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PubMed2000

Folic acid supplements are more effective than increased dietary folate intake in elevating serum folate levels.

In 1992, recommendations were disseminated aimed at reducing the incidence of neural tube defects. Women were advised to increase consumption of folic acid supplements and dietary folates during the periconceptional period and a major integrated national campaign was launched to help achieve this. In this study we found that only one-quarter of the women with an uncomplicated obstetric history and 51% with a complicated obstetric history took supplements for the recommended time period. Dietary modification was extremely unusual. Serum analysis demonstrated that intake of folic acid supplements provides a greater elevation in serum folate levels than dietary food intake, suggesting dietary manipulation is an ineffective strategy and that efforts would be better focused on increasing supplement intake at a clinically important time. More effective education strategies are required, and since approximately one-third of pregnancies are unplanned, fortification of foods with folic acid is warranted.

Adult↗
PubMed2001

Effects of homocysteine on proliferation, necrosis, and apoptosis of vascular smooth muscle cells in culture and influence of folic acid.

BACKGROUND: It is known that hyperhomocysteinemia is associated with an increased risk of vascular disease, yet little is known about the pathogenic mechanisms underlying the action of homocysteine (Hcy) itself. METHODS: We evaluated the effects of Hcy on cell proliferation, apoptosis, and necrosis in smooth muscle cells (SMCs) cultured for 24 h with different amounts of Hcy. The percentage of apoptotic and necrotic cells from the culture was evaluated using two different techniques: annexin V-FITC and propidium iodide (PI) fluorescence and apoptosis TUNEL assay. RESULTS: The addition of 10 microM/l of Hcy to the medium was followed by a significant increase in cell proliferation and death, through apoptosis and necrosis, respectively. Notwithstanding this apparent balance, a significant increase was found in the total number of cells present in Hcy-treated culture, thus demonstrating a positive dose-dependent correlation with Hcy concentrations in the culture medium. The addition of folic acid to the culture medium significantly reduced both Hcy concentrations in media and the effects of Hcy on the proliferation/apoptosis/necrosis balance of cells in culture. The percentages for apoptotic cells and for cells with a necrotic morphology continued to increase as Hcy concentrations increased, although the absolute values were lower in the culture treated than in that not treated with folic acid. CONCLUSIONS: In the presence of folic acid, at increasing concentrations of Hcy, the total number of cells in culture showed increases far less relevant with respect to the control. Also the percentage of apoptotic cells to that of cells with a necrotic morphology, although conserving the tendency to increase to growth of the concentrations of Hcy, have shown absolute values that were lower in the folic acid-treated cultures.

Apoptosis↗
PubMed1996

Folic acid and the prevention of birth defects.

Thirty years ago, it was suggested that maternal intake of certain vitamins during pregnancy affected the incidence of serious fetal malformations. Subsequent research has revealed that folate (folic acid), a B vitamin, plays a crucial role in the development of the central nervous system during the early weeks of gestation, which is generally before the pregnancy is confirmed. In a significant number of embryos, an inadequate supply of folate at this time leads to a failure of the primitive neural tube to close and differentiate normally and results in neural tube birth defects (NTD). Numerous studies have confirmed the importance of an adequate intake of folate during the weeks just before and after conception. Overall, the data predict that if women consume multivitamin supplements containing folic acid during the periconceptional period, the number of children born with serious malformations (such as spina bifida and anencephaly) could be reduced by half. Although programs to increase dietary folate intake of potential mothers may be effective in reducing NTD, the only proven and practical preventive measure currently available is to take oral multivitamin supplements containing folic acid. Multivitamin supplementation has also been associated with reduced incidence of other congenital malformations. Current research is focusing on the role of micronutrients in embryogenesis, and on methods to identify prospective mothers at increased risk for bearing a child with NTD or with other major malformations shown to occur at reduced frequency with multivitamin supplementation. Of equal importance is the development of methods to communicate current knowledge as a public health measure.

Congenital Abnormalities↗
PubMedDate not supplied

Differential expression of c-jun, c-fos and hsp 70 mRNAs after folic acid and ischemia-reperfusion injury: effect of antioxidant treatment.

