(OH)2D3, calcium, and albumin were significantly lower (p < 0.05) in the scorbutic animals than in the other groups. Bone mineral density and bone mineral content of the proximal and central femur were significantly lower in the scorbutic group than in the other groups (p < 0.05). Morphometric analysis of tibia indicated significantly lower bone volume, fewer and thinner trabeculae, and a thinner growth plate in the scorbutic group, compared to the pair-fed and ad libitum groups (p < 0.05). Osteoclast surface was about 60% higher in the scorbutic group than in the pair-fed and ad libitum control groups (0.05 < p < 0.10). Mechanical strength of the femur and lumbar vertebral body tended to be lower when bone mass was altered in the same group. Collagen synthesis of articular cartilage and tendons was lower in the scorbutic group than in the pair-fed or ad libitum groups (p < 0.05). In conclusion, scurvy but not food restriction, per se, results in alterations in bone mass and tissue collagen synthesis.

Analysis of Variance↗
PubMed2006

Scurvy in liver transplant patients.

We report on scurvy in 3 liver transplant recipients. Clinical presentation was limited to ecchymotic purpura and mild follicular keratosis with no mucosal involvement. Skin biopsies suggest vitamin C deficiency, which was confirmed by a low level of vitamin C in both sera and leukocyte specimens. Skin lesions dramatically improved within a few weeks after supplementation with ascorbic acid.

Aged↗
PubMed1988

Decreased extracellular matrix production in scurvy involves a humoral factor other than ascorbate.

Our recent studies suggested that decreased collagen synthesis in bone and cartilage of scorbutic guinea pigs was not related to ascorbate-dependent proline hydroxylation. The decrease paralleled scurvy-induced weight loss and reduced proteoglycan synthesis. Those results led us to propose that the effects of ascorbate deficiency on extracellular matrix synthesis were caused by changes in humoral factors similar to those that occur in fasting. Here we present evidence for this proposal. Exposure of chick embryo chondrocytes to scorbutic guinea pig serum, in the presence of ascorbate, led to effects on extracellular matrix synthesis similar to those seen in scorbutic animals. The rates of collagen and proteoglycan synthesis were reduced to approximately 30-50% of the levels in cells cultured in normal guinea pig serum plus ascorbate, but proline hydroxylation and procollagen secretion were unaffected. Similar results were obtained with serum from fasted guinea pigs supplemented in vivo with ascorbate. The growth rate of the chondrocytes was not significantly affected by scorbutic guinea pig serum.

Animals↗
PubMed1981

Adult scurvy.

Scurvy was diagnosed in two elderly alcoholic men in our emergency department. Both were ambulatory and had perifollicular petechiae and ecchymoses of the lower extremities and hypertrophic erythematous gingival lesions. There diets were deficient in fresh fruits and vegetables. Treatment with oral ascorbic acid resulted in dramatic resolution of the signs and symptoms. The first patient was admitted to the hospital, where extensive diagnostic studies failed to reveal other etiological explanations for the cutaneous lesions. The second patient was successfully treated as an outpatient.

Aged↗
PubMed1994

[Scurvy after a suicide attempt by starvation].

A 29-year-old man was admitted to hospital, unconscious and with extensive bleedings in skin and muscles. For many weeks he had been practically starving himself with suicidal intent. Physical examination revealed signs of anaemia and gingivitis with hypertrophy of the tooth borders and bleeding gums, as well as bright blood on rectal examination. There were extensive ecchymoses and petechiae, especially in the legs. Some of the body hair was corkscrew-curly. Haemoglobin level was 7.2 g/dl, mean corpuscular volume 93 fl, reticulocyte count 29/1000. The Rumpel-Leede test was abnormal (60 petechiae/4 cm2), as were the vitamin C level (0.026 mg/dl whole blood) and the ascorbic acid tolerance test. As these findings indicated scurvy, vitamin C was administered, 1 g daily intravenously for 5 days, followed by 500 mg daily by mouth. Remarkable improvement was apparent as early as 72 hours after onset of treatment. The endogenous depression, the underlying cause of the suicide attempt, was treated with clomipramine. When the patient was discharged after 13 days his physical and mental state was much improved.

