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PubMed1984

Is leucocyte ascorbic acid an unreliable estimate of vitamin C deficiency?

Leucocyte ascorbic acid levels failed to identify six of seven elderly patients shown to be deficient on an oral vitamin C saturation test. Compared to those with a normal saturation test, patients judged deficient had lower levels for triceps skinfold thickness, mean arm muscle circumference and Quetelet's index; there was a significant association with the habit of eating alone, and with a dietary intake of less than 30 mg of ascorbic acid daily (the recommended daily allowance in the U.K.). No significant difference was found in the values for haemoglobin, serum albumin or potassium concentrations between the two groups, and no association shown between a deficient saturation test and smoking, season, sublingual varicosities or an abnormal bleeding time.

Aged↗
PubMed1989

Ovarian aromatase activity in scorbutic mutant rats unable to synthesize ascorbic acid.

Osteogenic disorder syndrome rats are unable to synthesize ascorbic acid owing to the lack of l-gulonolactone oxidase, and become scorbutic within a few weeks without the supply of ascorbic acid. We studied effects of ascorbic acid deficiency on the ovarian aromatase activity in vivo using osteogenic disorder syndrome rats. The ovarian aromatase activity in ascorbic acid-deficient osteogenic disorder syndrome rats was significantly higher than that in normal or ascorbic acid-supplied osteogenic disorder syndrome rats. The activity in hypophysectomized immature rats was extremely low, but increased after treatment with pregnant mare serum gonadotropin, regardless of the presence or absence of ascorbic acid. The extent of the increase was the same among experimental groups. The present results indicate that ascorbic acid at physiological level lowers the ovarian aromatase activity, whereas it does not impair the responsiveness of the aromatase activity to gonadotropins.

Animals↗
PubMed1983

Internal distribution of excess iron and sources of serum ferritin in patients with thalassemia.

Liver and spleen iron concentrations, serum ferritin level and binding of S-ferritin to concanavalin A (Con A) were measured in 12 patients with thalassaemia major or intermedia at the time of splenectomy. All these subjects had increased liver iron concentration, most of them had hepatic fibrosis but none of them had histological evidence of chronic hepatitis. No patient had ascorbic acid deficiency. Serum ferritin concentration was increased in all cases, ranging from 266 to 5504 micrograms/l. In all but 2 subjects most of the protein did not bind to Con A, thus behaving as tissue ferritin. There were highly significant correlations between serum ferritin concentration, amount of blood transfused and liver iron concentration. On the average, iron concentration in the liver was about 3 times that in the spleen. The findings obtained suggest that in patients with thalassaemia major or intermedia most of the iron is deposited in parenchymal tissues and most of the S-ferritin derives by leakage from the cytosol of iron-loaded parenchymal cells. S-ferritin is a valid index of liver iron overload in thalassaemic patients without complications such as viral hepatitis and/or ascorbic acid deficiency.

Blood Transfusion↗
PubMed1992

Effects of ascorbate-deficiency on collagen secretion and resorption in cultured mouse incisor germs.

The effects of ascorbic acid deficiency on mouse incisors, grown in vitro, has been investigated at the histological and cytological levels. In this model, continuously growing mouse incisors are characterized by the existence of different type of predentin-dentin matrix on its lingual (root-analogue) and labial (crown-analogue) surface and the absence of enamel on the lingual surface. Our observations indicated that ascorbate-deficiency affected the behavior of mouse tooth germs in vitro: odontoblast differentiation was disturbed and morphological evidence for odontoblast-mediated collagen resorption were observed. An abnormal amorphous predentin-dentin matrix existed and the basement membrane was prematurely disrupted. The dentin mineralization, as well as functional differentiation of ameloblasts were strongly hampered. Chronic deficiency led to disorganization of the dental tissues.

Absorption↗
PubMed2001

Oral intake and serum levels of ascorbic acid in continuous ambulatory peritoneal dialysis patients.

Oral intake of ascorbic acid is essential for optimum health in human beings. Continuous ambulatory peritoneal dialysis (CAPD) patients have an increased need for ascorbic acid, because of increased loss through dialysate, reduced intake owing to nausea and loss of appetite, and increased oxidative stress. However, optimum intake is still controversial. We studied 50 clinically stable patients to determine the relationship between oral ascorbic acid intake and serum ascorbic acid (SAA) level. Total oral intake ranged from 28 mg daily to 412 mg daily. Only one patient had an oral intake of ascorbic acid below 60 mg per day. The SAA levels ranged from 1 mg/L to 36.17 mg/L. Although a strong correlation existed between intake and SAA (p < 0.001, R2 = 0.47), the variation in SAA at any given intake level was wide. Of the studied patients, 62% had an SAA < 8.7 mg/L, 40% had an SAA < 5.1 mg/L (below the level in a healthy population), and 12% had a level below 2 mg/L (scorbutic). None of the patients demonstrated clinical manifestations of scurvy. Our results show that, in CAPD patients, ascorbic acid deficiency can be reliably detected only with SAA measurements, and oral intake may influence SAA level. To maintain ascorbic acid in the normal range for healthy adults, daily oral intake needs to be increased above the U.S. recommended dietary allowance to 80-140 mg.

