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PubMed1989

Vitamin C lowers mutagenic and toxic effect of hexavalent chromium in guinea pigs.

The mutagenic effect of intraperitoneally injected K2Cr2O7 was significantly higher in vitamin C-deficient guinea pigs than in animals fed diet with high vitamin C content. Mutagenic and toxic effects of hexavalent chromium were more expressed in vitamin C-deficient guinea pigs administered K2Cr2O7 in drinking water: the number of micronuclei in polychromatic erythrocytes of bone marrow was increased, and the activity of O-demethylase and the levels of cytochromes P-450 and b5 in liver microsomes were decreased. In guinea pigs fed high vitamin C diet the same doses of bichromate in drinking water evoked no mutagenic changes in the bone marrow and no changes in microsomal enzymes in the liver. These results indicate that high intake of ascorbic acid in the diet reduces mutagenic effects of K2Cr2O7 and its toxic influence on drug metabolizing enzymes in hepatocytes. The protective effect ascorbic acid consists most probably in the enhanced extracellular and intracellular reduction of hexavalent chromium to the less toxic and less mutagenic trivalent chromium.

Animals↗

PubMed1975

A fine structural demonstration that some benzopyrones act as vitamin P in the rat.

In rats fed a diet lacking flavonoids (but which had supplementary vitamin C) definite fine structural alterations were found in blood capillaries and tissues. These fine structural alterations were quite different from those reported in C-avitaminosis and imply a different deficiency. They were largely prevented by feeding the benzopyrones, coumarin or coumarin plus troxerutin, thus pointing to the specificity of the lesions. This implies that, for the rat, benzopyrones are vitamins and that vitamin C and "vitamin P"-deficiency states are qute distinct. In "P-avitaminosis" the basic lesion is the opening of some blood capillary endothelial intercellular junctions. Unlike in C-avitaminosis, the endothelial cells are intact, without pale, grossly swollen cytoplasms.

Animals↗

PubMed2003

Combined deficiency of vitamins E and C causes paralysis and death in guinea pigs.

BACKGROUND: On the basis of in vitro studies, the antioxidant nutrients vitamins E and C are postulated to interact in vivo. OBJECTIVE: We developed a guinea pig model to evaluate the combined deficiency of vitamins E and C in vivo. DESIGN: Weanling guinea pigs were fed a control diet or a vitamin E-deficient diet for 14 d, after which one-half of each group had vitamin C removed from their diet, thus creating 4 diet groups. Some animals were observed for clinical signs. Others were killed for evaluation. RESULTS: Of 21 guinea pigs that were observed after being fed the diet deficient in both vitamins, 8 died 9 +/- 2 d (x +/- SD) after starting the diet. Eight additional guinea pigs developed a characteristic syndrome at 11 +/- 3 d. First, they became paralyzed in the hind limbs. Within a few hours, the paralysis progressed to include all 4 limbs and caused difficulty in breathing, which would have caused death had the animals not been euthanized. Histopathologic evaluation did not identify a lesion in the muscles or nervous system that could account for the paralysis. Biochemical measurements confirmed the deficiencies and indicated that the double deficiency caused lipid peroxidation in the central nervous system. CONCLUSIONS: A distinct clinical syndrome of combined vitamin E and vitamin C deficiency occurs in guinea pigs. This syndrome indicates that these antioxidant vitamins are related in vivo. We speculate that acute oxidative injury in the central nervous system underlies the clinical syndrome.

Animals↗

PubMed1976

Hepatic 7alpha-hydroxylation of cholesterol in ascorbate-deficient and ascorbate-supplemented guinea pigs.

Cholesterol 7alpha-hydroxylase activity was assayed in liver microsomes from guinea pigs supplemented with ascorbate and from guinea pigs in a state of ascorbate deficiency. A mass fragmentographic method was used by which the 7alpha-hydroxylation of endogenous cholesterol could be measured. The 7alpha-hydroxylation was markedly reduced in the ascorbate-deficient animals as compared to animals treated with ascorbate. Addition of ascorbate to the incubations did not increase this activity. 11- and 12-Hydroxylation of laurate as well as 25- and 26-hydroxylation of 5beta-cholestane-3alpha, 7alpha-diol were not significantly affected by the ascorbate status of animals. In the presence of excess NADPH-cytochrome P-450 reductase and a phospholipid, partially purified cytochrome P-450 from the microsomal fraction of liver of an ascorbate-deficient guinea pig had a much lower capacity to 7alpha-hydroxylate [4-14C]cholesterol than a corresponding system containing cytochrome P-450 from liver of an ascorbate-supplemented guinea pig. It is suggested that ascorbate affects the synthesis or breakdown of the 7alpha-hydroxylating system, in particular the cytochrome P-450 component.

