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PubMed1993

[Effect of folic acid for treatment of homocystinuria due to 5,10-methylenetetrahydrofolate reductase deficiency].

Deficiency of 5,10-methylenetetrahydrofolate reductase (MTHFR) leads to deficient remethylation of homocysteine and is one of the causes of homocystinuria. Only 28 patients have been reported so far. A 15-year-old boy with mild mental retardation was admitted in our hospital because of progressive difficulty in walking. He is the second child. The paternal grandparents are first cousins. On admission, clinical examination revealed mild disturbance of consciousness, left hemiparesis, truncal ataxia, pyramidal tract signs in the lower limbs and sensory disturbance in his feet. There was no marfanoid symptoms nor ectopia lentis. EEGs showed slow activity with sporadic spike and wave complexes. Peak latencies of N20 of median nerves SEPs, the third and 5th wave of ABR and P100 of VEP were delayed. The CT scan showed mild cortical atrophy and MRI revealed increased intensity on T2-weighted images in the cerebral white matter. Biochemical studies revealed homocystinuria with homocystinemia. Both plasma methionine and serum folic acid were low. Serum vitamin B12 and methylmalonic acid in urine were normal. The lymphoblastoid cell line, transformed by Epstein-Barr virus of lymphocytes of the patient, could not grow when homocysteine was substituted in the culture medium for methionine. The normal control cell line grew naturally under the same condition. A diagnosis of homocystinuria due to MTHFR deficiency was made. The patient was on various therapeutic regimens for about 70 days. Treatment with high doses of folic acid (400 mg/day) resulted in disappearance of homocysteine in plasma, remarkable decrease of homocysteine in urine and increase of methionine in plasma of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2004

Radiation-induced sensitizing effect of folic acid (vitamin B11) and its synergistic action to mitomycin C: in vitro experiments and radiolysis.

Folic acid (FA; vitamin B11) is found to exhibit very strong cytostatic effects upon gamma-irradiation in neutral media. This effect depends on the FA concentration, pH of the media, and on the presence of air. The largest cytostatic efficiency of FA was observed in an air-free environment (pH 7.4), where deltaD37 = -90 for 10(-4) mol/dm3 FA and deltaD37 = -160 for 10(-3) mol/dm3 FA was found. FA also acts as a very efficient electron donor and is therefore able, in air-free neutral media, to enhance the efficiency of 7.5 x 10(-7) mol/dm3 mitomycin C (MMC) from deltaD37 = -80 up to deltaD37 = -200 in the presence of 5 x 10(-5) mol/dm3 FA, respectively. This synergistic effect offers a new pathway for more efficient radiation therapy by joint implementation of MMC and FA. Additionally, FA radiolysis was studied in the absence and presence of air as well as in media saturated with N20 (conversion of e(aq)- into OH). As a result of these investigations, various products were detected: ammonia, aldehydes, and a mixture of carboxylic acids, in addition to some not yet identified compounds. Their individual yields could not be identified at present.

Antibiotics, Antineoplastic↗
PubMed1998

An audit of the investigation and treatment of folic acid deficiency.

On the suspicion that folate deficiency was not being thoroughly investigated we conducted a retrospective study of management in a teaching hospital. Notes from 84 consecutive patients with low red cell folates (mean age 69.5 years, range 21-95, M:F 33:51) were reviewed for haemoglobin, mean cell volume, dietary history, alcohol consumption, drug history, relevant medical history, relevant investigations, treatment, repeat measurement of red cell folate and diagnosis of deficiency. In 52 (61.9%, mean age 72.9 years, range 33-95, M:F 21:51) no diagnosis was reached. In only 32 (38.1%, mean age 63.9 years, range 21-89, M:F 12:20) was a definitive diagnosis established: 5 had coeliac disease, 1 had Crohn's disease, 9 had drug-associated deficiency (4 methotrexate, 3 phenytoin, 1 trimethoprim and 1 valproate), 1 had combined variable immunodeficiency and 16 had dietary deficiency. In most cases of folic acid deficiency no attempt was made to establish aetiology. We recommend that younger patients without an obvious cause are investigated initially by dietary assessment and measurement of anti-endomysial antibody and by duodenal biopsy with small-bowel follow-through if clinically indicated.

Adult↗
PubMedDate not supplied

Influence of dietary folic acid on the developmental toxicity of methanol and the frequency of chromosomal breakage in the CD-1 mouse.

The proposed increased use of methanol (MeOH)-based fuels raises the concern for an increased risk for MeOH toxicity. MeOH, which is detoxified in part via a folate-dependent pathway, is known to be teratogenic in rodents. Previous observations have implicated maternal folate status as a critical modulator for the developmental toxicity of MeOH. The current study extends these findings, examining the effect of maternal dietary folate intake on fetal folate stores, as well as identifying a possible marker for the prediction of the developmental toxicity of MeOH. Virgin female CD-1 mice were assigned to diets containing either 400 (marginal) or 1200 (control) nmol folic acid (FA)/kg, and and 1% succinylsulfathiazole for 5 weeks prior to mating and throughout breeding and gestation. From gestation day (GD) 6 through 10 dams were given by gavage deionized, distilled water (dH2O) or MeOH at 2.5 g/kg body weight, twice daily. On GD 18, mice were weighed and killed and the liver, kidneys, and gravid uteri removed and weighed. Implantation sites, live and dead fetuses, and resorptions were counted; fetuses were weighed individually and examined for cleft palate and exencephaly. The marginal FA dietary treatment resulted in low maternal liver (50% reduction) and red cell folate (30% reduction) concentrations, as well as low fetal tissue folate concentrations (60 to 70% reduction) relative to the adequate FA dietary groups. Marginal FA treatment alone resulted in cleft palate in 13% of the litters; there were no litters affected with cleft palate in the adequate FA-control group. Marginal FA-MeOH treatment resulted in a further increase in the litters affected by cleft palate (72% of litters affected). The percent of litters affected by exencephaly was highest in the marginal FA-MeOH group. The frequency of micronuclei in maternal and fetal reticulocytes, a marker for chromosomal abnormalities, was not influenced by either the marginal FA diet or by MeOH treatment. These results show that marginal folate deficiency in pregnant dams significantly increases the teratogenicity of MeOH.

Abnormalities, Drug-Induced↗
PubMed1989

Homocysteinemia in rats induced by folic acid deficiency.

The effect of folate deficiency on homocysteine metabolism was examined in rats given a folate-deficient diet. Total homocysteine was determined in serum stored at -22 degrees C for 3 wk. All animals in the control group had more than 20 ng.ml-1 of serum folate and more than 1000 pg.ml-1 of serum cyanocobalamin throughout the experimental period. In contrast, serum folate in animals given the folate-deficient diet decreased to less than 3 ng.ml-1 after 4 wk and to less than 2 ng.ml-1 (a subnormal level) after 10 wk of the experiment while serum cyanocobalamin remained at more than 1000 pg.ml-1 throughout the experiment. In the control group, mean serum total homocysteine +/- SD was 4.04 +/- 1.07 nmol.ml-1 during the 20 wk of experiment. At the 10th wk before serum folate reached subnormal levels, the animals given the folate-deficient diet had a mean serum total homocysteine of 7.67 +/- 1.53 nmol.ml-1, demonstrating a significant increase (P less than 0.001). No further significant increase of mean serum total homocysteine concentrations was observed after serum folate became subnormal. This study demonstrated for the first time that a selective deficiency of folic acid caused a 2-4 fold increase in serum total homocysteine when serum folate was at low normal and at subnormal levels in rats.

Animals↗
PubMedDate not supplied

[Folic acid].

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Folic Acid↗