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At least 883 records · Page 49Linked to original sources
PubMed1990

Vitamin C deficiency in patients with sickle cell anemia.

Because peroxidative damage to red cell membranes may contribute to the pathophysiology of sickle cell disease, deficiency of fat- and water-soluble antioxidants could be a determinant in the pathogenesis of this disease. We have previously reported a deficiency of vitamin E in sickle cell disease. The present study was undertaken to see if a deficiency in vitamin C might also be detected. Leukocyte vitamin C, which reflects total body vitamin C reserve, was measured by a modified 2,4-dinitrophenylhydrazine method. Sickle cell patients (N = 18) had lower leukocyte vitamin C levels (18.3 +/- 9.4 micrograms/10(8) cells) than normal controls (N = 12; 30.3 +/- 7.5 micrograms/10(8) cells; p less than 0.01). Furthermore, 50% of the patients had vitamin C levels below 15 micrograms/10(8) cells, a value consistent with vitamin C deficiency. A statistically significant correlation (r = -0.62 with 0.01 less than p less than or equal to 0.025) was found between leukocyte vitamin C levels and serum ferritin concentration. Because dietary vitamin C intake appeared to be adequate, increased vitamin C utilization may account for this deficiency. However, the mechanisms for this deficiency as well as its pathophysiologic consequences remain to be established.

Anemia, Sickle Cell↗
PubMed1985

Hormonal, drug, and dietary factors affecting peptidyl glycine alpha-amidating monooxygenase activity in various tissues of the adult male rat.

The factors controlling levels of peptidyl glycine alpha-amidating monooxygenase (PAM) activity in its major tissue sources in the adult male rat were investigated by carrying out a variety of endocrine, pharmacological, and dietary manipulations. Levels of PAM activity and alpha MSH immunoactivity in the neurointermediate lobe of the pituitary gland rose and fell in parallel in rats treated with the dopamine antagonist haloperidol or the dopamine agonist bromocriptine, respectively. PAM activity in the anterior pituitary lobe was increased after adrenalectomy or castration and decreased after thyroidectomy or treatment with haloperidol. PAM activity in the submandibular gland was increased after treatment with the alpha-adrenergic antagonist phenoxybenzamine and decreased after treatment with the alpha-adrenergic agonist phenylephrine. Serum levels of PAM activity were unaltered after hypophysectomy, adrenalectomy, sialectomy, or castration, but rose after thyroidectomy and declined after treatment with the ganglionic blocker chlorisondamine or phenoxybenzamine. Chronic dietary copper deficiency in rats resulted in increased PAM activity in homogenates of anterior pituitary lobe and submandibular gland assayed under optimized conditions; chronic dietary ascorbate deficiency in guinea pigs did not produce consistent changes in PAM activity in the tissues examined.

Animals↗
PubMed2006

Regional transient osteoporosis of the foot and vitamin C deficiency.

We describe the clinical presentation and diagnostic tests of a patient with regional transient osteoporosis (RTO) of the foot. This patient presented with a 4-month history of left-foot pain, nonpitting edema, and brownish discolorations of both feet. He had a history of tobacco abuse, alcohol abuse, and malnutrition. Radiological studies revealed severe osteopenia in the feet, and a MRI revealed bone marrow edema. The bone biopsy was consistent with RTO. This patient also had vitamin C deficiency. This case suggests a link between vitamin C deficiency and RTO, a hypothesis supported by our review of relevant literature on osteoporosis and vitamin C.

Ascorbic Acid↗
PubMed2004

Vitamin C deficiency exerts paradoxical cardiovascular effects in osteogenic disorder Shionogi (ODS) rats.