Animals↗

PubMed2004

[Micronutrients status of Ile-de-France inhabitants. A literature review].

PURPOSE: A review of the literature about micronutrients status of Ile-de-France inhabitants. CURRENT KNOWLEDGE AND KEY POINTS: During the last decades, substantial changes in the French diet had an impact on micronutrients intake. Over this time, several studies conducted in Ile-de-France showed that a large part of its inhabitants is subject to an increased risk of mild to severe deficiency in one or more micronutrient(s). Teenagers and subjects over 70 years-old are groups at risk for vitamin D deficiency. During the 1980s, iron intake was insufficient in a majority of menstruating women and iron deficiency was common during pregnancy. Vitamin C deficiency is constantly present in homeless people and often associated with an insufficient intake in a number of micronutrients. FUTURE PROSPECTS AND PROJECTS: Identification of the groups at risk favours a better adequacy of preventive action on micronutrient deficiencies in this population. However, the efficacy of prevention is to be determined. Controlled trials of micronutrients' supplementation may be useful to value the beneficial effects of micronutrient supplementation on the incidence of cardiovascular diseases and cancer.

Adolescent↗

PubMed1977

Vitamin C status of elderly men in a residential home.

The vitamin C status of 35 men, over 70 years of age from a residential home has been studied by measuring the plasma and leucocyte vitamin C levels and by assessing the intake of vitamin C. The mean plasma vitamin C level of the group was 16 +/- 15 mumol/l which was significantly lower (P less than 0.005) than that of a similar group of elderly men living alone (26 +/- 20 mumol/l). The mean leucocyte vitamin C levels of the two groups did not differ significantly. Twenty-nine (83 percent) of the institution group had plasma vitamin C levels below 23 mumol/l and 13 men (37 percent) had leucocyte vitamin C levels below 10 microgram/10(8)WBC. The residents who supplemented the institution diet with their own fresh fruit supplies had higher plasma and leucocyte vitamin C levels than the men who did not (P less than 0.01). Some clinical signs possible related to vitamin C deficiency were recorded but these could not later be statistically related to either plasma or leucocyte vitamin C levels. A case is made for vitamin C supplementation of puddings in institutional meals for the elderly.

Aged↗

PubMed2006

Vitamin C deficiency increases the lung pathology of influenza virus-infected gulo-/- mice.

This study was designed to determine the effects of vitamin C deficiency on the immune response to infection with influenza virus. l-Gulono-gamma-lactone oxidase gene-inactivated mice (gulo-/- mice) require vitamin C supplementation for survival. Five-wk-old male and female gulo-/- mice were provided water or water containing 1.67 mmol/L vitamin C for 3 wk before inoculation with influenza A/Bangkok/1/79. There were no differences in lung influenza virus titers between vitamin C-adequate and -deficient mice; however, lung pathology in the vitamin C-deficient mice was greater at 1 and 3 d after infection but less at d 7 compared with vitamin C-adequate mice. Male vitamin C-deficient mice had higher expression of mRNA for regulated upon activation normal T expressed and secreted (RANTES), IL-1beta, and TNF-alpha in the lungs at d 1 after infection compared with male controls. However, at d 3 after infection, male vitamin C-deficient mice had less expression of mRNA for RANTES, monocyte chemotactic protein-1 (MCP-1), and IL-12 compared with male controls. None of these differences were observed in female mice. Vitamin C-deficient male mice also had greater nuclear factor-kappaB activation as early as 1 d after infection compared with male controls. These data suggest that vitamin C is required for an adequate immune response in limiting lung pathology after influenza virus infection.

Animals↗

PubMed1978

Parenteral vitamin requirements during intravenous feeding.

Serum vitamin levels of 40 patients undergoing parenteral nutrition over a 5-to 42-day period were studied while the subjects received daily water-soluble and once weekly fat soluble vitamin formulations intravenously. Initial serum deficiencies of vitamins A, C, and folate were noted in a large portion of the severely malnourished population. At the replacement levels used in this study a small number of patients developed subnormal levels of vitamins A and D. Improvement in levels for vitamin C and folate were noted for most patients. Vitamin B12 deficiencies were not noted in any patient. Currently available commercial vitamin preparations can be used with safety in the parenterally nourished population and recommended guidelines for weekly infusion of both water and fat soluble vitamins are presented.

