Complement-fixing murine typhus antibodies in vitamin deficiency states. III. Riboflavin and folic acid deficiencies.
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Animals↗
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Influence of folic acid on birthweight and growth of the erythroblastotic infant. I. Birthweight.
The birthweights of 100 infants with erythroblastosis were carefully matched as to sex, gestational age, and parity with the birthweights of 200 control infants born during the same period. At all gestational ages the average birthweight of the affected infants was below that of the controls, the average reduction being 227 g. The more severely affected infants tended to be at a lower centile for birthweight than were the mildly affected ones. The relationships between maternal serum folate, cord blood serum folate, and centile for birthweight among affected infants were also studied. There was a strong correlation between low maternal serum folate and the incidence of small-for-dates babies among the affected infants. There was also a strong correlation between maternal and cord blood serum folate values. There was a lack of correlation between maternal serum folate and cord blood haemoglobin. It is concluded that infants with erythroblastosis are lighter than controls and that the reason for this may be a shortage of folic acid available for fetal growth.
Birth Weight↗
In vivo plasma and urine folate binding after ingestation of 3H-folic acid and 14C-methyl-folate.
After simultaneous ingestion of equivalent amounts of [3H]folic acid (3H-PteGlu) and [14C]N5-methyl-tetrahydrofolic acid (14C-CH3-H4PteGlu) we were able to demonstrate progressive macromolecular binding of radiofolate in plasma, which appeared to be near maximal at 6 h. Bound radiofolate was predominantly of 14C-CH3H4PteGlu origin, and only at 24 h could 3H incorporation be demonstrated. The binder eluted with albumin from Sephadex DEAE-A50 columns. In urine a smaller bound radiofolate fraction, with approximately equal amounts of 3H and 14C, appeared after 5.5 h. Plasma chromatography showed radio-PteGlu (peak 1) to be rapidly converted to CH3-H4PteGlu (peak 2), with subsequent appearance of two further radiofolate peaks (peaks 3 and 4) the nature of which is as yet unclear. Urine showed similarly placed fractions but their magnitude differed, and urinary peak 3 in particular was much more prominent than its plasma counterpart.
Administration, Oral↗
Knowledge and use of folic acid in Croatian pregnant women--a need for health care education initiative.
Adequate periconceptional folic acid (FA) intake reduces the risk of neural tube defects. There are still no official FA supplementation guidelines, FA fortification policies or larger studies of awareness regarding FA or number of planned pregnancies in Croatia. This study assesses the knowledge and practice regarding FA supplementation and reports the trends in pregnancy planning in Croatia. A total of 569 pregnant women completed an anonymous questionnaire and about 72% of them were aware of the benefits of FA. Despite 75.53% of planned pregnancies, only 14.41% of all women took FA appropriately. Croatian women get information about FA from the media, health professionals and friends, but 63.77% got this information too late. The present study showed low percentage of appropriate FA intake despite high number of planned pregnancies in Croatia. It emphasizes the need for immediate and continuous public health education initiative about FA intake targeted to the women of childbearing age before their pregnancies have occurred.
Croatia↗
Synergistic embryotoxicity of combination pyrimethamine and folic acid in rats.
The increased embryotoxicity of pyrimethamine (PYM) with concomitant oral dosing of folic acid (FA) was examined in rats. The preventive effects of folinic acid (FNA) on PYM embryotoxicity were also examined. Six groups were constructed: PYM I (PYM 1.2 mg/kg/day), FA (FA 50 mg/kg/day), PYM I+FA (1.2 and 50 mg/kg/day, respectively), PYM II (2.7 mg/kg/day), PYM II+FNA (2.7 and 12 mg/kg/day, respectively), and a vehicle control group. The agents were administered for 11 days from day 7 throughout 17 of gestation. PYM and FA were administered by gavage and FNA was administered intraperitoneally. Visceral and skeletal malformations were observed in the fetuses of both PYM I+FA and PYM II groups; these included dilatation of the lateral ventricle and fused ribs. No malformed fetuses were observed in the fetuses of the other four groups. External malformations were observed only in the fetuses of PYM II groups; these included cleft palate, cleft lips, and brachygnathia, among others. These results show that the concomitant gavage dosing of FA augments PYM embryotoxicity. The preventive effects of FNA were also confirmed.