The regenerative repair response to folic acid and ischemia-reperfusion injury is characterized by different patterns of renal tubular cell proliferation. The purpose of this study was to examine the time course of the expression of two early growth response genes, c-jun and c-fos, and of the stress response gene hsp70 after such renal injuries and to determine the role played by reactive oxygen species generated during reperfusion, on gene induction. Ischemic injury caused an almost immediate increase of c-jun, c-fos and hsp70 mRNA expression, that reached a maximum at 1 h of reperfusion. Folic acid treatment increased c-fos and hsp70 mRNAs at 2 h, while c-jun accumulated at 1 h, although to a lesser extent. The intravenous administration of two antioxidant drugs, allopurinol or dimethyl sulfoxide (DMSO), 20 min before ischemia, to prevent the generation of oxygen free radicals during reperfusion, did not cause any change in gene expression. In contrast, the combined administration of allopurinol and DMSO reduced c-jun and c-fos mRNA expression as well as tubular cell damage at 1 h of reperfusion, although not at earlier times while hsp70 mRNA expression remained almost unchanged. Taken together, the results suggest that these scavengers, by reducing reactive oxygen species and renal damage during reperfusion, may affect the expression and/or persistence of transcripts involved in the control of epithelial cell proliferation.

Acute Kidney Injury↗
PubMed1984

Covalent binding of folic acid to dimethylglycine dehydrogenase.

Dimethylglycine dehydrogenase (EC 1.5.99.2) carries out the oxidative demethylation of dimethylglycine to sarcosine in liver mitochondria. In vivo, the enzyme uses tightly bound tetrahydropteroyl pentaglutamate (H4PteGlu5) as an acceptor of the one-carbon group generated during the reaction. The purified enzyme can use, but does not require, H4PteGlu5 and under these conditions formaldehyde is the one-carbon unit produced. It is reported that folic acid may be covalently linked to dimethylglycine dehydrogenase in a specific and saturable manner so that only 1 mole of folic acid is bound per mole of enzyme. Covalently bound folic acid blocks the subsequent binding of H4PteGlu, and does not inhibit the rate of dimethylglycine dehydrogenase activity in vitro.

Animals↗
PubMed2003

[Folic acid reduces risks of having fetus affected with neural tube defects: dietary food folate and plasma folate concentration].

OBJECTIVES: Risk of having fetus affected with neural tube defects can be reduced by maternal periconceptional folic acid supplementation. The purpose of the present study is to investigate how folate is taken from diets and to measure plasma folate concentrations. SUBJECTS AND METHODS: A total of 222 women comprising 5 groups, i.e., healthy women, mothers of myelodysplastic patients, pregnant women, myelodysplastic patients, nurse students, participated in our study. Food frequency questionnaires kept 3 days were analyzed based on the 5th standard table of food composition in Japan. Plasma folate concentrations were measured by means of chemiluminescent immunoassay method. Changes in plasma folate concentrations and possible adverse effects following the folic acid supplementation for 16 weeks were also investigated. RESULTS: The dietary intake of folate, plasma folate concentration and energy intake averaged 293 micrograms/day, 8.1 ng/ml and 1,857 Kcal, respectively, among the subjects. Pregnant women took the largest amount of folate from diets and demonstrated the highest plasma folate concentration among the groups. The dietary folate in myelodysplastic patients and nurse students was significantly lower compared to that of healthy women. The Recommended Dietary Allowance of folate was not fulfilled in 22% of non-pregnant adult women and 72% of pregnant women. The dietary folate was mainly taken from the 3rd food group but the 4th group of food was consumed most. Mean folate intake was significantly correlated with circulating concentrations of serum folate (p = 0.012 r = 0.186). The consecutive administration of 400 micrograms supplements for 16 weeks increased a baseline plasma value of 8.7 ng/ml to 32.6 but fell down rapidly to 17.3 24 hours later without any adverse effects. CONCLUSIONS: The dietary folate and serum folate concentrations averaged 293 micrograms/day and 8.1 ng/ml, respectively. The former is the first report based on the 5th standard table of food composition in Japan. Majority of pregnant women took less dietary folate than what recommended by the government. Those who are capable of becoming pregnant are recommended to consume much of the 3rd food group and those who are planning to become pregnant are recommended to take 400 micrograms of folic acid supplements from 4 weeks before to 12 weeks after conception.

Adolescent↗
PubMed1999

Effects of high-dose folic acid and pyridoxine on plasma and erythrocyte sulfur amino acids in hemodialysis patients.