Vitamin C is considered to be a very efficient water-soluble antioxidant, for which several new cardiovascular properties were recently described. The aim of this study was to determine in vivo the effects of a severe depletion of vitamin C on cardiac and vascular variables and reperfusion arrhythmias. For this purpose, we used a mutant strain of Wistar rats, osteogenic disorder Shionogi (ODS). After 15 d of consuming a vitamin C-deficient diet, ODS rats had a 90% decrease in plasma and tissue levels of ascorbate compared with ODS vitamin C-supplemented rats and normal Wistar rats. However, plasma antioxidant capacity, proteins, alpha-tocopherol, urate, catecholamines, lipids, and nitrate were not influenced by the vitamin C deficiency in ODS rats. Moreover, there was no difference between ODS vitamin C-deficient and -supplemented rats in heart rate and arterial pressure. After 5 min of an in vivo regional myocardial ischemia, various severe arrhythmias were observed, but their intensities were not modified by vitamin C in vitamin C-deficient ODS rats. The vascular reactivity, measured in vitro on thoracic arteries, was not altered by ascorbate deficiency in ODS rats. These unexpected results suggest that unidentified compensatory mechanisms play a role in maintaining normal cardiac function and vascular reactivity in vitamin C-deficient rats.

Acetylcholine↗
PubMed1996

Utilization of the bone/liver alkaline phosphatase activity ratio in blood plasma as an indicator of ascorbate deficiency in salmonid fish.

The goal of this study was to test the hypothesis that the ratio of liver to bone alkaline phosphatase in blood plasma reflects the ascorbate status in scurvy-prone teleost fish (rainbow trout [Oncorhynchus mykiss]). The studies focused on finding a method for distinguishing bone alkaline phosphatase present in blood plasma from other alkaline phosphatase isoforms. We tested temperature optima and thermostability of liver, kidney, gill cartilage, and intestinal alkaline phosphatases. We did not observe differences among liver, bone, and kidney enzymes with respect to temperature optima and thermostability. We partially purified alkaline phosphatase from juvenile rainbow trout vertebrae and liver using n-butanol solubilization and ammonium sulfate fractionation. We found a difference between bone alkaline phosphatase, which precipitated in 0%-20% ammonium sulfate saturation, and liver enzyme, which required 40%-50% ammonium sulfate saturation to precipitation. We conducted a series of urea inactivation studies on partially purified enzymes from liver and vertebrae. Urea differentially inhibited the enzymes with t 1/2 = 1.1 and 0.4 min, for bone and liver, respectively. Subsequently, we subjected blood plasma alkaline phosphatase to urea inhibition, and using regression analysis we calculated the ratio of liver to bone alkaline phosphatase. We found that thus obtained ratios of bone enzyme in blood plasma correlated with liver ascorbate concentration. Bone alkaline phosphatase declined in ascorbate deficiency 10-fold, whereas low ascorbate status resulted in a 3.5-fold decrease. In order to draw a general conclusion on the linearity of the response of blood plasma/bone alkaline phosphatase as an indicator of ascorbate deficiency in fish, further studies must include analysis of individual fish followed in the process of developing avitaminosis.

Alkaline Phosphatase↗
PubMedDate not supplied

[Vitamin supply of miners employed in modern highly-mechanized coal mines].

The author studied vitamin C, B2, B6, E, A and carotinoid supply of the miners of modern highly mechanized coal mines. The reduction in the supply of the miners with individual vitamins and frequent manifestations of the microsymptoms of their deficiency were of the microsymptoms of their deficiency were linked to a definite degree with high physiological requirements of the miners, associated with the specificity of work at highly mechanized mines.

Ascorbic Acid Deficiency↗
PubMed1995

Evaluation of vascular and metabolic deficiency in patients with large leg ulcers.

A consecutive series of 50 patients with large leg ulcers (surface area > 100 cm2) were investigated for evidence of arterial, venous and nutritional problems. Arterial insufficiency was found in 34%, venous reflux in 50%. A group of eight patients had no arterial or venous problem but had serious deficiencies of vitamin C and zinc. Arterial bypass was performed successfully in 15 of the 17 patients with arterial disease. All patients had a mesh split-skin graft. The 25 with venous incompetence had compression bandaging; in these patients the ulcer had healed on discharge but 10 had recurrent ulceration within 6 months. The leg ulcers in patients with corrected arterial insufficiency healed significantly more rapidly than those with venous incompetence. The ulcers in those with nutritional deficiency healed promptly after skin grafting and correction of the deficiency. It is important to be aware of arterial insufficiency and nutritional deficiency in patients with leg ulcers, as such deficiencies may contribute to the non-healing of an apparently straightforward leg ulcer.

