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Results for “FOLIC ACID DEFICIENCY”

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PubMed1975

Metabolic studies of a family with massive formiminoglutamic aciduria.

We have described two siblings who excrete massive amounts (up to 3.89 mmol/24 hr) of N-formiminoglutamic acid (FIGLU) in their urine. This unusual compound was isolated from urine, purified, and firmly identified as FIGLU by combined gas chromatography-mass spectrometry. The patients presumably have a deficiency in activity of the hepatic enzyme, glutamate formiminotransferase, which carries out the fourth sequential step in the main pathway of histidine degradation. Unlike children reported previously with this disorder, our patients had normal serum folate levels, had no hematologic abnormalities, and were not mentally retarded. Very small amounts of FIGLU were present in the plasma of one of the patients, but FIGLU was not detectable in the cerebrospinal fluid of either patient. Administration of pharmacologic doses of folic or folinic acid produced a decrease in excretion of FIGLU in urine. Histidine loading caused a small and comparable urinary excretion of FIGLU in the children's parents and in control adult subjects.

Amino Acid Metabolism, Inborn Errors↗
PubMed2005

Chronic ethanol feeding and folate deficiency activate hepatic endoplasmic reticulum stress pathway in micropigs.

Previously, we showed that feeding micropigs ethanol with a folate-deficient diet promoted the development of hepatic injury while increasing hepatic levels of homocysteine and S-adenosylhomocysteine (SAH) and reducing the level of S-adenosylmethionine (SAM) and the SAM-to-SAH ratio. Our present goals were to evaluate mechanisms for hepatic injury using liver specimens from the same micropigs. The effects of ethanol feeding or folate-deficient diets, singly or in combination, on cytochrome P-450 2E1 (CYP2E1) and signal pathways for apoptosis and steatosis were analyzed using microarray, real-time PCR, and immunoblotting techniques. Apoptosis was increased maximally by the combination of ethanol feeding and folate deficiency and was correlated positively to liver homocysteine and SAH. Liver CYP2E1 and the endoplasmic reticulum stress signals glucose-regulated protein 78 (GRP78), caspase 12, and sterol regulatory element binding protein-1c (SREBP-1c) were each activated in pigs fed folate-deficient or ethanol diets singly or in combination. Liver mRNA levels of CYP2E1, GRP78, and SREBP-1c, and protein levels of CYP2E1, GRP78, nuclear SREBP, and activated caspase 12 each correlated positively to liver levels of SAH and/or homocysteine and negatively to the SAM-to-SAH ratio. The transcripts of the lipogenic enzymes fatty acid synthase, acetyl-CoA carboxylase, and stearoyl-CoA desaturase were elevated in the ethanol-fed groups, and each was positively correlated to liver homocysteine levels. The induction of abnormal hepatic methionine metabolism through the combination of ethanol feeding with folate deficiency is associated with the activation of CYP2E1 and enhances endoplasmic reticulum stress signals that promote steatosis and apoptosis.

Animals↗
PubMed1985

Theoretical involvement of vitamin B6 in tumour initiation.

Vitamin B6 is a co-enzyme involved in the biosynthesis of thymidine. Thymidine deficiency has been reported to increase DNA replication errors and hence increase mutagenesis. Carcinogenic stimulae increase the rate of DNA repair, and increase cell multiplication, both of which increase the requirement for thymidine. Vitamin B6 deficiency occurring at the same time as contact with carcinogens could well lead to tumour initiation and subsequent cancer development.

DNA↗
PubMedDate not supplied

Maternal-fetal folate transfer: effect of ethanol and dietary folate deficiency.

The effects of acute ethanol treatment and dietary folate deficiency on maternal-fetal folate transfer were studied to asses the hypothesis that the potentiation of ethanol's toxic effect on the fetus during ongoing folate deficiency was due to the impairment of folate transfer. Sprague-Dawley rats were fed either a folate-deficient diet (0.2 mg/kg) or a folate-sufficient diet (2 mg/kg) for an average of 11 weeks before pregnancy and continued until gestation day 11 when they were sacrificed. On gestation day 11, pregnant rats were treated with either ethanol (2.5 g/kg body weight) or isocaloric sucrose (control) followed by an intravenous administration of 3H-folate (2 muCi/100 g body weight) at 120 minutes. At 210 minutes, maternal blood and feto-placental tissues were removed for radioactivity measurement. Folate status and ethanol treatment had no effect on the distribution of 3H-folate in maternal circulation. However, contrary to the hypothesis, the uptake of 3H-folate by feto-placental tissues was increased in folate deficiency and by ethanol treatment, indicating that folate transfer was not impaired by the ethanol treatment. Other possibilities are discussed.

Animals↗
PubMed2003

Folate intake and risk of oral and pharyngeal cancer.