In this investigation, sulfur amino acids (sAA) and sulfhydryls were determined in the plasma and erythrocytes (RBC) of 10 uremic patients on regular hemodialysis (HD) treatment and 10 healthy subjects, before and after supplementation with 15 mg/d of folic acid and 200 mg/d of pyridoxine for 4 wk. The basal total plasma concentrations of homocysteine (Hcy), cysteine (Cys), cysteinylglycine (Cys-Gly), gamma-glutamylcysteine (gamma-Glu-Cys), glutathione (GSH), and free cysteinesulfinic acid (CSA) were significantly higher in HD patients when compared to healthy subjects, whereas methionine (Met) and taurine (Tau) concentrations were the same in the two groups. HD patients showed significantly higher RBC levels of Hcy and Cys-Gly, whereas the RBC concentrations of Met, Cys, Tau, and GSH were not different from those in the healthy subjects. The plasma concentrations of sAA and sulfhydryls differed compared with RBC levels in the healthy subjects and HD patients. In both groups, supplementation with high doses of folic acid and pyridoxine reduced the plasma Hcy concentration. In addition, increased plasma concentrations of Cys-Gly and GSH were found in the HD patients and of CSA in the healthy subjects. After vitamin supplementation, the RBC concentrations of Hcy, Cys, and GSH increased and that of Tau decreased in healthy subjects. The only significant finding in RBC of HD patients was an increase in GSH levels after supplementation. This study shows several RBC and plasma sAA and sulfhydryl abnormalities in HD patients, which confirms earlier findings that RBC and plasma pools play independent roles in interorgan amino acid transport and metabolism. Moreover, high-dose supplementation with folic acid and pyridoxine significantly reduced Hcy levels, but did not restore the sAA and sulfhydryl abnormalities to normal levels. The increase that was observed in GSH after vitamin supplementation may have a beneficial effect in improving blood antioxidant status in uremic patients. Finally, the findings of elevated plasma Cys levels correlating to the elevated plasma Hcy levels in the presence of elevated plasma CSA levels, both before and after vitamin supplementation, led to the hypothesis that a block in decarboxylation of CSA is linked to hyperhomocysteinemia in end-stage renal failure.

Adult↗
PubMed1977

Structural and functional abnormalities of the small intestine due to nutritional folic acid deficiency in infancy.

Structural abnormalities and disaccharidase deficiency were demonstrated in biopsies of duodenal mucosa from four infants who had symptoms of failure to thrive and chronic diarrhea associated with a megaloblastic anemia. Goat's milk was the main dietary constituent for each infant for six to eight months prior to presentation. The structural abnormalities consisted of villous blunting, crypt hypertrophy, megaloblastic changes in epithelial cells, and nuclear enlargement. All changes reverted to normal with the addition of folic acid to the diet. This study provides evidence that nutritional folic acid deficiency can cause structural and functional alterations of the small intestine in infants.

Anemia, Megaloblastic↗
PubMed1977

The influence of folate antagonists on the metabolism of folic acid and its reduced derivatives in rat liver and kidney.

Uptake and conversion of [3H]folic acid to polyglutamate derivatives by rat liver and kidney were inhibited by methotrexate or aminopterin (15 mg/kg body weight) and DL-tetrahydromethotrexate (30 mg/kg body weight). In contrast, these antagonists did not influence the conversion of L-5-formyl-[3H]tetrahydrofolic acid or L-5-methyl[3H]tetrahydrofolic acid to polyglutamine derivatives and had little effect on the uptake of reduced folate derivatives. When [3H]methotrexate, [3H]aminopterin, and DL-[3H]tetrahydromethotrexate were administered in small amounts (15 mug/kg body wieght), no metabolites of these compounds were observed. However, at higher doses of [3H]methotrexate (300 mug/kg body weight), more than 30% of the radioactivity remaining in the tissue 24 hr after administration could be attributed to a metabolite of methotrexate. This metabolite was tentatively identified as methotrexate diglutamate.

Aminopterin↗
PubMed1963

Studies on the physiology of Rickettsiae. IV. Folic acids of Coxiella burnetii.