Aged↗
PubMed1999

Respiratory chain complex III [correction of complex] in deficiency with pruritus: a novel vitamin responsive clinical feature.

We report a child with an isolated complex III respiratory chain deficiency and global developmental delay who had severe pruritus with elevated plasma bile acid levels. A liver biopsy showed micronodular cirrhosis, and enzymologic evaluation demonstrated an isolated complex III deficiency in both liver and muscle. His pruritus improved and serum bile acid levels decreased after treatment with menadione and vitamin C.

Anemia, Iron-Deficiency↗
PubMed1979

Relevance of a borderline vitamin deficiency in relation to the question of vitamin requirement.

A definition is given for the terms of latent and borderline vitamin deficiency, and the vitamin requirement and optimal vitamin supply, respectively, are discussed in relation to these two terms. The upper limit of the latent vitamin deficiency status can be used to define the optimal intake of vitamins, whereas the lower limit indicates the minimum requirement. The impact on health of a latent vitamin deficiency lies in the risk of falling into a manifest vitamin deficiency during sudden stress, whereas, in borderline vitamin deficiency status, some health functions are affected so that a problem of public health may arise and countermeasures should be taken.

Adolescent↗
PubMedDate not supplied

[Various aspects of the effect of nutritional factors on the metabolism and biological action of aflatoxin B1 in the rat liver].

Interrelationships between the quality of nutrition, oxidative hydroxylation of aflatoxin B1 and lipid peroxidation were studied in biomembranes of hepatocyte endoplasmic reticulum of growing male rats of the WAG strain. Activity of the liver microsomal monooxygenase, lipid peroxidation as well as metabolism of aflatoxin B1 were shown to depend on presence of three essential amino acids (lysine, methionine and threonine) and vitamins A, E and C. Deficiency of these compounds altered the aflatoxin metabolism causing formation of highly reactive metabolites, which might accelerate the carcinogenic effect of the xenobiotic. However, formation of free toxic metabolites of aflatoxin was stimulated under conditions of balanced nutrition as a result of which its toxic effect might be increased.

Aflatoxin B1↗
PubMed2006

The effect of intravenous iron on oxidative stress in hemodialysis patients at various levels of vitamin C.

BACKGROUND/AIMS: Vitamin C levels decrease during hemodialysis (HD), which deteriorates antioxidant defense. Vitamin C may also act pro-oxidatively, via reduction in Fe(III). We sought to determine whether intravenous iron (Fe(iv))-induced oxidative stress differs in HD patients with low and physiological vitamin C levels and whether intravenous vitamin C (C(iv)) administration during HD would change the response to Fe(iv). PATIENTS AND METHODS: Twenty patients with vitamin C deficiency (median 15.7 micromol/l, range 8.0-22.7) received Fe(iv) (100 mg iron sucrose between 150 and 180 min of HD). After 4 weeks of oral supplementation, the levels of vitamin C were comparable with those of controls (60.1 micromol/l, range 47.4-70.9). Patients were subsequently treated with (1) Fe(iv), (2) Fe(iv) and continuous 2 mg/min C(iv) throughout HD, (3) saline (S), and (4) S+C(iv). Plasma thiobarbituric acid reacting substances (TBARS) and vitamin C were assessed before, during and after FE(iv)(S), and 15, 30 and 60 min after infusion. RESULTS: Fe(iv) induced a comparable rise in TBARS in patients with vitamin C deficiency (before Fe(iv), 1.9 micromol/l, range 1.4-1.9; after Fe(iv), 2.6 micromol/l, range 2.3-2.9; p < 0.01) and in those with normal vitamin C (before Fe(iv), 1.9 micromol/l, range 1.7-2.1; after Fe(iv), 2.6 micromol/l, range 2.5-2.9; p < 0.01). Fe(iv)+C(iv) resulted in a greater increase in TBARS (after Fe(iv), 3.1 micromol/l, range 2.8-3.2) compared with Fe(iv) (p < 0.01). CONCLUSION: Iron sucrose-induced oxidative stress is comparable in HD patients with vitamin C deficiency and in those with normal vitamin C. We documented a pro-oxidative effect of vitamin C during Fe(iv)+C(iv) administration.