Abnormalities, Drug-Induced↗
Folate deficiency-induced hyperhomocysteinemia attenuates, and folic acid supplementation restores, the functional activities of rat coagulation factors XII, X, and II.
Hyperhomocysteinemia (HH) constitutes a risk marker for thrombosis, but the pathophysiological mechanisms in thrombus formation are still unresolved. We investigated the influence of HH on single coagulation factor functions and evaluated the platelet GpIIb/IIIa receptor function in HH-induced changes in whole-blood coagulation profiles (WBCP). Three groups of 12 rats were investigated: control rats, folate deficient-HH (FD-HH) rats, and treated rats. Plasma total homocysteine was 7.1 micromol/L in controls, 31.3 micromol/L in FD-HH rats, and 7.6 micromol/L in treated rats. Factor (F) II:C, FX:C, and FXII:C were reduced in FD-HH rats compared with controls and normalized in treated rats (P < 0.05). FVII:C activity did not differ among the groups. Factor VIII:C activity was greater in FD-HH rats than in controls (P < 0.05). Blockage of the platelet GpIIb/IIIa receptor by Integrilin (Schering-Plough A/S) did not abolish the FD-HH-induced increase in whole-blood coagulation velocity, irrespective of the dosage of Integrilin. In conclusion, FD-HH reduced the functional activities of FXII:C, FX:C and FII:C, whereas FVII:C was unchanged and FVIII:C increased. These findings may partially explain the prolonged initiation phase of WBCP in FD-HH rats. The changes in single coagulation factor functions and WBCPs in FD-HH rats were reversed by treatment with folic acid.
Animals↗
Failure of folic acid derivatives to mimic the actions of kainic acid in brain in vitro or in vivo.
The ability of three derivatives of folic acid, N-5-methyltetrahydrofolic acid (MTHF), tetrahydrofolic acid (THF) and dihydrofolic acid (DHF) to mimic the actions of kainic acid (KA) in a number of in vitro and in vivo systems known to be sensitive to KA was examined. None of the three folate derivatives at 100 microM concentration significantly inhibited the specific binding of [3H]-KA to striatal membranes although 2 microM L-glutamate produced a 40% inhibition. None of the three folate derivatives stimulated the formation of cyclic GMP in cerebellar slices incubated in vitro although KA (0.5 mM) increased cyclic GMP levels by 2.5-fold. Whereas intrahippocampal injection of 2.3 nmoles of KA produces prolonged abnormalities of the EEG, limbic-type seizures and a characteristic pattern of neuronal degeneration in the hippocampal formation and related structures, intrahippocampal injection of a 100-fold greater dose of THF caused only minor and transient EEG abnormalities, no overt seizures and a highly restricted lesion. Whereas intrastriatal injection of 5.6 nmoles of KA caused a profound reduction in the specific activities of choline acetyltransferase and glutamate decarboxylase, markers for striatal intrinsic cholinergic and GABAergic neurons, 50-fold greater doses of MTHF did not affect either enzyme although this high dose of THF did cause a significant 33% reduction in choline acetyltransferase activity. These findings support the suggestion that THF may have weak neurotoxic effects in brain but indicate that the actions of this compound and the related MTHF and DHF are not mediated through KA-specific receptors.
Animals↗
The effect of long-term intravenous high dose B-complex vitamins with or without folic acid on serum homocysteine in hemodialysis patients.
