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At least 127 records · Page 7Linked to original sources
PubMed1995

[Intake of folic acid in the total daily diet--effect of food preparation on its folic acid content].

The folic acid content of total daily diet was determined by means of high-performance liquid chromatography (HPLC). The contents of tetrahydrofolic acid (THF), 5-methyl-THF and 5-formyl-THF were differentiated. The mean of the folic acid content of the total daily diet samples determined analytically was 205 +/- 60 micrograms and the mean of the individual ingredients of the samples was 401 +/- 78 micrograms, which implies that about 50% of folic acid is destroyed by common household food preparation methods. If the contents of pteroylglutamic acid (PteGlu) and 10-formyl-PteGlu (which cannot be determined analytically) are added, it can be assumed that the folic acid content with only be reduced by about 40%. THF and 5-methyl-THF proved to be less stable than 5-formyl-THF. The monoglutamate portion of the total folat content was higher in the total diet samples than in the individual foodstuffs as a consequence of the action of the enzyme "deconjugase" which is released when the matrix of food-stuffs is destroyed.

Chromatography, High Pressure Liquid↗
PubMed1961

Conventional voltage electrophoresis for formiminoglutamic-acid determination in folic acid deficiency.

A new method for the determination of urinary formiminoglutamic acid (FIGLU) using conventional electrophoresis at 200 to 500 v. on cellulose acetate strips is reported. Experience in 166 determinations on 137 patients shows the method to be a simple, practical, and apparently sensitive one for the determination of FIGLU in the urine. Results of the application of the measurement of urinary FIGLU with histidine loading as a test for folic acid deficiency are also reported.

Cellulose↗
PubMed1975

Binding of folic acid to serum proteins. V. Tritiated folic acid in the liver.

Sephadex G-200 chromatographies of the liver cell sap of rabbits, 1, 3 and 6 days after an injection of 3H-folic acid activity (FAA) into the circulation, were used in an attempt to study the binding of this labelled FAA to liver proteins. The labelled FAA was quickly accumulated in the liver, and in the cell sap it was grouped chromatographically to two maxima, which corresponded to the two maxima of microbiological FAA (L. casei). The maxima were eluated in the chromatography together with cell sap proteins. The possible coupling of FAA to proteins in the liver is discussed.

Animals↗
PubMed1975

Studies of folic acid compounds in nature. IV. Folic acid compounds in soybeans and cow milk.

Folate compounds in soybean and cow's mild were identified by Sephadex chromatography and differential microbiological assaymsoybean contained mainly monoglutamates (ca. 52%), some diglutamates (ca. 16%), and polyglutamates (pentaglutamates representing the major portion). 5-CHO-H4PteGlun(1-6) constituted 65-70% of total folate activity; Cow's milk contained monoglutamates (60%) and polyglutamates (ranging from di- to hepta-conjugates). In contrast to soybean, 90-95% of milk folate was in the 5-CH3h4pteGlun(1-7) form.

Animals↗
PubMed1981

Folic acid and pterin deaminases in Dictyostelium discoideum: kinetic properties and regulation by folic acid, pterin, and adenosine 3',5'-phosphate.

Kinetic data obtained for deamination of pterin by the extracellular fraction from Dictyostelium discoideum yielded apparently linear Lineweaver-Burk plots for pterin. The Michaelis constant for pterin was 30 microM. The data for folic acid deamination yielded convex Lineweaver-Burk plots. Convex Lineweaver-Burk plots could result from the presence of two types of enzymes with different affinities. The data for folic acid deamination were analyzed mathematically for two types of enzymes. This analysis produced Michaelis constants for folic acid of 1.8 and 23 microM competition studies suggested that an enzyme with low affinity nonspecifically catalyzed the deamination of folic acid and pterin, whereas an enzyme with high affinity was a specific folic acid deaminase. A specific folic acid deaminase with high affinity appeared to be present on the surface of D. discoideum cells. The Michaelis constant for this enzyme was 2.6 microM. Cells growing in nutrient broth and cells starved in phosphate buffer released folic acid and pterin deaminases. The quantity of deaminase activities released by the cells appeared to be controlled by chemoattractants. Starving cells that were supplied with folic acid, pterin, or adenosine 3',5'-phosphate increased their extracellular folic acid and pterin deaminase activities to a larger extent than did cell suspensions to which no chemoattractants were added. Administration of folic acid or pterin to starving cells caused increases of the activity of extracellular adenosine 3',5'-phosphate phosphodiesterase and repressed increases of the activity of phosphodiesterase inhibitor.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

[Management, prevention and control of megaloblastic anemia, secondary to folic acid deficiency].

Folic acid deficiency is the second most common cause of anemia in our environment, after anemia secondary to iron deficiency. Folates are essential components of human and animal diet. Folic acid is mainly in poliglutamate form, and it is hydrolyzed in the proximal jejunum. It is important to identify adequately the exact vitamin deficiency that causes megaloblastic anemia, because vitamin B12 administration in folate deficiency may correct partially megaloblastic alterations, but administration of folic acid in cobalamin deficient patients improves haematological parameters but deteriorates the neurological syndrome. Main causes of anemia secondary to folate deficiency are inadequate dietetic administration, increased requirements, impaired absorption and pharmacologic interactions. Folates are altered by light, high temperature and by water affinity, which facilitates its elimination by washing or cooking.