Adolescent↗

PubMed1984

Carnitine biosynthesis from gamma-butyrobetaine and from exogenous protein-bound 6-N-trimethyl-L-lysine by the perfused guinea pig liver. Effect of ascorbate deficiency on the in situ activity of gamma-butyrobetaine hydroxylase.

The production of carnitine from peptide-bound 6-N-trimethyl-L-lysine (Lys(Me3)) or 4-N-trimethyl-aminobutyrate(gamma-butyrobetaine) perfused through isolated guinea pig livers was investigated. [Methyl-3H] Lys(Me3)-labeled agalacto-orosomucoid (AGOR) and asialofetuin were rapidly taken up and degraded by the perfused liver. Most of the free Lys(Me3) derived from Lys(Me3)-AGOR was released unmodified into the perfusion medium. However, Lys(Me3), arising from Lys(Me3)-asialofetuin was converted mostly to gamma-butyrobetaine and carnitine. gamma-Butyrobetaine added to the perfusion medium was hydroxylated to carnitine by the liver at a rate of 2.3 mumol/h. Guinea pigs maintained on an ascorbate-free diet for 17-60 days showed lowered ascorbate contents in all tissues measured and, coincidentally, a sharp reduction in carnitine levels in kidney, liver, and cardiac, and skeletal muscle. Carnitine production from [1,2,3,4-14C]gamma-butyrobetaine and [methyl-3H]Lys(Me3)-asialofetuin was reduced in perfused livers obtained from ascorbate-deficient guinea pigs. Although hydroxylation of gamma-butyrobetaine to carnitine was effectively depressed in the perfused isolated livers from ascorbate-deficient animals, hydroxylation of [methyl-3H]Lys(Me3) (derived from asialofetuin) to [methyl-3H]3-hydroxy-6-N-trimethyl-L-lysine was unaffected. Prior administration of ascorbate to the medium perfusing the isolated livers caused carnitine biosynthesis from all precursors examined to return to control values.

Animals↗

PubMed1979

Drugs and vitamin deficiency.

During the past 10 to 20 years it has become increasingly clear that a certain number of drugs may lead to increased vitamin requirements. However, it is unusual for symptomatic avitaminosis to develop, and then only when circumstances are present which in themselves increase the risk of vitamin deficiency. Therapeutic doses of drugs will interfere with the vitamin status only to a restricted degree, provided they are administered for brief periods and to patients receiving a normal supply of vitamins. Most cases of vitamin deficiency have in fact been described in connection with drugs usually taken for a longer period of time by patients who were already in negative vitamin balance as a result of disease or marginal supply of the necessary vitamins. This review describes some of the more important articles covering this topic.

Ascorbic Acid Deficiency↗

PubMed2005

[Ferro-folgamma--a good alternative in the treatment of iron deficiency anemia and depleted iron stores in pregnant women].

OBJECTIVE: To study the effect of different therapeutical regimens of Ferro-Folgamma, in pregnant patients with iron deficiency anemia. MATERIALS AND METHODS: 22 pregnant patients between 20 and 35 week of gestation (mean 29 gestational week) with hemoglobin levels between 83.1-106 g/l were included. They were divided in two groups: group 1 included patients with hemoglobin levels up to 100g/l and group 2--with hemoglobin levels between 100 and 110. The dosage of the preparation in group 1 was 1 tablet Ferro-Folgamma tid for 40 days, and 1 tablet Ferro-Folgamma bid for the same period. Blood samples were taken four times during the study on day 0, 10th day, 20th day and in the week after the 40th completed day of therapy. The samples were tested for CBC, iron, transferine, feritine, folic acid. All patients were given complete information about the possible risks of iron deficiency anemia during pregnancy and parturition. DISCUSSION AND RESULTS: The mean hemoglobin level at initiation of treatment was 91.22 g/l (day 0). After initiation of treatment the the following rise in hemoglobin levels was detected 10th day - 103.8 g/l, 20th day - 112.6 g/l, after the 40th completed day - 136.0 g/l. The mean levels of the rest of hematological parameters were, day 0 - Er - 3.25 mln/microl, Fe - 7.53 micromol/l, transferine - 3.65 gr/l, feritine - 15.02 ngr/ml, folic acid - 14.08 ng/ml, vit. B12 - 219.68 pg/ml; 10th day - Er- 3.5 mln/microl, Fe - 14. 12 micromol/l; 20th day - Er - 4.10 mln/microl, Fe - 20.46 micromol/l; 40th completed day - Er- 4.69 mln/microl, Fe - 13.12 micromol/l, transferine - 3.82 gr/l, feritine - 27.42 ngr/ml, folic acid - 15.67 ng/ml, vit. B12 - 484.52 pg/ml respectively. CONCLUSIONS: Oral treatment with Ferro-Folgamma, according the described dosage regimen, demonstrates its fast and stable effect in treatment of moderate iron deficiency and recovery of depleted iron pool in pregnant patients as well. It could be administered as a prophylactic preparation for borderline anemic states.