Adult↗
PubMed2006

Senescence marker protein 30 functions as gluconolactonase in L-ascorbic acid biosynthesis, and its knockout mice are prone to scurvy.

We originally identified senescence marker protein 30 (SMP30) as a distinctive protein whose expression decreases in an androgen-independent manner with aging. Here, we report its sequence homology found in two kinds of bacterial gluconolactonases (GNLs) by using the blast search. Then, through a biochemical study, we identify SMP30 as the lactone-hydrolyzing enzyme GNL of animal species. SMP30 purified from the rat liver had lactonase activity toward various aldonolactones, such as d- and l-glucono-delta-lactone, d- and l-gulono-gamma-lactone, and d- and l-galactono-gamma-lactone, with a requirement for Zn(2+) or Mn(2+) as a cofactor. Furthermore, in SMP30 knockout mice, no GNL activity was detectable in the liver. Thus, we conclude that SMP30 is a unique GNL in the liver. The lactonase reaction with l-gulono-gamma-lactone is the penultimate step in l-ascorbic acid (AA) biosynthesis, and the essential role of SMP30 in this synthetic process was verified here by a nutritional study using SMP30 knockout mice. These knockout mice (n = 6), fed a vitamin C-deficient diet, did not thrive; i.e., they displayed symptoms of scurvy such as bone fracture and rachitic rosary and then died by 135 days after the start of receiving the deficient diet. The AA levels in their livers and kidneys at the time of death were <1.6% of those in WT control mice. In addition, by using the SMP30 knockout mouse, we demonstrate that the alternative pathway of AA synthesis involving d-glucurono-gamma-lactone operates in vivo, although its flux is fairly small.

Aging↗
PubMed1976

Immunologic evidence that the gene for L-gulono-gamma-lactone oxidase is not expressed in animals subject to scurvy.

L-Gulono-gamma-lactone oxidase (L-gulono-gamma-lactone:oxygen 2-oxidoreductase, EC 1.1.3.8) is the enzyme that catalyzes the terminal step of L-ascorbic acid biosynthesis in mammalian liver. The absence of the oxidase activity in primates and guinea pigs is the reason why these animals are subject to scurvy, which must be considered an inborn error of metabolism. Attempts were made to determine if a protein immunologically crossreactive with L-gulono-gamma-lactone oxidase is present in these animals. Detergent-solubilized microsomal preparations from guinea pig and African green monkey liver did not precipitate the antisera directed to either rat or goat enzyme, nor did any of the other cell fractions obtained from guinea pig liver react with either antiserum. No crossreactive protein was detectable in guinea pig microsomes even with the sensitive procedure or micro-complement fixation. On the other hand, extracts of all 10 other mammalian (4 orders) liver microsomes tested were shown to contain L-gulono-gamma-lactone oxidase activity that did crossreact with antibodies to the rat and goat enzymes. One explanation of these findings is that, in the guinea pig, and perhaps in primates too, the structural gene for L-gulono-gamma-lactone oxidase is not expressed.

Alcohol Oxidoreductases↗
PubMed1996

Induction by 4-nitroquinoline-1-oxide of oral epithelial dysplasia and neoplasia in scurvy-prone osteogenic disorder Shionogi (ODS) rats.

