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PubMedDate not supplied

Intravenous ascorbic acid in hemodialysis patients with functional iron deficiency: a clinical trial.

BACKGROUND: Hemodialysis (HD) patients with functional iron deficiency (FID) often develop resistance to recombinant human erythropoietin (rHuEpo). In these patients, iron therapy may be a hazard, leading to iron overload and consequently to hemosiderosis. Recent studies suggest that intravenous ascorbic acid (IVAA) may circumvent rHuEpo resistance. The aim of our study was to show the effects of IVAA on FID and whether this results in a better correction of anemia in HD patients with stable hemoglobin (Hb) concentration and FID. METHODS: Twenty-seven HD patients with serum ferritin >300 microg/l, transferrin saturation (TS) <20% and hemoglobin (Hb) <10 g/dL were selected andrandomly divided into two groups to enter a cross-over trial with IVAA. In group I IV vitamin C 500 mg was administered three times a week for three months and discontinued in the next three months of the study. Vitamin C was not given the first three months in group II (control group, first three months of the study), who then received 500 mg IV three times a week for the next three months. RESULTS: Hb and TS% significantly increased (baselines vs 3 months, Hb 9.2 +/- 0.2 vs 10.0 +/- 0.3 g/dL, TS% 17.5 +/- 0.6 vs 25.7 +/- 1.7, respectively p < 0.01 and p <0.001) in group I after three months; ferritin fell significantly from 572 +/- 40 to 398 +/- 55 microg/L (p<0.004). Ten patients completed the study: mean Hb and TS% fell significantly (3 months vs final, Hb 9.9 +/- 0.3 vs 8.9 +/- 0.2 g/dL, TS% 25.1 +/- 1.2 vs 19.1 +/- 1.1, respectively p < 0.01 and p <0.001), while mean ferritin did not change. Mean Hb, ferritin and TS% remained unchanged in group II after three months. Hb and TS% mean values rose significantly (3 months vs final, Hb 9.0 +/- 0.2 vs 9.9 +/- 0.2 g/dl, TS% 18.4 +/- 1.0 vs 27.0 +/- 1.0, respectively p < 0.005 and p <0.001), and ferritin markedly decreased from 450 +/- 50 to 206 +/- 24 microg/L (p < 0.001) at the end of the study. The rHuEpo dose was kept unchanged throughout the study. Differences were analyzed after three months. Mean Hb rose (0.8 +/- 0.2 g/dL) in group I but dropped (-0.1 +/- 0.1 g/dL) (p< 0.009) in group II. Ferritin dropped in both groups (group I vs group II, -173 + /-48 vs - 33 +/- 21 microg/L) (p < 0.01) while TS% increased (group I vs group II, 8.2 +/- 1.5 vs 0.4 +/- 0.7) (p < 0.001). CONCLUSION: IVAA may partially correct FID and consequently help rHuEpo hyporesponsive anemia.

Adult↗
PubMed2004

Iron absorption by heterozygous carriers of the HFE C282Y mutation associated with hemochromatosis.

BACKGROUND: Research conducted before genotyping was possible suggested that subjects heterozygous for the genetic mutation associated with hemochromatosis absorbed nonheme iron more efficiently than did control subjects when tested with a fortified meal. Heme-iron absorption in these subjects has not been reported. OBJECTIVE: We compared the absorption of heme and nonheme iron from minimally or highly fortified test meals between HFE C282Y-heterozygous and wild-type control subjects. DESIGN: After prospective genotyping of 256 healthy volunteers, 11 C282Y-heterozygous and 12 wild-type control subjects were recruited, and their iron absorption was compared by using a hamburger test meal with or without added iron and ascorbic acid. After retrospective genotyping of 103 participants in previous iron-absorption studies, 5 C282Y-heterozygous subjects were compared with 72 wild-type control subjects. RESULTS: HFE C282Y-heterozygous subjects did not differ significantly from wild-type control subjects in their absorption of either heme or nonheme iron from minimally or highly fortified test meals. No differences were detected in blood indexes of iron status (including serum ferritin, transferrin saturation, and non-transferrin-bound iron) or in blood lipids or transaminases, but heterozygotes had significantly greater, although normal, fasting glucose concentrations than did wild-type control subjects. Compound heterozygotes (those who had both HFE C282Y and H63D mutations) absorbed more nonheme (but not heme) iron from meals with high (but not low) iron bioavailability. CONCLUSIONS: HFE C282Y-heterozygous subjects did not absorb dietary iron more efficiently, even when foods were highly fortified with iron from ferrous sulfate and ascorbic acid, than did control subjects. Iron fortification of foods should not pose an additional health risk to HFE C282Y heterozygotes.