BACKGROUND: Many regimens using different doses of folic acid (FA) alone or with supplementation of B-complex vitamins (BCV) have been tested for the reduction of total homocysteine (tHcy) levels in hemodialysis (HD) patients. BCV are usually administered orally and for a short period. In the present study, we assessed the effect of long-term intravenous (IV) BCV on serum tHCy levels in HD patients, and the effect produced by moderate oral supplementation with FA. METHODS: In a cohort of 37 patients under chronic HD treatment for a mean of 50.2 +/- 46.7 months, serum concentrations of tHcy, folate and vitamin B12 were determined at the end of four sequential periods: (A) three months without any FA supplementation, (B) three months with oral supplementation of 5 mg of FA three times weekly, (C) six months without FA supplementation, and (D) three months without BVC or FA supplementation. From the start of HD treatment and throughout the study until the beginning of period D, patients received a standard IV dose of BCV (B1 250 mg + B6 250 mg + B12 1.5 mg) three times per week, post-dialysis. RESULTS: At the end of period B, mean serum tHcy levels were significantly lower than in periods A and C (13.7 +/- 3.6 micromol/L vs 19.6 +/- 10.8 micromol/L and 21.3 +/- 9.4 micromol/L, respectively, p < 0.001) and mean serum folate levels were significantly higher (20.7 +/- 7.4 ng/mL vs 5.0 +/- 2.8 ng/mL and 4.5 +/- 1.4 ng/mL, respectively, p < 0.01). At the end of period D, mean serum tHcy levels were significantly higher than in all the previons periods (29.3 +/- 13.5 micromol/L, p < 0.001). Twenty-six of the 37 patients (70.2%) had normal (< 15 micromol/L) serum tHcy levels at the end of period B and only one (2.7%) had normal tHcy at the end of period D. Mean serum vitamin B12 levels at the end of periods A, B and C were 100 times the usual normal values. At the end of period D, although significantly lowered (p < 0.001), they remained above the normal range. CONCLUSIONS: Long-term high-dose BCV IV three times a week post-dialysis reduced serum tHcy levels only when combined with oral FA supplementation.
Administration, Oral↗
[Quality of data on folic acid content in vegetables included in several Spanish Food Composition Tables and new data on their folate content].
The relationship between adequate folate intake, adequate serum levels, and lowering the risk of suffering from cardiovascular diseases, neural tube defects, neural illness and some kind of cancers have been widely studied. Because of the expected health benefits, the consumption of foods with high folate content or enriched foods is increasing. Therefore, an adequate folate intake is important in order to reach acceptable serum levels. Reliable food composition data are necessary in order to evaluate and estimate the populations folate intake, elaborate diets and formulate recommended dietary intakes. For this reason, we revised folic acid data in Spanish Food Composition Tables (FCT). The quality of the data was evaluated and compared with other well-known international Food Composition Tables as well as with a high-resolution liquid chromatographic method (HPLC) validated in our laboratory. We evaluated all data about folate content, as well as all the information given like data origin, analytical method, sampling or original database. For the HPLC method, the food samples were incubated with hog kidney conjugase. After that, the samples were purified and concentrated by strong anion exchange (SAX), then the folate content was quantified by HPLC with a combination of two ultraviolet and fluorescence detectors. The evaluation and comparison of data was established according to some parameters, which define the quality of data, giving punctuation depending on the compliance with these parameters. The study of different sources showed that nutrients were different in definition, analysis method, units and expression of data, and that this fact could have a potential influence on TCA data values. In addition, it has been possible to show a wide variation in food number, name of these foods as well as the analysis of raw or cooked products with different composition. When the quality conditions were tested, the Spanish FCT had the lowest punctuation in folate content data. That is because the Spanish FCT did not use a validated method to quantify folic acid in foods (Direct method of FCT elaboration), but they used folate content data from others FCT (Indirect method of FCT elaboration). These data manifest the importance of getting a consensus method to determine folate content in foods with the aim to obtain a FCT with reliable folate data.
Folic Acid↗
Nutrition and disease: folic acid deficiency in the mouse.
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Animals↗
[Folic acid deficiency of pregnant rats as an effect of pantothenic acid deficiency].
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Animals↗
Effect of homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 on clinical outcome after percutaneous coronary intervention: the Swiss Heart study: a randomized controlled trial.