Carcinogenesis by 4-nitroquinoline-1-oxide (NQO) in the oral mucosa is a reliable method of obtaining oral mucosal squamous cell carcinoma (OMSCC) and allows examination of various stages of oral cancer development. In vivo and in vitro studies have indicated that L-ascorbic acid (AA) may have a role in cancer prevention. The Wistar "scurvy-prone" osteogenic disorder Shionogi (ODS) rat of the od/od substrain is unable to synthesize AA and requires supplementation for its survival. This study examined the effects of NQO on the oral mucosa of ODS and outbred Wistar rats. NQO (0.5%) was applied topically to the palatal mucosa of 72 male ODS and 36 outbred Wistar rats three times weekly for 4, 8, 12, 16, 20, and 24 wks. The ODS rats were divided so that 36 rats were given 2.5 g/l AA in the drinking water and 36 rats were given 0.33 g/l AA. Vehicle-treated and untreated control animals were included. The rats were killed two weeks after the final NQO application, and the tissues were examined. Epithelial dysplasia was assessed using a modified Smith and Pindborg (1969) index. The ordered categorical scores were analyzed appropriately. Plasma AA levels were checked in ODS and outbred rats at the start and end of the experiment. The results indicated that the oral mucosa of the ODS and outbred rats were susceptible to NQO but that the rate of dysplasia and OMSCC development differed between them, with more rapid changes being found in the ODS rats (p < or = 0.05). No significant difference was found in the dysplasia scores and in the rate of OMSCC development between ODS rats given 2.5 g/l of AA and ODS rats given 0.33 g/l of AA (p > 0.05). No epithelial changes were observed in the palatal mucosa of vehicle-treated and untreated controls. The plasma AA level mean (+/- SEM) was 56 +/- 6 microM for the outbred rats, 8 +/- 1 microM for the ODS rats given 0.33 g/l AA supplementation, and 29 +/- 2 microM for the ODS rats given 2.5 g/l AA. It was concluded that the chronic AA-deficient state in ODS rats played an insignificant role in oral carcinogenesis and that other factors, for example, genetic differences in susceptibility to NQO, contributed to the present findings.

4-Nitroquinoline-1-oxide↗
PubMed1991

Ascorbate requirement for hydroxylation and secretion of procollagen: relationship to inhibition of collagen synthesis in scurvy.

Vitamin C deficiency is associated with defective connective tissue, particularly in wound healing. Ascorbate is required for hydroxylation of proline residues in procollagen and hydroxyproline stabilizes the collagen triple helical structure. Consequently, ascorbate stimulates procollagen secretion. However, collagen synthesis in ascorbate-deficient guinea pigs is decreased with only moderate effects on proline hydroxylation. Proteoglycan synthesis, which does not require ascorbate, also is decreased and both effects are correlated with the extent of weight loss during scurvy. Fasting, with ascorbate supplementation, produces similar effects. Both functions are inhibited in cells cultured in sera from either scorbutic or starved guinea pigs and inhibition is reversed with insulin-like growth factor (IGF)-I. The inhibitor appears to consist of two IGF-binding proteins induced during vitamin C deficiency and starving and may be responsible for in vivo inhibition of collagen and proteoglycan synthesis.

Animals↗
PubMed1992

Treatment of iron-deficiency anemia complicated by scurvy and folic acid deficiency.

We present a case of a child with iron-deficiency anemia, folic acid deficiency, and scurvy. His anemia proved refractory to treatment with iron until he received both folic acid and vitamin C supplementation. This case illustrates the importance of the evaluation of ascorbic acid and folate status in treating iron-deficiency anemia initially refractory to iron supplementation, because multiple nutrient deficiencies may coexist.

Anemia, Hypochromic↗
PubMed1979

Scurvy and vitamin C deficiency in Crohn's disease.

A case of scurvy presenting in a patient with Crohn's disease is reported. A normal response to replacement therapy is seen. Vitamin C (ascorbic acid) deficiency was found in 7 out of 10 patients with clinically quiescent Crohn's disease, 4 of whom had an adequate oral intake of vitamin C. There was no significant difference in oral intake between patients with Crohn's disease and matched controls but there was a significant difference (P less than 0.001) in leucocyte ascorbic acid levels. It is recommended that patients with Crohn's disease be screened for vitamin C deficiency and receive prophylactic vitamin C supplements daily.

Adult↗
PubMed1970

Autonomic reflexes and vascular reactivity in experimental scurvy in man.

