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Results for “ASCORBIC ACID DEFICIENCY”

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PubMed1986

A comparative study on the effects of ascorbic acid deficiency and supplementation on endurance and mitochondrial oxidative capacities in various tissues of the guinea pig.

The aim of this study was to ascertain the effects of ascorbic acid deficiency and supplementation on endurance and mitochondrial oxidative capacities in various tissues of guinea pigs. Endurance capacity was significantly reduced by ascorbic acid deficiency and supplementation. Oxidative capacities were reduced in heart, liver and brown adipose tissue but it seems as if skeletal muscle is protected against ascorbic acid deficiency and supplementation-induced oxidative damage. Skeletal muscle and liver but not heart appear to be susceptible to exercise-induced oxidative damage. To a certain extent oxidative capacities could be related to the glutathione status in the various tissues.

Animals↗
PubMed1983

Lack of effect of experimental ascorbic acid deficiency on bile acid metabolism, sterol balance, and biliary lipid composition in man.

Extensive studies in animal models indicate that subclinical ascorbic acid deficiency impairs the conversion of cholesterol to bile acid, elevates plasma cholesterol levels, and predisposes to development of cholesterol cholelithiasis. The present study was designed to see if this is also true in man. Five normal volunteers were hospitalized in a metabolic ward and placed on a controlled diet containing 3-4 mg of ascorbic acid each day. Ascorbic acid supplementation was given as follows: control period I (days 1-33), 75 mg/day; deficient period (days 34-96), 0 mg/day; and repletion period (days 97-101), 1000 mg/day. In addition, three of the subjects were studied during a second control period (days 102-139) during which they were given 75 mg/day of ascorbic acid. Ascorbate levels at the end of both control periods were 0.87-1.34 mg/dl in plasma and 19.4-29.5 micrograms/10(8) cells in leukocytes. At the end of the deficient period these levels were 0.09-0.15 mg/dl in plasma and 6.2-10.0 micrograms/10(8) cells in leukocytes, levels approaching those seen in scurvy. There was no effect of ascorbic acid deficiency on plasma cholesterol and triglycerides; plasma cholesterol in high, very low, and low density lipoprotein fractions; biliary lipid composition and saturation index of gallbladder bile; synthesis, fractional turnover, or pool size of either cholic or chenodeoxycholic acids; output of fecal acid or neutral sterols; and fecal sterol balance. Total bile acid pool size calculated by the one-sample technique was reduced 11% in the deficient period compared to control period I (P less than 0.005), and increased to 98.7% of the baseline levels in control period II. However, total bile acid pool calculated by the Lindstedt method did not change during deficiency. These data demonstrate that short-term subclinical ascorbic acid deficiency near the scorbutic range has no significant effect on bile acid and cholesterol metabolism in man.

Adult↗
PubMed1987

Re-evaluation of ascorbic acid deficiency in hemodialysed patients.

In 92 uremic patients under chronic hemodialysis without ascorbic acid supplementation, serum ascorbic acid was measured before hemodialysis and between two sessions. The results indicated a more serious ascorbic acid deficiency of patients than in previous studies. This difference might be explained by the highly specific enzymatic method applied in the present study, excluding any potential interference of various serum reducing substances.

Adult↗
PubMed1967

Ascorbic acid deficiency in cultured human fibroblasts.

Fibroblasts grown in medium containing less than 1 microg of ascorbic acid per milliliter showed evidence of ascorbic acid deficiency when compared with cells grown in medium containing 50 microg of ascorbic acid per milliliter. This was manifested morphologically by dilated endoplasmic reticulum, a decrease in number, size, and intensity of staining of the mitochondria, by defective intercellular fibril formation, and by easy disaggregation of the cells from the intercellular matrix after treatment with pronase. When 50 microg per milliliter of ascorbic acid was incorporated into the medium, the altered morphology was corrected, banded fibrils were produced which were organized into bundles, and the cells were tightly bound in a matrix which was resistant to disaggregation with a variety of proteolytic enzymes. Collagen and sulfated glycosaminoglycan synthesis were less in the control than in the ascorbic acid supplemented cells. Similar morphological and chemical changes have been reported in the connective tissue of scorbutic animals. The effects of low ascorbic acid concentration on fibroblasts in culture indicate that these cells require ascorbic acid to maintain connective tissue functions.