BACKGROUND: Diet has been recognised as having a role in the aetiology of oral and pharyngeal cancer, and dietary factors may account for 10-15% of cases in Europe. Folate deficiency has been linked to risk of several cancers, but has not been studied adequately with respect to oral cancer. PATIENTS AND METHODS: This case-control study, conducted in Italy and French-speaking Switzerland, included 749 patients with incident cancer of the oral cavity and pharynx, and 1772 hospital controls with acute, non-neoplastic conditions. The interviews used a validated food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multiple logistic regression. RESULTS: The ORs were 0.68 (95% CI 0.52-0.88) for the intermediate tertile and 0.53 (95% CI 0.40-0.69) for the highest tertile of dietary folate intake, compared with the lowest tertile. No heterogeneity was found in strata of gender, age, methionine intake or alcohol consumption. The combined OR for low-folate and high-alcohol intake versus high-folate and low-alcohol intake was 22.3 (95% CI 13.1-38). CONCLUSIONS: Our study supports a protective role of folate against oral and pharyngeal carcinogenesis. Compared with low folate intake, a consistent reduction in risk was already observed from intermediate levels of intake, suggesting that cancer risk may be related to relative folate deficiency.

Adult↗
PubMed1981

Methotrexate accumulation and folate depletion in cells as a possible mechanism of chronic toxicity to the drug.

Methotrexate has been associated with chronic toxicities such as cirrhosis and neurological impairments ranging from mild learning disorders to a fatal leucoencephalopathy. The mechanism(s) for this toxicity is not completely understood. Certain tissues can convert methotrexate to polyglutamates. This results in a more persistent intracellular form of the drug. In this study the intracellular levels of folate and methotrexate were measured in the erythrocytes and liver of patients treated chronically with methotrexate. These tissues showed an accumulation of methotrexate as polyglutamates and a concomitant loss of folate. Folate concentrations were below normal in nine of 12 red cell and three of five liver samples. It is proposed that persistent methotrexate concentrations and/or the associated folate deficiency may be related to the toxicity of methotrexate, especially in time of cellular stress.

Erythrocytes↗
PubMed1982

Vitamin B-12 (cobalamin) deficiency: a heretofore undescribed control mechanism for plasma corticosteroid-binding globulin concentration in man.

Six of eight patients with Addisonian pernicious anemia were found to have diminished corticosteroid-binding globulin (CBG) concentrations, which returned within 2 weeks to normal after the im administration of cobalamin. T4-binding globulin was found to be completely normal before and after cobalamin replacement. Other estrogen-responsive proteins, i.e. ceruloplasmin, alpha 1-trypsin inhibitor, haptoglobin, transferrin, and alpha 2-macroglobulin, also did not follow CBG concentration in a parallel fashion. The immunoglobulins similarly did not follow a course parallel to that of CBG. The CBG concentration in two untreated patients had a normal increase in response to estrogen administration, similar to that described in CBG deficiency from other causes. No clue was found regarding the mechanism by which B12 influences the putative hepatic control of CBG concentration. It is speculated that at least two control points may be necessary for a normal CBG concentration. Patients with a genetic deficiency of CBG may also have to have cobalamin deficiency in order for them to reach a concentration approaching zero.

Anemia, Pernicious↗
PubMed1991

High performance liquid chromatography method for rapid and accurate determination of homocysteine in plasma and serum.

Determination of homocysteine in plasma or serum for evaluation of cobalamin and folate deficiency is becoming an important diagnostic procedure. Accurate, rapid and low cost methods for measuring homocysteine are therefore required. We have improved an HPLC method and made it suitable for clinical application. The more important changes are the addition of an internal standard, mercaptopropionylglycine, and the use of a plasma/serum based calibration material. The method consists of the following steps: reduction of the sample with tri-n-butylphosphine, precipitation of proteins, derivatisation with ammonium 7-fluorobenzo-2-oxa-1,3-diazole-4-sulphonate, and HPLC separation followed by fluorescence detection. The linearity of the assays is established and the coefficient of variation is 3.0%. Stability studies show that blood samples must be cooled or centrifuged immediately after venipuncture. The method is useful for evaluation of cobalamin or folate deficiency, especially in patients with normal or moderately depressed cobalamin or folate concentrations in blood.

Chromatography, High Pressure Liquid↗
PubMed1990

[Role of zinc deficiency in the etiology of neural tube malformations].

The authors study the hypothesis of zinc deficiency as an etiology of malformations of the neural tube. This hypothesis is based on several facts: decrease of maternal zinc levels in this disease found by many authors, malformations of the neural tube induced by experimental deficiency in several animal species, zinc membrane transfer disorders found in fibroblasts cultures in affected newborns. Numerous zinc related biochemical mechanisms could explain this effect. But the most interesting would a disturbance of folate metabolism. In fact, neither a strict isolated zinc deficiency nor a strict folate deficiency can clearly explain these malformations. On the contrary, an interaction, genetic as well as nutritional, between these nutrients would explain these anomalies.