CONTEXT: Plasma homocysteine level has been recognized as an important cardiovascular risk factor that predicts adverse cardiac events in patients with established coronary atherosclerosis and influences restenosis rate after percutaneous coronary intervention. OBJECTIVE: To evaluate the effect of homocysteine-lowering therapy on clinical outcome after percutaneous coronary intervention. DESIGN, SETTING, AND PARTICIPANTS: Randomized, double-blind placebo-controlled trial involving 553 patients referred to the University Hospital in Bern, Switzerland, from May 1998 to April 1999 and enrolled after successful angioplasty of at least 1 significant coronary stenosis (> or = 50%). INTERVENTION: Participants were randomly assigned to receive a combination of folic acid (1 mg/d), vitamin B12 (cyanocobalamin, 400 micro g/d), and vitamin B6 (pyridoxine hydrochloride, 10 mg/d) (n = 272) or placebo (n = 281) for 6 months. MAIN OUTCOME MEASURE: Composite end point of major adverse events defined as death, nonfatal myocardial infarction, and need for repeat revascularization, evaluated at 6 months and 1 year. RESULTS: After a mean (SD) follow-up of 11 (3) months, the composite end point was significantly lower at 1 year in patients treated with homocysteine-lowering therapy (15.4% vs 22.8%; relative risk [RR], 0.68; 95% confidence interval [CI], 0.48-0.96; P =.03), primarily due to a reduced rate of target lesion revascularization (9.9% vs 16.0%; RR, 0.62; 95% CI, 0.40-0.97; P =.03). A nonsignificant trend was seen toward fewer deaths (1.5% vs 2.8%; RR, 0.54; 95% CI, 0.16-1.70; P =.27) and nonfatal myocardial infarctions (2.6% vs 4.3%; RR, 0.60; 95% CI, 0.24-1.51; P =.27) with homocysteine-lowering therapy. These findings remained unchanged after adjustment for potential confounders. CONCLUSION: Homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 significantly decreases the incidence of major adverse events after percutaneous coronary intervention.
Angioplasty, Balloon, Coronary↗
Reduction of plasma homocysteine and serum methylmalonate concentrations in apparently healthy elderly subjects after treatment with folic acid, vitamin B12 and vitamin B6: a randomised trial.
OBJECTIVES: To investigate, in an elderly population: (1) the effects of oral B-vitamin therapy on P-tHcys, S-MMA and Hb/MCV, (2) the appropriate decision limit for 'high' metabolite concentrations and (3) the estimated prevalence of vitamin B(12)/folate deficiency on the basis of different decision limits. DESIGN: Double-blind placebo-controlled intervention study. SETTING: Outpatient clinic. SUBJECTS: A total of 209 community-dwelling subjects, median age 76 y (range 70-93) y. INTERVENTION: Four months of oral daily supplementation with 0.5 mg cyanocobalamin, 0.8 mg folic acid and 3 mg vitamin B(6). RESULTS: High P- tHcys was found in 64% of men and 45% of women, high S-MMA in 11% of both. Vitamin B(12) deficiency was observed in 7.2% and folate deficiency in 11% of all subjects. Health-related upper reference limits for the metabolites at the start were higher than the laboratory's upper reference limits. The latter were, however, similar to those of the vitamin replete group. There was a significant decrease in P-tHcys (P<0.001) and S-MMA (P=0.009) after 4 months of vitamin treatment. In a multivariate analysis, the P-Hcys change correlated positively with baseline P-tHcys and inversely with baseline P-folate and transferrin saturation (Fe/TIBC ratio). The S-MMA change correlated with baseline S-MMA and inversely with baseline vitamin B(12) and age. CONCLUSIONS: Suboptimal vitamin status is an important cause of elevated P-tHcys and S-MMA in apparently healthy elderly subjects. Oral B-vitamin therapy is an effective and convenient way to normalise P-tHcys and S-MMA.
Aged↗
Folic acid binding protein and folate balance in uremia.