Anemia, Iron-Deficiency↗

PubMed2004

Elevated blood histamine caused by vaccinations and Vitamin C deficiency may mimic the shaken baby syndrome.

The findings of subdural hematoma and retinal hemorrhages in infants, without any documented history of major trauma, do not always indicate child abuse. A combination of ascorbate depletion and the injection of foreign proteins can cause a very high blood histamine level, leading to capillary fragility and venular bleeding. This can be prevented by the administration of vitamin C.

Ascorbic Acid↗

PubMed1998

Vitamin C nutriture and risk of atherosclerotic heart disease.

There is substantial evidence for a role of dietary antioxidants in the prevention of cardiovascular disease, but evidence for a protective effect of vitamin C is inconclusive. Two recent reports add to the supporting evidence and provide some new observations. The first study, a 5-year prospective population study of Finnish men, suggests that vitamin C-deficient men may be at increased risk of myocardial infarction. The second study suggests that vitamin C may play a role in preventing manifestations of existing coronary artery disease, rather than in limiting disease progression. Although these results suffer from the limitations of observational studies, they provide impetus for further investigation.

Antioxidants↗

PubMed1985

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) does not destroy nigrostriatal neurons in the scorbutic guinea pig.

Guinea pigs were injected subcutaneously with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in maximal tolerated doses (8 mg/kg, once daily) for 10 or 15 days. No neurological effects were noted, other than sedation and hypotonia lasting a few hours after each injection, either in animals maintained on normal diet or in animals fed an ascorbate-deficient diet and rendered severely scorbutic. Subsequent chemical analyses of the striatum showed no evidence of lasting damage to nigrostriatal dopaminergic neurons in MPTP treated guinea pigs on normal diet, and minimal evidence of permanent damage to these neurons in scorbutic animals. MPTP was undetectable in the urine of MPTP-treated animals, although a metabolite, presumably 1-methyl-4-phenylpyridinium ion (MPP+) was regularly present in urine. The relative lack of neurotoxicity of MPTP in the guinea pig remains unexplained. This species clearly is not a suitable small animal for MPTP-induced parkinsonism.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMedDate not supplied

Zinc and antioxidant vitamin deficiency in patients with severe sickle cell anemia.

BACKGROUND: Patients with severe sickle cell anemia (SCA) have a higher potential for oxidative damage due to chronic redox imbalance in red blood cells that often leads to hemolysis, endothelial injury and recurrent vaso-occlusive episodes. This study evaluated the plasma levels of vitamins A, C and E as indicators of antioxidant status. In addition, serum levels of zinc and copper were also estimated. PATIENTS AND METHODS: Twenty-five adult patients with severe sickle cell anemia (12 males and 13 females aged 29.72+/-12.94 years) and 25 matched controls were studied. Plasma levels of vitamins A, C and E were measured by HPLC technique. Serum zinc and copper levels were measured by atomic absorption spectrometry. RESULTS: There was a significant decrease in plasma levels of vitamins A, C and E and in serum levels of zinc in patients with SCA as compared with controls (P<0.0001). Serum copper levels were signficantly elevated compared with controls (P<0.0001). CONCLUSION: These findings emphasize the significant deficiencies of the antioxidant vitamins A, C and E and the trace element zinc along with the significant elevation of serum copper in patients with severe sickle cell disease. Further studies are needed to find out whether supplementation of antioxidant vitamins and zinc may ameliorate some sickle cell disease complications.