Mattheis, Martha S. (University of Kansas, Lawrence), M. Silverman, and D. Paretsky. Studies on the physiology of rickettsiae. IV. Folic acids of Coxiella burnetii. J. Bacteriol. 85:37-41. 1963.-Yolk, yolk sac, and embryo tissues of uninfected eggs, and those infected with Coxiella burnetii, were analyzed for folic acid derivatives by employing diethylaminoethyl (DEAE)-cellulose column chromatography. Infected tissues contained quantitatively less folate, but the elution profiles of both infected and uninfected tissues were identical. Purified C. burnetii contained some types of folate apparently unique to these rickettsiae, and not found in infected tissue. The major folate fraction of C. burnetii was partially characterized by (i) elution position from DEAE columns; (ii) treatment with conjugase; (iii) growth response by Lactobacillus casei, Streptococcus faecalis R, and Pediococcus cerevisiae; and (iv) response to oxidation, reduction, and formylation.

Coxiella↗
PubMed2001

Folic acid fortification increases red blood cell folate concentrations in the Framingham study.

In 1996 the Food and Drug Administration (FDA) issued a regulation to take effect in January 1998 that all enriched cereal grain products include 140 microg of folic acid/100 g. The present cross-sectional study was undertaken to assess the effect of this fortification on RBC folate concentrations in the Framingham Offspring Cohort. Among those who did not take B-vitamin supplements, we compared RBC folate in 561 individuals who were examined before implementation of the FDA mandatory folic acid fortification (not exposed) vs. 354 individuals who were examined after implementation of fortification (exposed). We calculated the prevalence of deficient (<160 microg/L, 362.6 nmol/L) and acceptable (>200 microg/L, 453.2 nmol/L) RBC folate concentrations in both groups. Those exposed to folic acid fortification had a mean RBC folate of 450.0 microg/L (1019.7 nmol/L), a value 38% higher than the mean RBC folate of 325.3 microg/L (737.1 nmol/L) in those who were not exposed to fortification (P < 0.001). The prevalence of individuals with deficient RBC folate was 4.9% in the group not exposed to fortification compared with 1.9% in the group exposed to fortification (P < 0.02), and the prevalence of individuals with acceptable RBC folate was 87.0% in the group not exposed to fortification compared with 96.1% in the group exposed to fortification (P < 0.001). Similar results were seen in individuals who used supplements containing B-vitamins. The results of this study showed that in this cohort, the introduction of folic acid fortification significantly improved folate nutritional status measured as RBC folate.

Adult↗
PubMed1975

Methotrexate and folic acid effect in normal and sarcoma 180 bearing mice.

Four- to six-fold surplus of folic acid in oral application reduced the toxicity of methotrexate administered repeatedly in high therapeutic doses. The therapeutic effect of methotrexate applied intraperitoneally to mice with the ascitic S 180 sarcoma, as measured by their survival, can be reliably demonstrated; moreover, the survival can be prolonged by adding folic acid into drinking water. In the solid form S 180 the intraperitoneal administration of methotrexate did not significantly reduce the weight of tumors of treated aminals as compared to untreated animals. The maximum tolerated dose of methotrexate was lower in animals with the ascitic tumor than in non-tumorous animals.

Administration, Oral↗
PubMed1982

Evaluation of X-methyl folate preparations as possible folic acid antagonists.

Crude X-methyl folate and two purified fractions (purified X-methyl folate and 9-methyl folate) were evaluated as possible folic acid antagonists. Antifolate activity was measured by the deoxyuridine suppression assay, direct measurement of dihydrofolate reductase and morphological changes characteristic of folate deficiency. Cytotoxicity was evaluated by cell growth curves. These drugs were studied in freshly obtained human normal evaluated by cell growth curves. These drugs were studied in freshly obtained human normal bone marrow and leukemia cells as well as in three established cell lines HL-60 (human promyelocytic leukemia), CEM (human T lymphocytes), and L1210 (murine lymphoid leukemia). Purified X-methyl folate and 9-methyl folate at concentrations up to 2X10(-5) M failed to induce cell toxicity or inhibit deoxyuridine suppression of 3H-thymidine into DNA. Dihydrofolate reductase was not inhibited by 9-methyl folate but was partially inhibited by purified X-methyl folate. Crude X-methyl folate (2X10(-1) M) is a weak folate antagonist as compared to methotrexate since it requires a 1,000-fold higher concentration to inhibit cell growth and dihydrofolate reductase activity. In addition, the crude X-methyl folate contains a folate-like fraction since it will correct the abnormal deoxyuridine suppression in folate-depleted cells. None of the drugs tested were able to induce myeloid differentiation in the HL-60 cells. The data suggest that 9-methyl folate would not be active as a folate antagonist antitumor agent and that purified and crude X-methyl folate in large concentrations will inhibit folate metabolism. Additional studies are needed to remove the folate-like activity in the crude material in order to further establish the antitumor effects of the crude X-methyl folate.