Adult↗
PubMed1980

Effect of ascorbic acid on the resistance of the extracellular matrix to hydrolysis by tumor cells.

Extracellular matrices produced by cultured rat smooth muscle cells in the presence or absence of ascorbic acid wee used as substrates for the human fibrosarcoma cell line HT1080. The matrix elaborated by smooth muscle cells in the presence of ascorbic acid contained glycoproteins, elastin, and collagen, and all of these components were digested by the tumor cells. In contrast, the matrix elaborated in the absence of ascorbic acid which contained glycoproteins and underhydroxylated elastin but no collagen was more resistant to tumor-induced hydrolysis. The underhydroxylated elastin was particularly refractory to the tumor proteases, suggesting that the elastolytic activity produced by HT1080 cells showed a marked preference for the natural substrate containing hydroxyproline. The digestion by HT1080 cells of elastin from living cultures of smooth muscle cells was also retarded if the extracellular proteins were produced under ascorbic acid-deficient conditions. These experiments therefore do not support the notion that connective tissues made under scorbutic conditions are inherently more susceptible to tumor hydrolysis.

Ascorbic Acid↗
PubMedDate not supplied

[Ascorbic acid supply and cytochrome P-450 levels in guinea pig liver after dimethylformamide poisoning].

The universal solvent dimethylformamide (DMFA) administered to guinea-pigs in a dose of 400 mg/kg bw per os for 14 days produced a considerable decrease in the content of total and reduced ascorbic acid (AA) in the liver, in all forms of AA in the adrenals, and lowering of vitamin C excretion with daily urine. The liver showed an increase in the concentration of dehydroascorbic acid and diminution of the concentration of cytochrome P-450 detected in liver homogenates. Additional administration of AA (50 mg/day) recovered the lowered level of the vitamin in the liver and adrenals but did not make the daily excretion of AA with urine return to normal. Additional administration of vitamin C to guinea-pigs recovered the level of cytochrome P-450 in liver homogenates, which was reduced during DMFA poisoning. One of the reasons for the development of vitamin C deficiency during DMFA poisoning is likely to be high oxidation of AA.

Adrenal Glands↗
PubMed1984

[Deficiency anemias in tropical countries].

Nutritional anaemias are common in tropical areas. The commonest cause is iron deficiency, which mainly arises from impaired absorption of iron from food. Substances which inhibit iron absorption in various diets play an important role in the pathogenesis of iron deficiency anaemia. Iron deficiency is further aggravated by blood loss in hook-worm infestation. Folic acid and vitamin B 12 deficiency are less important causes of nutritional anaemia. The efforts of the World Health Organization to supplement iron in food are described.

Anemia, Hypochromic↗
PubMed1976

Vitamin A deficiency and the metabolism of glycosaminoglycans and ascorbic acid in the rat.