To determine the incidence and importance of folate deficiency in uremia, we studied 41 patients who had chronic uremia but who were not receiving hemodialysis. Serum folate level was assayed by microbiological, whole serum radioassay, and heat-extracted radioassay techniques. Mean serum folate level, as determined with the Lactobacillus casei method, was 6.9 ng/ml (normal, more than 3.0 ng/ml). The mean heat-extracted radioassay serum folate level was 6.6 ng/ml. Only 10% of our patients had subnormal serum folate values, as determined with these techniques. No cases of megaloblastic anemia were discovered, and the hematologic profiles correlated with L casei and heat-extracted radioassay serum folate values. The mean serum folic acid binding protein (FABP) level was significantly greater for the uremic patients than for control patients (26% vs 9.9%, respectively; P = .0005). Our results show that elevated levels of serum FABP spuriously depress the serum folate level, as determined with the whole serum radioassay technique, but apparently do not retard delivery of folate to the tissue in vivo.
Creatinine↗
Hyperhomocysteinemia increases damage on brain slices exposed to in vitro model of oxygen and glucose deprivation: prevention by folic acid.
In the present study we evaluate the effects of homocysteine on cellular damage using hippocampal slices from Wistar rats exposed to oxygen and glucose deprivation (OGD, followed by reoxygenation), an in vitro model of hypoxic-ischemic events. For chronic treatment, we induced elevated levels of homocysteine in blood (500 microM), comparable to those of human homocystinuria, and in brain (60 nmol/g wet tissue) of young rats by subcutaneous injections of homocysteine (0.3-0.6 micromol/g of body weight), twice a day with 8 h intervals, from the 6 th to the 28 th postpartum day and controls received saline. Rats were sacrificed 1, 3 or 12 h after the last injection. For acute treatment, 29-day-old rats received one single injection of homocysteine (0.6 micromol homocysteine/g body weight) or saline and were sacrificed 1h later. In another set of experiments rats were pretreated with Vitamins E (40 mg/kg) and C (100 mg/kg) or folic acid (5 mg/kg) during 1 week; 12 h after the last administration they received a single injection of homocysteine or saline and were sacrificed 1 h later. Results showed that both chronic (1 h after homocysteine administration) and acute hyperhomocysteinemia increased the cellular damage measured by LDH released to de incubation medium, suggesting an increase of tissue damage caused by OGD. Pretreatment with folic acid completely prevented the damage caused by acute hyperhomocysteinemia, whereas Vitamin E just partially prevented such effect. These findings may be relevant to explain, at least in part, the higher susceptibility of hyperhomocysteinemic patients to be susceptible to ischemic events and point to a possible preventive treatment.
Analysis of Variance↗
Folic acid metabolism and mechanisms of neural tube defects.
Folate acts as a cofactor for enzymes involved in DNA and RNA biosynthesis. Folate is also involved in the supply of methyl groups to the so-called methylation cycle, which uses methionine and makes homocysteine. The folate cofactor, N5-methyltetrahydrofolate, donates its methyl group to a vitamin B12-dependent enzyme, methionine synthase, which recycles homocysteine back to methionine. The cell's ability to methylate important compounds such as proteins, lipids and myelin will be compromised by deficiency of folate or vitamin B12, resulting in impaired cellular function. Methionine synthase plays another role: it converts circulating N5-methyltetrahydrofolate into tetrahydrofolate. The latter but not the former can act as a substrate for polyglutamate synthase, thereby becoming retained in the cell as polyglutamate. Interruption of DNA biosynthesis or methylation reactions could prevent the proper closure of the neural tube. Such inhibition could be caused by simple deficiency of either folic acid or vitamin B12. Studies comparing serum folate and vitamin B12 status in women who have had an affected pregnancy to those in control women indicate no difference between the two groups and show that most cases are not clinically deficient in either vitamin. A small number of studies using the level of folate in red blood cells, which is a better reflection of tissue stores, confirm this, suggesting instead a metabolic impairment in the biochemical functions of one of these vitamins. The trials using folic acid to prevent neural tube defects thus seem to be effectively overcoming a metabolic block rather than treating folate deficiency.
Female↗
Experimental anemias in animals resulting from folic acid and vitamin B12 deficiencies.
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Anemia↗
Effects of folic acid antagonist therapy on urinary excretion of formic acid by humans.
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Body Fluids↗