Adolescent↗

PubMed1995

Ozone-induced pulmonary functional, pathological, and biochemical changes in normal and vitamin C-deficient guinea pigs.

Since Vitamin C (ascorbate, AH2) is an important airway antioxidant and is an essential component of tissue repair, and since acute (4 hr) O3 toxicity is enhanced by AH2 deficiency, we hypothesized that longer-term O3 effects might also be increased. Female Hartley guinea pigs (260-330 g) were fed either an AH2-sufficient or an AH2-deficient diet 1 week prior to exposure, and were maintained on their respective diets during 1 week of continuous exposure to O3 (0, 0.2, 0.4, and 0.8 ppm, 23 hr/day), and during 1 week postexposure recovery in clean air. The AH2-deficient diet caused lung AH2 to drop to about 30% of control in 1 week, and to below 10% by the end of exposure and recovery. Body weight gains during exposure were decreased in the 0.8 ppm O3 group, while the AH2 deficiency began to affect body weights only during recovery. O3 caused a concentration-dependent decrease in total lung capacity, vital capacity, carbon monoxide diffusing capacity, nitrogen washout, and static compliance, while increasing forced expiratory flow rates and residual or end-expiratory volume (suggestive of pulmonary gas-trapping). The lung/body weight ratio and fixed lung displacement volume were also increased in O3-exposed animals. Lung pathology consisted of mononuclear cell and neutrophil infiltration, airway as well as alveolar epithelial cell hyperplasia, and general decrease in epithelial cell cytoplasm. Thickening of the interstitium and an apparent increase in collagen staining were seen at the terminal bronchiolar regions. Some of these effects were marginally exacerbated in AH2-deficient guinea pigs. One week postexposure to air reversed all O3-induced abnormalities, irrespective of AH2 deficiency. Whole lung hydroxyproline and desmosine were not changed at any time by either O3 or AH2 deficiency. Measurement of lung prolyl hydroxylase activity suggested that AH2 deficiency as well as O3 exposure may have increased the tissue levels of this enzyme. The lack of a significant increase in toxicity with the longer-term exposure scenario suggests that AH2 has minimal influence on other compensatory mechanisms developed over time.

Animals↗

PubMedDate not supplied

Depletion of iron and ascorbate in rodents diminishes lung injury after silica.

Exposures of the lung to iron chelates can be associated with an injury. The catalysis of oxygen-based free radicals is postulated to participate in this injury. Such oxidant generation by mineral oxide particles can be dependent on availability of both iron and a reductant. We tested the study hypothesis that lung injury after silica is associated with the availability of both iron and ascorbate in the host by depleting this metal and reductant in the lungs of rats and guinea pigs, respectively. Rats were fed either a normal diet or a diet deficient of iron. After 30 days, animals were instilled with either saline or 1.0 mg Minusil-5 silica. Relative to saline, silica significantly increased neutrophils and lavage protein. Iron depletion significantly diminished both the cellular influx and injury but only at 1 week after silica exposure. Guinea pigs were provided either a normal diet supplemented with 1,000 ppm vitamin C or a diet deficient in ascorbate. After 14 days, the guinea pigs were instilled with either saline or 1.0 mg silica. Silica exposure significantly increased neutrophils and lavage protein. Ascorbate depletion significantly diminished the influx of inflammatory cells and injury at both 1 day and 1 week after silica exposure. We conclude that host concentrations of both iron and ascorbate can affect lung injury after silica exposure.

Animals↗

PubMed1987

Experimental vitamin C depletion and supplementation in young men. Nutrient interactions and dental health effects.

Biochemical indices of AA clearly showed that the young men in this study were brought into various states of AA depletion and repletion according to their dietary AA intakes. While previous studies have postulated that supplemental intakes of AA may adversely affect body status of vitamins B6 and B12, we found no changes in the B vitamin status of the young men receiving varying AA intakes. Moderate AA supplementation (605 mg/day) showed no antagonistic effect on markers of vitamins B6 and B12. Blood markers of fat-soluble vitamins A and E and iron status were not affected by AA intakes. The propensity of the gingiva to become inflamed or bleed on probing was reduced after normal (65 mg/day) AA intakes as compared to deficient (5 mg/day) intakes and upon supplementary (605 mg/day) AA intakes as compared to normal intakes. The results suggest that AA status may influence early stages of gingival inflammation and crevicular bleeding, and warrant further study of the relationship between AA and periodontal health.

Adult↗