Weanling rats were fed diets with and without the addition of retinyl palmitate at 6,500 units/kg. The supplemented groups were fed either ad libitum or food was restricted daily to that amount consumed by the group of rats receiving the unsupplemented diet. After a 10 week experimental period, signs of vitamin A deficiency were observed (growth plateau, xerophthalmia) and liver values as retinol were only 1% of control values. Relative to the two control groups, vitamin A deficiency resulted in approximately 30% lower liver, 50% lower blood and 40% lower urinary ascorbic acid. Vitamin A deficiency did not appear to result in significant and direct impairment of GAG sulfate metabolism. Although the total amount of GAG in rat skin was increased, the composition of GAG fractions did not appear to be altered by vitamin A deficiency. Studies regarding the incorporation and disappearance of 35S-sulfate in vivo into GAG fractions obtained from skin indicated no serious impairment in GAG turnover with vitamin A deficiency. Twenty-four hour urine samples were also collected for estimation of 35SO4 excreted in GAG and non-GAG fractions. Likewise, little change was observed with respect to radioactivity associated with sulfate fractions excreted in urine. Although many previous studies have directly linked vitamin A with sulfation of GAG, the results reported here suggest that if there is an alteration in GAG sulfate metabolism, it is probably an indirect consequence of vitamin A status.

Animals↗
PubMed1995

Ozone-induced tissue injury and changes in antioxidant homeostasis in normal and ascorbate-deficient guinea pigs.

It has been reported previously that ozone (O3) toxicity from acute (4 hr) exposure is enhanced by ascorbate (AH2) deficiency in guinea pigs. We hypothesized that lung injury from continuous 1-week O3 exposure would also be increased under conditions of AH2 deficiency because of (1) a diminished antioxidant pool to counteract the oxidant challenge, (2) impaired reparation of tissue injury, and/or (3) altered antioxidant redox homeostasis. Female Hartley guinea pigs (260-330 g) were made AH2 deficient by providing a diet similar to guinea pig chow, but having no AH2. The dietary regimen was started 1 week prior to exposure and was continued during exposure to O3 (0, 0.2, 0.4, or 0.8 ppm, 23 hr/day, 7 days) as well as 1 week post-exposure. Bronchoalveolar lavage (BAL) and tissue AH2 were measured in subgroups at the beginning of exposure (1 week on the AH2-deficient diet), at its termination and 1 week post-exposure. AH2 measured in ear tissue punches proved to be an easy and effective monitor for AH2 deficiency. One week on the AH2-deficient diet caused a 70-80% drop in ear, lung and liver AH2, while AH2 in BAL was decreased by 90%. Immediately after the exposure, total BAL protein and albumin (markers of lung permeability) were increased (approximately 50%) at 0.8 ppm with no difference between the dietary groups. O3 caused an increase in total BAL cells and neutrophils in a concentration-dependent manner with only a slight augmentation due to diet. Exposure to O3 caused an increase in lung and BAL AH2 in normal guinea pigs. Glutathione and uric acid were also increased in the lung and BAL after O3 exposure (40-570%) in both dietary groups, and the levels remained elevated during the recovery period. Lung alpha-tocopherol was not changed due to O3. A significant overall diet-related decrease was seen in AH2-deficient guinea pigs, immediately after the exposure and recovery. In summary, lung injury/inflammation following 1 week O3 exposure and recovery were minimally affected by AH2 deficiency. Antioxidants also appeared to increase in response to O3 exposure despite the deficiency in AH2.

Animals↗
PubMed1982

The effect of chemical and physiological factors on the kinetics for product formation as it relates to enzyme activity and concentration, reaction time and to substrate adsorption and affinity.

1. The dependency of product formation on reaction time and on enzyme concentration was studied with certain purified enzymes and liver microsomal mixed-function oxidase system. 2. The product-formation-time relation was estimated with different enzyme and/or substrate concentrations for the reactions limited by diffusion. 3. The kinetic constants of the product-time relations in these diffusion systems have been verified experimentally to give a more specific and detailed characterization of an enzyme system under a variety of physiologic and reaction conditions. 4. The influence of inhibitors and activators in vitro, the effect of enzyme preparation technic, aging, starvation, pretreatment with somatotropic hormone, phenobarbital or 3-methylcholanthrene, and the effect of a tumor were studied. 5. The influence of vitamin C deficiency in guinea pig was also studied.

Adenocarcinoma↗