Ascorbic acid is a required cofactor in the conversion of dopamine to norepinephrine in vitro, and the deficiency of this vitamin in guinea pigs is associated with degeneration of autonomic ganglion cells and with cardiac supersensitivity to norepinephrine. Because of these findings, we tested the hypothesis that ascorbic acid deficiency in man alters autonomic cardiovascular reflexes and vasomotor responses to adrenergic stimuli. We studied five normal volunteers who had been deprived of ascorbic acid for a period of 3 months; they had developed symptoms and signs of scurvy and their plasma levels of ascorbic acid averaged 0.178 +/-SE 0.07 mg/100 ml. We repeated the studies after giving the subjects vitamin C for a period of 4 months; they had become asymptomatic and their plasma ascorbic acid had increased to an average of 1.68 +/-0.151 mg/100 ml. Blood flow to the left forearm (plethysmograph), arterial and central venous pressures, and heart rate were measured before and after exposure of the lower half of the body to subatmospheric levels of pressure and before and after intravenous and intra-arterial (left brachial artery) infusions of norepinephrine and tyramine. Average values of blood flow (7.9 +/-1.4 ml/min per 100 ml), arterial pressure (91.2 +/-4.6 mm Hg), heart rate (68 +/-4.4 beats/min), central venous pressure (6.1 +/-1.1 mm Hg), and plasma catecholamines (0.68 +/-0.20 mug/liter) obtained during ascorbic acid deficiency were not altered significantly after correction of the deficiency. Vasoconstrictor responses to intra-arterial norepinephrine and tyramine were augmented after vitamin repletion. During ascorbic acid deficiency, four subjects had reduced responsiveness of resistance vessels of the forearm to lower body negative pressure as compared to the responsiveness observed after vitamin repletion. Reflex tachycardia during lower body negative pressure and reflex bradycardia during the pressor responses to intravenous tyramine and norepinephrine were similar during the two studies. The results suggest that the decreased vascular responsiveness to intra-arterial norepinephrine and tyramine and to lower body negative pressure during ascorbic acid deficiency is caused by a defect in the ability of resistance vessels to constrict in response to adrenergic stimuli. Ascorbic acid deficiency in man does not interrupt autonomic reflexes and does not appear to cause significant depletion of endogenous norepinephrine.

Ascorbic Acid↗
PubMed1997

A case of scurvy rarely encountered in Japan.

We report a case of scurvy, which is rarely encountered in Japan. A 75-year-old male was hospitalized with diffuse subcutaneous hemorrhaging of both feet, pain on walking, and shortness of breath. A remarkably low serum level of vitamin C was confirmed. Administration of ascorbic acid dramatically improved his clinical symptoms. Improvement paralleled the increase of serum vitamin C level. This case underscores the important role of vitamin C on the integrity function of the vessel wall.

Aged↗
PubMed2006

Ascorbic acid deficiency stimulates hepatic expression of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1, in scurvy-prone ODS rats.

ODS rat has a hereditary defect in ascorbic acid biosynthesis and is a useful animal model for elucidating the physiological role of ascorbic acid. We previously demonstrated by using ODS rats that ascorbic acid deficiency changes the hepatic gene expression of acute phase proteins, as seen in acute inflammation. In this study, we investigated the effects of ascorbic acid deficiency on the production of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 (CINC-1), in ODS rats. Male ODS rats (6 wk of age) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Obvious symptoms of scurvy were not observed in the ascorbic acid-deficient rats. Ascorbic acid deficiency significantly elevated the serum concentration of CINC-1 on d 14. The liver and spleen CINC-1 concentrations in the ascorbic acid-deficient rats were significantly elevated to 600% and 180% of the respective values in the control rats. However, the lung concentration of CINC-1 was not affected by ascorbic acid deficiency. Ascorbic acid deficiency significantly elevated the hepatic mRNA level of CINC-1 (to 480% of the value in the control rats), but not the lung mRNA level. These results demonstrate that ascorbic acid deficiency elevates the serum, liver and spleen concentrations of CINC-1 as seen in acute inflammation, and suggest that ascorbic acid deficiency stimulate the hepatic CINC-1 gene expression.

Animals↗
PubMed1976

Aortic endothelial and sub-endothelial lesions in early stages of experimental atherogenesis and in scurvy.

The endothelial and sub-endothelial lesions during early stages of experimental atherogenesis and scurvy have been studied by means of scanning EM and transmission EM, making use also of the Con-A reaction. The surface coat modifications were accompanied by formation of vacuoles in the endothelial cells and by sub-endothelial 'oedema', not only in rabbits fed a hypercholesterolic diet but also in scorbutic guinea pigs. The endothelial lesions were sometimes found even before clear modifications of the Con-A surface reactive layer were apparent.

Animals↗