Amino Sugars↗
PubMed2004

Ascorbic acid deficiency, iron overload and alcohol abuse underlie the severe osteoporosis in black African patients with hip fractures--a bone histomorphometric study.

Osteoporosis and femoral neck fractures (FNF) are uncommon in black Africans although osteoporosis accompanying iron overload (from traditional beer brewed in iron containers) associated with ascorbic acid deficiency (oxidative catabolism by iron) has been described from sub-Saharan Africa. This study describes histomorphometric findings of iliac crest bone biopsies and serum biochemical markers of iron overload and of alcohol abuse and ascorbic acid levels in 50 black patients with FNFs (29 M, 21 F), age 62 years (40-95) years (median [min-max]), and in age- and gender-matched black controls. We found evidence of iron overload in 88% of patients and elevated markers of alcohol abuse in 72%. Significant correlations between markers of iron overload and of alcohol abuse reflect a close association between the two toxins. Patients had higher levels of iron markers, i.e., siderin deposits in bone marrow (P < 0.0001), chemical non-heme bone iron (P = 0.012), and serum ferritin (P = 0.017) than controls did. Leukocyte ascorbic acid levels were lower (P = 0.0008) than in controls. The alcohol marker mean red blood cell volume was elevated (P = 0.002) but not liver enzymes or uric acid. Bone volume, trabecular thickness, and trabecular number were lower, and trabecular separation was greater in patients than in controls, all at P < 0.0005; volume, surface, and thickness of osteoid were lower and eroded surface was greater, all at P < 0.0001. There was no osteomalacia. Ascorbic acid deficiency accounted significantly for decrease in bone volume and trabecular number, and increase in trabecular separation, osteoid surface, and eroded surface; iron overload accounted for a reduction in mineral apposition rate. Alcohol markers correlated negatively with osteoblast surface and positively with eroded surface. Relative to reported data in white FNF patients, the osteoporosis was more severe, showed lower osteoid variables and greater eroded surface; FNFs occurred 12 years earlier and were more common among men. We conclude that the osteoporosis underlying FNFs in black Africans is severe, with marked uncoupling of resorption and formation in favor of resorption. All three factors--ascorbic acid deficiency, iron overload, and alcohol abuse--contributed to the osteoporosis, in that order.

Adult↗
PubMed1978

Effects of ascorbic acid deficiency on adrenal mitochondrial hydroxylations in guinea pigs.

The effect of ascorbic acid deficiency on adrenal hydroxylation of cholesterol and deoxycorticosterone in guinea pigs was studied by using mitochondria and isolated cytochrome P-450 fractions. The effects obtained were compared with the effects of long-term treatment with ACTH. Advanced scurvy as well as treatment with ACTH resulted in an increase in the weight of the adrenals, the total amount of cytochrome P-450, the cholesterol side-chain cleavage activity, the cortisol level in plasma, and the excretion of unconjugated cortisol in urine. Total 11beta- and 18-hydroxylation of deoxycorticosterone were not stimulated or were stimulated only to a small extent. It is suggested that the major effects observed in advanced scurvy are due to ACTH, the level of which was significantly increased, most probably as a consequence of the stress. In animals kept on a scorbutogenic diet for 2-4 weeks or, with a small dose of ascorbate added, for several weeks, changes were observed that could not be fully explained as effects of ACTH on normal adrenals. Although the plasma levels of ACTH and cortisol were increased only to a small extent and excretion of unconjugated cortisol in urine was unaffected, there was a significant increase in the total capacity of adrenal mitochondria to hydroxylate exogenous cholesterol. It is concluded that the level of ascorbate in the adrenals might be of some importance for the capacity to convert cholesterol into pregnenolone. The normal feed-back regulation is, however, intact in moderate ascorbate deficiency and the plasma level of cortisol is kept within normal limits.

Adrenal Glands↗
PubMed1977

The effects of ascorbic acid deficiency on collagen synthesis by mouse molar tooth germs in organ culture.