Fetus↗
PubMed1973

Iron, folate, and vitamin B 12 nutrition in pregnancy: a study of 1000 women from southern India.

As part of a WHO collaborative programme the prevalence of anaemia was studied and the serum concentrations of iron, folate, and vitamin B(12) were measured in 1 000 pregnant women from southern India. The results of the study show a high prevalence of anaemia, resulting from iron and folate deficiency with iron deficiency predominating. Interrelationships between these nutrients and their effect on pregnancy and the fetus were investigated. The results indicate that, in comparison with populations in developed countries, there was a high prevalence of iron and vitamin B(12) deficiency in the community, but the state of folate nutrition was similar to that found elsewhere.

Adolescent↗
PubMed1980

Phytohemagglutinin-stimulated normal human peripheral blood lymphocytes in folate-depleted medium: an in vitro model for megaloblastic hemopoiesis.

Normal human peripheral blood lymphocytes cultured with phytohemagglutinin in folate-free RPMI 1640 medium supplemented with normal human serum exhibit megaloblastic maturation. These changes are accompanied by a decrease in intracellular folate content, and when compared to folate-replete cells, reveal increased 3H-thymidine incorporation into DNA together with a decreased inhibitory effect of deoxyuridine on 3H-thymidine incorporation. This in vitro system of cellular folate deficiency is a convenient model for analysis of biochemical events accompanying megaloblastic maturation.

Cells, Cultured↗
PubMed1993

Nutritional assessment of folate and cyanocobalamin status in a Spanish elderly group.

This study is part of a broader examination of the nutritional status of elderly people in Spain. Cyanocobalamin and folate status were determined in a group of 72 non-institutionalized elderly (34 males and 38 females), aged 65 to 89, living in the Comunidad Autonoma de Madrid (Spain) by means of dietetic and biochemical data. We also studied the influence of the vitamin status on some haematologic parameters, as for example the MCV (mean corpuscular volume). Our results show that the average intake of vitamin B12 (6.3 +/- 0.9 micrograms/day) was three times the recommended amount, and that the blood levels were, in general, satisfactory (721.61 +/- 93 pg/ml). However, in 41.6% of the cases folate intake (213.8 +/- 92.4 micrograms/day) was below the recommended amount and serum (4.74 +/- 15 ng/ml) and red blood cells folate levels (115.37 +/- 36.7 ng/ml) also showed a deficient situation for 80% of the studied elderly. The influence of folate status on MCV of the studied elderly was evident. Elderly with MCV > or = 100 mu 3 (7.4% of the cases), had significantly lower intakes of folate (132.8 +/- 36.1 micrograms/day) and lower serum levels (3.93 +/- 0.4 ng/ml) than elderly with MCV < 100 mu 3 (who had intakes of 235.3 +/- 14.8 micrograms/day and serum levels of 4.81 +/- 1.48 ng/ml). Our results show that cyanocobalamin deficiency is not very frequent among the studied elderly, whereas folate deficiency has a great incidence and can have negative effects on their health.

Aged↗
PubMed1997

Micronutrient regulation in pregnant and lactating women from Rio de Janeiro.

Studies with low-income pregnant and lactating women from the city of Rio de Janeiro, concerned mainly with the changes in micronutrient homeostasis during pregnancy and lactation in the absence of overt clinical deficiencies, are reported. These studies focused on folate, cobalamin, iron, zinc and vitamin A. Factors that may affect the maternal micronutrient state, such as dietary intakes, use of supplements and interrelationships of micronutrients have been considered, as well as the implications of these changes for maternal-fetal transfer and milk composition. Although these studies were not designed to evaluate the prevalence of sub-clinical micronutrient deficiencies in pregnant and lactating women, they indicate that high frequencies of sub-clinical deficiencies of folate, iron, zinc and vitamin A, especially in pregnant women, are expected to be found in Rio de Janeiro.

Appetite Regulation↗
PubMed1995

Folate requirements for health in different population groups.

Folate coenzymes are required for the transfer and utilisation of one-carbon units in essential reactions involving amino acid metabolism, and the synthesis of purines and pyrimidines. Much of our understanding of human folate requirement comes from the study of folate deficiency, as it progresses from early haematological changes to eventual clinical manifestations. In population studies folate status may be assessed during the early stages of negative balance, before functional and clinical changes occur, by means of both dietary evaluation and biochemical measurements. Sub-optimal folate status may arise as a result of a number of environmental, physiological or pathological factors which cause decreased availability, increased requirement, or both. Current reference values for folate apply to intakes in healthy population groups. New recommendations for folic acid in the prevention of both first occurrence and recurrence of neural tube defects have recently been published. Folate nutrition may also have a role in coronary heart disease and various cancers.

Adolescent↗