Aged↗
PubMedDate not supplied

Vanadium and ascorbate effects on 3-hydroxy-3-methylglutaryl coenzyme A reductase, cholesterol and tissue minerals in guinea pigs fed low-chromium diets.

Vanadium has been reported to affect numerous physiological processes; however, a demonstration that vanadium deficiency consistently impairs biological function is lacking. The purpose of this study was to determine if the activity of hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in cholesterol synthesis, is affected by dietary supplementation of vanadate and/or chronic ascorbic acid deficiency. To determine if vanadium and/or ascorbic acid affected mineral metabolism, tissue minerals also were analyzed. Weanling male guinea pigs were assigned randomly to groups of 10 in a 2 x 2 factorial design. The dietary variables were ascorbate, 0.5 or 10 mg/day, and vanadium < 0.01 microgram or 0.5 microgram/g diet as NH4VO3 in a low Cr diet containing < 0.07 microgram Cr/g diet. After 21 weeks on this diet, guinea pigs receiving more ascorbate had lower liver weight/body weight ratios and increased bone copper. Testes weight/body weight ratios, hepatic glycogen and bone copper decreased while hepatic lipids, fecal bile acids, plasma cortisol and bone calcium and magnesium were increased by vanadium supplementation. An interaction between vanadium and ascorbate affected cholesterol excretion in feces, hepatic iron, plasma cholesterol concentration and the activity of HMG CoA reductase. This study provides evidence of increased bone mineral concentrations with vanadium supplementation and of an interaction between vanadium and ascorbate which affected cholesterol metabolism.

Animals↗
PubMed1984

The effects of various levels of ascorbic acid intake upon growth and organ weights of guinea pigs.

The purpose of this study was to evaluate the systemic effects of varying levels of orally administered ascorbic acid during wound healing in guinea pig oral mucosa. Forty five Murphy/Hartley guinea pigs were randomly placed into four groups and fed an ascorbic acid deficient diet for 2 weeks. Each group of animals then received a daily oral supplement of the following doses of ascorbic acid: 0.5 mg, 5.0 mg, 50 mg, and 250 mg. All animals were weighed twice a week. Twenty eight days later, a standardized wound was made in the premaxilla. On day 35, all animals were sacrificed. Blood samples were evaluated for levels of ascorbic acid. Thirty nine samples showed insignificant levels of vitamin C, 32 of which showed no ascorbic acid. Organ to body weight ratios were calculated and compared. Spleen to body weight ratios were not affected by different ascorbic acid levels. High levels of ascorbic acid caused a significant increase in adrenal gland to body weight ratios. Varying the levels of ascorbic acid did not affect growth prior to surgical wounding. Increased levels of ascorbic acid enhanced body weight recovery post surgically.

Adrenal Glands↗
PubMed1989

Role of plasma ascorbate in diabetic microangiopathy.

Plasma total ascorbate status measured by 2.4 dinitrophenyl hydrazine method showed that diabetics (N = 100) had significantly lower plasma total ascorbate compared with 45 age and sex matched non-diabetic controls; 0.34 +/- 0.16 mg/dl vs 0.68 +/- .06 mg/dl, P less than 0.001) regardless of presence or absence of retinopathy and irrespective of mode of treatment. The finding unique to this study was that plasma total ascorbate status in diabetics with retinopathy (0.19 +/- 0.07 mg/dl) was significantly lower than that of uncomplicated diabetics (0.49 +/- 0.06 mg/dl; P less than 0.001). Plasma Glucose had no correlation with plasma ascorbate levels and effect of duration of Diabetes Mellitus (DM) on ascorbate status in diabetics was ambiguous. Diabetics had abnormally fragile cutaneous capillaries detected by Hess test. The incidence of capillary fragility was more in patients with retinopathy. Hess test can be used as an easy and non-invasive test to assess plasma ascorbate status to detect microvascular involvement in DM. The experience of this study reflects that the two distinct microvascular lesions in diabetes, i.e. abnormal dermal capillary fragility and retinopathy may have a common link to ascorbic acid deficiency. An early switching on of the supplementation of ascorbic acid may retard the development of microvascular complications in diabetes.

Adult↗
PubMed1986

Coordinate regulation of collagen and proteoglycan synthesis in costal cartilage of scorbutic and acutely fasted, vitamin C-supplemented guinea pigs.