Cell Differentiation↗
PubMed2005

Vitamin B12, homocysteine and carotid plaque in the era of folic acid fortification of enriched cereal grain products.

BACKGROUND: Carotid plaque area is a strong predictor of cardiovascular events. High homocysteine levels, which are associated with plaque formation, can result from inadequate intake of folate and vitamin B12. Now that folic acid fortification is widespread in North America, vitamin B12 has become an important determinant of homocysteine levels. We sought to determine the prevalence of low serum levels of vitamin B12, and their relation to homocysteine levels and carotid plaque area among patients referred for treatment of vascular disease since folic acid fortification of enriched grain products. METHODS: We evaluated 421 consecutive new patients with complete data whom we saw in our vascular disease prevention clinics between January 1998 and January 2002. We measured total carotid plaque area by ultrasound and determined homocysteine and serum vitamin B12 levels in all patients. RESULTS: The patients, 215 men and 206 women, ranged in age from 37 to 90 years (mean 66 years). Most were taking medications for hypertension (67%) and dyslipidemia (62%). Seventy-three patients (17%) had vitamin B12 deficiency (vitamin B12 level < 258 pmol/L with homocysteine level > 14 mumol/L or methylmalonic acid level > 271 nmol/L). The mean area of carotid plaque was significantly larger among the group of patients whose vitamin B12 level was below the median of 253 pmol/L than among those whose vitamin B12 level was above the median: 1.36 (standard deviation [SD] 1.27) cm2 v. 1.09 (SD 1.0) cm2; p = 0.016. CONCLUSIONS: Vitamin B12 deficiency is surprisingly common among patients with vascular disease, and, in the setting of folic acid fortification, low serum vitamin B12 levels are a major determinant of elevated homocysteine levels and increased carotid plaque area.

Adult↗
PubMed1983

Growth of Trichinella spiralis larvae in rats receiving folic-acid-deficient diet.

A study of the effect of growth of Trichinella spiralis in rats fed a folic-acid-deficient diet is described. Trichinella spiralis larvae encysted in the diaphragms of two groups-rats fed a folic acid-deficient diet and rats fed a complete (normal) diet-were examined. In rats fed a folic-acid-deficient diet, the number of the encysted larvae was larger than that in the controls. However, the encysted larvae were substantially longer in the control group of rats fed complete (normal) diets.

Animals↗
PubMed2000

Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial.

BACKGROUND: A high plasma homocysteine concentration is associated with increased risk of atherothrombotic disease. We investigated the effects of homocysteine-lowering treatment (folic acid plus vitamin B6) on markers of subclinical atherosclerosis among healthy siblings of patients with premature atherothrombotic disease. METHODS: We did a randomised, placebo-controlled trial among 158 healthy siblings of 167 patients with premature atherothrombotic disease. 80 were assigned placebo and 78 were assigned 5 mg folic acid and 250 mg vitamin B6 daily for 2 years. The primary endpoint was the development or progression of subclinical atherosclerosis as estimated from exercise electrocardiography, the ankle-brachial pressure index, and carotid and femoral ultrasonography. FINDINGS: Ten participants in the treatment group, and 14 in the placebo group dropped out. Vitamin treatment, compared with placebo, was associated with a decrease in fasting homocysteine concentration (from 14.7 to 7.4 micromol/L vs from 14.7 to 12.0 micromol/L), and in postmethionine homocysteine concentration (from 64.9 to 34.9 micromol/L vs from 64.8 to 50.3 micromol/L). It was also associated with a decreased rate of abnormal exercise electrocardiography tests (odds ratio 0.40 [0.17-0.93]; p=0.035). There was no apparent effect of vitamin treatment on ankle-brachial pressure indices (0.87 [0.56-1.33]), or on carotid and peripheral-arterial outcome variables (1.02 [0.26-4.05] and 0.86 [0.47-1.59], respectively). INTERPRETATION: Homocysteine-lowering treatment with folic acid plus vitamin B6 in healthy siblings of patients with premature atherothrombotic disease is associated with a decreased occurrence of abnormal exercise electrocardiography tests, which is consistent with a decreased risk of atherosclerotic coronary events.

Blood Pressure↗