Second molar tooth germs from 2-day-old Swiss-Webster mice, grown in organ culture for 7 days in ascorbic-acid-deficient medium, synthesized about 65% as much protein (measured by incorporation of [14C]proline during a 24-h pulse) as did ascorbic-acid-supplemented controls. The newly synthesized proteins from ascorbic-acid-deficient cultures contained only about 7% of the hydroxyproline content of the controls. Collagenase digestion of the newly synthesized proteins showed that collagen comprised the same fraction of the total protein synthesized under both culture conditions. This result indicates that the ascorbate-deficient cultures made significant quantities of underhydroxylated collagen. Partial characterization of the collagen alpha chains on carboxymethyl cellulose columns showed an alpha1/alpha2 ratio of about 5, suggesting that at least two different species of collagen were synthesized. The alpha1/alpha2 ratio of the chains recovered from the ascorbate-deficient cultures was also about 5 but the chains were slightly underhydroxylated and the total amount of these chains which could be identified accounted for only a small fraction of the total collagen which was synthesized. A large fraction of the synthesized collagenous protein was found in the culture medium, mostly in the form of lower molecular weight peptides. It is concluded that most of the collagen which is synthesized by ascorbate-deficient tooth-bud cultures is not utilized by the component tissues, but is probably degraded and released into the medium.

Animals↗
PubMed1995

Effect of marginal ascorbic acid deficiency on saliva level of cortisol in the guinea pig.

Male guinea pigs subjected to prolonged marginal ascorbic acid deficiency developed moon facies and oedema, features of functional adrenal hypercorticism. Compared with age- and sex-matched controls fed an adequate diet for a similar period, ascorbate deficiency had no effect on submandibular gland weight but elicited a significant (p < 0.005) reduction in stimulated whole-saliva flow rate. Plasma cortisol concentration (nmol/L) was significantly increased (p < 0.005) in the deficient animals (998.21 +/- 57.19 compared to 254.66 +/- 15.62 for the controls). Associated with marked hypercortisolaemia in the deficient animals was a significant (p < 0.01) but less prominent increase in the whole-saliva cortisol level, resulting in a mean saliva/plasma cortisol ratio of 46% for this group compared to 72% for the controls. Increased corticosteroid levels suppress immunological and inflammatory responses, particularly neutrophil function, impair production of some cytokines, inhibit collagen synthesis, and impair wound healing and bone matrix formation. Numerous conditions such as ageing, stress, smoking, ionizing radiation, ingestion of drugs, protein malnutrition, diabetes, and several other pathological states, which are among the risk factors for xerostomia and periodontal/oral mucosal lesions, promote tissue depletion of ascorbate. This study suggests that increased salivary and blood levels of glucocorticoids in these conditions may be important in reducing the ability of the host to mount an effective immune response to oral pathogens.

Adrenocortical Hyperfunction↗
PubMed1984

The role of ascorbic acid deficiency in human gingivitis--a new hypothesis.

Periodontal disease is one of the most prevalent health problems in the world and is the major cause of tooth loss in the adult population. Its two major subdivisions are gingivitis where disease is confined to the gingiva, and periodontitis where disease is present both in the gingiva and the supporting periodontal tissues. During the first stage there is a vasculitis of vessels subjacent to the junctional epithelium which is followed by exudation of fluid from the gingival sulcus and migration of leukocytes. There is variable expression of this stage throughout the mouth with new areas of involvement appearing in place of healed areas. Mast cells which are present in the gingival connective tissues may participate in this inflammatory response by liberating histamine. Ascorbic acid deficiency has been shown to be a conditioning factor in the development of gingivitis. When humans are placed on ascorbic acid deficient diets there is increased edema, redness and swelling of the gingiva. These changes have been attributed to deficient collagen production by gingival blood vessels. However, this may be due to an antihistamine role of ascorbic acid. This vitamin may act to directly detoxify histamine or effect a change in the level of enzymes responsible for histamine metabolism. This could occur through the influence of ascorbic acid in altering cyclic AMP (c-AMP) levels. Such changes in the level of this regulatory molecule could result in increased histamine-N-methyl transferase and other enzymes responsible for the breakdown of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