The effects of ascorbic acid deficiency and acute fasting (with ascorbate supplementation) on the synthesis of collagen and proteoglycan in costal cartilages from young guinea pigs was determined by in vitro labeling of these components with radioactive proline and sulfate, respectively. Both parameters were coordinately decreased by the second week on a vitamin C-free diet, with a continued decline to 20-30% of control values by the fourth week. These effects were quite specific, since incorporation of proline into noncollagenous protein was reduced by only 30% after 4 weeks on the deficient diet. The time course of the decrease in collagen and proteoglycan synthesis paralleled the loss of body weight induced by ascorbate deficiency. Hydroxylation of proline in collagen synthesized by scorbutic costal cartilage was reduced to about 60% of normal relatively early, and remained at that level thereafter. Neither collagen nor proteoglycan synthesis was returned to normal by the addition of ascorbate (0.2 mM) to cartilage in vitro. Administration of a single dose of ascorbate to scorbutic guinea pigs increased liver ascorbate and restored proline hydroxylation to normal levels by 24 h, but failed to increase the synthesis of collagen or proteoglycan. Synthesis of both extracellular matrix components was restored to control levels after four daily doses of ascorbate. A 96-h total fast, with ascorbate supplementation, produced rates of weight loss and decreases in the synthesis of these two components similar to those produced by acute scurvy. There was a linear correlation between changes in collagen and proteoglycan synthesis and changes in body weight during acute fasting, scurvy, and its reversal. These results suggest that it is the fasting state induced by ascorbate deficiency, rather than a direct action of the vitamin in either of these two biosynthetic pathways, which is the primary regulatory factor.

Animals↗
PubMed1990

Decrease of nitrate biosynthesis in scorbutic mutant rats unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on the urinary excretion of nitrate was investigated using a mutant strain of rats (osteogenic disorder syndrome rats; ODS rats) unable to synthesize ascorbic acid. The amount of urinary nitrate excreted by ODS rats with or without ascorbic acid supplementation were measured before and after the intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS). Urinary nitrate excretion increased markedly after LPS injection. Urinary nitrate excretion by ODS rats not supplied with ascorbic acid was significantly less than that of those supplied with ascorbic acid both before and after LPS injection. These results show that ascorbic acid enhances both LPS-stimulated and constitutive nitrate production in vivo.

Adrenal Glands↗
PubMed1983

Relation between ascorbic acid intake and periodontal disease in the United States.

Only a weak association between periodontal disease and ascorbic acid deficiency has been shown in the analysis of nutritional and periodontal health data collected from a representative sample of the US population. Intake of ascorbic acid in amounts larger than those recommended by the dietary standards does not seem to be associated with better periodontal health. The results of this study also suggest that dental practitioners are better advised to concentrate on plaque control rather than vitamin C supplements to prevent and control periodontal disease in their patients.

Adult↗
PubMed1991

Bone histomorphometric analysis for the cause of osteopenia in vitamin C-deficient rat (ODS rat).

A particular strain of rat, the osteogenic disorder rat (ODS rat), was established in 1973. Phenotypic expression of od/od in ODS rat develops signs characteristics of a vitamin C-deficient animal, with bleeding tendencies and limb fractures. We investigated the bone histomorphometry to clarify the pathogenesis of osteopathy found in ODS rat. Bone histomorphometry revealed that static parameters reflecting bone formation were found to be remarkably decreased in od/od rats. These observations were more prominent in the metaphysis of distal femurs of od/od rats than those in the tail vertebrae. Parameters reflecting bone resorption in od/od rats were reduced in the distal femoral metaphysis, but were similar to those of controls in the tail vertebrae. These parameters were restored to control levels after ascorbic acid supplementation to pair-fed od/od rats. The mineral appositional rate in od/od rats was not significantly different from that in controls. Although body weight gain in pair-fed controls was significantly reduced compared to those fed ad libitum, histomorphometric parameters, on the contrary, were unaltered between these groups. Our present study provides evidence that the cause of osteopenia found in od/od rat is attributable to an imbalance between the total amounts of resorption and formation, and the pathogenesis of osteopathy could be due to ascorbic acid deficiency itself rather than malnutrition.

Alkaline Phosphatase↗
PubMed1971

Ascorbic acid status in iron-deficiency anaemia.

Leucocyte ascorbic acid concentration declines with age. Patients with iron-deficiency anaemia have higher concentrations than normal while those with iron overload have a reduced concentration. It is suggested that these phenomena may be a result of reduced ascorbate catabolism in iron-deficiency anaemia and they provide support for the suggestion that the amount of iron in the tissues may be an important factor in determining ascorbic acid utilization.

Adolescent↗
PubMed1978

The effect of vitamin supplementation upon antipyrine metabolism in the elderly.

1 Antipyrine plasma half-life and clearance rates were studied in 19 elderly patients shortly after admission to a geriatric ward and again 2 weeks after a course of dietary supplementation with Vitamins A, B complex, C and D. 2 Antipyrine half-life fell and clearance increased in the nine who had sub-clinical evidence of ascorbic acid deficiency. No correlation was found with other indices of nutritional status. 3 Vitamin supplementation in elderly people with no demonstrable deficiencies did not alter the metabolism of antipyrine.

Aged↗