Anemia, Megaloblastic↗
PubMed2006

Population reference values for plasma total homocysteine concentrations in US adults after the fortification of cereals with folic acid.

BACKGROUND: Folic acid fortification has resulted in a dramatic increase in folate intake in the United States. Folate intake is inversely associated with circulating total homocysteine (tHcy). Elevated tHcy is directly associated with cardiovascular disease risk. OBJECTIVE: The aim of this study was to present the distribution of plasma concentrations of tHcy in US adults by using data from nationally representative sample surveys conducted since folic acid fortification was implemented. DESIGN: Data from the National Health and Nutrition Examination Surveys from 1999-2001 and 2001-2002 were used to study tHcy distribution by age, sex, and race-ethnicity in 9196 persons. RESULTS: Plasma concentrations of tHcy were higher in men than in women and in older persons than in younger persons. In those aged 19-30, 31-50, and 51-70 y but not in those aged >70 y, men had significantly (P < 0.0001) higher mean plasma concentrations of tHcy than did women. A race-ethnicity difference in plasma tHcy existed only in persons aged >70 y. Non-Hispanic blacks aged >70 y had significantly (P < 0.05) higher tHcy concentrations than did non-Hispanic white or Mexican American or Hispanic subjects in the same age group. Age-adjusted plasma tHcy concentrations did not differ significantly between non-Hispanic white (8.39 micromol/L), non-Hispanic black (8.92 micromol/L), and Mexican American or Hispanic (8.12 micromol/L) subjects. The rate of increase in plasma tHcy was greater in non-Hispanic blacks aged >/=50 y than in persons of similar age but of other races-ethnicities. CONCLUSIONS: These plasma tHcy data reflect the effects of folic acid fortification. Sex, age, and race-ethnicity differences persist in plasma tHcy concentrations.

Adult↗
PubMed1998

Plasma homocysteine, vitamin B6, vitamin B12 and folic acid in end-stage renal disease during low-dose supplementation with folic acid.

In order to see whether conventional low-dose folic acid supplement along with vitamin B6 and B12 reduces hyperhomocysteinemia in patients with ESRD, we compared the levels of homocysteine, vitamin B6, B12 and folic acid among 3 groups of patients: 44 ESRD patients on hemodialysis with replacement of folic acid, vitamin B6, and B12 (dialysis group); 27 chronic renal failure patients without vitamin replacement (predialysis group); and 17 hypertensive patients without vitamin replacement (control group). Mean plasma total homocysteine concentration was higher in the dialysis (15.5 +/- 6.6 micromol/l) and the predialysis groups (15.7 +/- 4.2 micromol/l) than in the control group (6.2 +/- 1.5 micromol/l) (p < 0.001). However, there was no difference in homocysteine concentrations between the dialysis and predialysis groups. In the control and predialysis groups, the homocysteine concentration showed a reverse correlation with the concentrations of folic acid (r = 0.584, p = 0. 014 for the control group; r = 0.431, p = 0.247 for the predialysis group) and vitamin B12 (r = 0.485, p = 0.049 for the control group; r = -0.562, p = 0.023 for the predialysis group) but not with vitamin B6. In conclusion, plasma folic acid concentrations were 3-4 times higher in the dialysis than in the predialysis group. But these levels of folic acid are not enough to reduce hyperhomocysteinemia in ESRD.

Adult↗
PubMed2000

Do patients with rheumatoid arthritis established on methotrexate and folic acid 5 mg daily need to continue folic acid supplements long term?

BACKGROUND: It is postulated that some aspects of methotrexate toxicity may be related to its action as an anti-folate. Folic acid (FA) is often given as an adjunct to methotrexate therapy, but there is no conclusive proof that it decreases the toxicity of methotrexate and there is a theoretical risk that it may decrease the efficacy of methotrexate. OBJECTIVES: To look at the effect of stopping FA supplementation in UK rheumatoid arthritis (RA) patients established on methotrexate <20 mg weekly and FA 5 mg daily, to report all toxicity (including absolute changes in haematological and liver enzyme indices) and to report changes in the efficacy of methotrexate. METHODS: In a prospective, randomized, double-blind, placebo-controlled study, 75 patients who were established on methotrexate <20 mg weekly and FA 5 mg daily were asked to stop their FA and were randomized to one of two groups: placebo or FA 5 mg daily. Patients were evaluated for treatment toxicity and efficacy before entry and then at intervals of 3 months for 1 yr. RESULTS: Overall, 25 (33%) patients concluded the study early, eight (21%) in the group remaining on FA and 17 (46%) in the placebo group (P = 0.02). Two patients in the placebo group discontinued because of neutropenia. At 9 months there was an increased incidence of nausea in the placebo group (45 vs. 7%, P = 0.001). The placebo group had significantly lower disease activity on a few of the variables measured, but these were probably not of clinical significance. CONCLUSIONS: It is important to continue FA supplementation over the long term in patients on methotrexate and FA in order to prevent them discontinuing treatment because of mouth ulcers or nausea and vomiting. Our data suggest that FA supplementation is also helpful in preventing neutropenia, with very little loss of efficacy of methotrexate.

Aged↗