Administration, Oral↗
PubMed1990

Controlled vitamin C restriction and physical performance in volunteers.

A double-blind study on the effects of vitamin C restriction on physical performance was executed with 12 healthy men. During seven weeks of low vitamin C intake six subjects were on a daily diet of regular food products, providing 20% of the Dutch Recommended Dietary Allowances (RDA) for vitamin C (Dutch RDA is 50 mg/day). Other vitamins were supplemented at twice the RDA level. After three weeks of low vitamin intake an additional vitamin C dose of 15 mg/day was provided, resulting in a total intake of 25 mg/day (50% of the Dutch RDA). Six control subjects consumed the same diet supplemented with twice the RDA for all vitamins. In the restriction group blood vitamin C levels decreased significantly (p less than 0.01). Vitamin C restriction had no harmful effects on health, aerobic power (VO2-max), and onset of blood lactate accumulation (OBLA). However, an increased heart rate at OBLA level was observed during the period of low vitamin C intake (p less than 0.05), possibly by interference with either catecholamine or carnitine metabolism. These results suggest that short-term marginal vitamin C deficiency does not affect physical performance in single bouts of intensive exercise.

Adult↗
PubMed1981

The nutritional status of patients with an alcohol problem.

73 patients with an alcohol problem seen in a hospital medical unit over a two year period were examined specifically for signs suggestive of nutritional deficiency and of organ or system damage due to alcohol. A seven day dietary recall was carried out on most of them. Clinical signs of nutritional deficiency were relatively uncommon but nine patients had Wernicke-Korsakoff syndrome and ten had peripheral neuropathy. Thiamine was present in less than recommended amounts in 81.5% of the diets. Vitamin D and vitamin C were the next most common dietary deficiencies. 66.1% were deficient in energy intake and about a third of patients derived more than 40% of their energy from alcohol.

Adult↗
PubMed2000

[Scurvy presenting with ecchymotic purpura and hemorrhagic ulcers of the lower limbs].

INTRODUCTION: The risk of vitamin C deficiency is underestimated in industrialized countries and is only disclosed in rare cases of severe scurvy. CASE REPORT: We report three cases of scurvy presenting with ecchymotic purpura and hemorrhagic ulcerations of the lower limbs. Vitamin C supplementation led to rapid improvement of the skin lesions. DISCUSSION: Clinical diagnosis of low-grade deficiency can be difficult. Biological diagnosis requires special care in sample taking and transport.

Aged↗
PubMedDate not supplied

[Effect of acute and chronic lindane poisoning on the function of the liver microsome mono-oxygenase system in rats maintained on a diet deficient in lysine, methionine, threonine and vitamins A, C and E].

Polynutrient deficiency in essential amino acids and vitamins A, C and E led to induction of liver tissue microsomal monooxygenase system in male rats of WAG strain within first 2 hrs and to inhibition of the induction within the subsequent hours after a single dose administration of a pesticide lindane (18 mg/kg) as compared with control animals maintained on a normal diet. The deficiency in essential nutrients caused also a delay in the monooxygenase induction in rats treated daily within 3 months with lindane at a dose of 0.9 mg per kg of body mass. No distinct nutritionally-dependent differences in the rate of the monooxygenase induction were observed after 6 months of the chronic treatment with the pesticide. Activity of monooxygenases in nutritionally-deprived and lindane-treated rats was decreased as compared with the similarly treated rats which were maintained on a normal diet. The induction of monooxygenases in experimental rats was accompanied by an increase in relative mass of liver tissue. The increase in liver tissue mass appears to occur as an adaptive response to the polynutrient deficiency and the effect of xenobiotics in order to maintain the enzymatic system at an adequate functional level.

Amino Acids, Essential↗