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At least 73 records · Page 4Linked to original sources
PubMed2006

A folate-dependent metabolite in amniotic fluid from pregnancies with normal or trisomy 21 chromosomes.

INTRODUCTION: Previous studies have given conflicting results as to whether or not folate metabolism is altered in Down syndrome. Folate is necessary to facilitate metabolism of one-carbon units. Folate accepts one-carbon units from one-carbon unit donors, including formiminoglutamate (FIGLU). Folate deficiency leads to accumulation of FIGLU and impairment of one-carbon unit metabolism. FIGLU is a functional measure of folate deficiency. MATERIALS AND METHODS: Archived anonymized amniotic fluid specimens were obtained from normal pregnancies and those with Down syndrome. Gas liquid chromatography/mass spectrometry was used to quantitate FIGLU, which is elevated in folate deficiency. A tetra-deuterated FIGLU was used as a standard, and single-ion monitoring was performed. Nonparametric statistical analysis was performed with the Mann-Whitney U test. RESULTS: FIGLU was significantly lower in pregnancies with Down syndrome. The median FIGLU level was 0.9 micromol/l in amniotic fluid from fetuses with Down syndrome. The median FIGLU level was 1.3 in amniotic fluid from control fetuses. This difference was statistically significant (p = 0.009). No statistically significant differences were found with histidine or glutamate. DISCUSSION: There was no evidence of folate deficiency. FIGLU was decreased, not increased. Decreased FIGLU might result from accelerated activity of one or more genes on chromosome 21, by a gene dosage effect. Genes which might explain the reduced FIGLU include one which degrades FIGLU (glutamate formiminotransferase-cyclodeaminase), one which participates in purine synthesis, and one which degrades homocysteine (cystathionine-beta-synthase).

Amniocentesis↗
PubMed2002

The role of histidine in the anemia of folate deficiency.

The amino acid histidine is metabolized to glutamic acid in mammalian tissue. Formiminoglutamic acid (FIGLU) is an intermediary in this reaction, and tetrahydrofolic acid is the coenzyme that converts it to glutamic acid. A test for folate deficiency concerns the measurement of urinary FIGLU excretion after a histidine load. It was observed that folate-deficient individuals receiving the histidine for the FIGLU test made hematological response that alleviated the anemia associated with this deficiency. This was unusual in that a biochemical test to determine the deficiency results in a beneficial effect for one aspect of the deficiency. The studies reported in this paper give a metabolic explanation for this phenomenon. Urine was collected for 24 hr from 25 folate-deficient subjects, 10 vitamin B(12)-deficient subjects, and 15 normal controls. Urinary excretion of histidine was a mean of 203 mg with a range of 130-360 mg for the folate-deficient subjects; 51.5 mg with a range of 30-76.6 mg for normal subjects; and 60.0 mg with a range of 32.3-93.0 mg for the vitamin B(12)-deficient subjects. All the folate-deficient subjects subsequently made a hematological response to the histidine administered for the FIGLU test. No hematological response was observed in the vitamin B(12)-deficient individuals. When folic acid was given to folate-deficient subjects who received no histidine, urinary histidine levels returned to normal levels rapidly and this was followed by a hematological response. Others have shown that volunteers fed a histidine-free diet developed anemia. In normal subjects, histidine is excreted much more in the urine than other essential amino acids are. Hemoglobin protein contains 10% histidine. Under normal conditions, dietary histidine can supply sufficient histidine to prevent anemia. When the dietary intake is diminished or the urinary excretion is greatly increased, anemia results. It is concluded that folate deficiency causes histidine depletion through increased urinary excretion of this amino acid. Feeding histidine replenishes tissue levels of histidine, resulting in hemoglobin regeneration. Folic acid administration results in return of histidine to normal urinary levels. Thus, a combination of folic acid histidine would be beneficial for folate deficient individuals.

Anemia, Macrocytic↗
PubMed1976

Hydantoin-5-propionic aciduria in folic acid nondependent formiminoglutamic aciduria observed in two siblings.

Hydantion-5-propionic acid was detected in massive amounts in the urine of two previously described sisters with folic acid nondependent formiminoglutamic aciduria. HPA was identified rigorously, e.g. by gas chromatography-mass spectrometry, and was measured quantitatively by selected ion monitoring (mass fragmentography) using deuterated HPA as internal standard. Before histidine loading, both girls with the postulated formiminotransferase deficiency excreted an amount of HPA more than 50 times greater than the control subjects. After histidine ingestion, HPA excretion was still doubled or tripled. With the exception of the father, the values for the other members of the family also markedly exceeded the normal range and were of the same order of magnitude as in folate deficiency. Measurement of HPA excretion in urine seems to be a valuable supplement or alternative to the enzymatic FIGu test for the detection of general or functional folate deficiency or impaired folate utilization and it will be indispensable for the detection of (as yet unknown) 4-imidazolone-5-propionic acid hydrolase deficiency.

Adolescent↗
PubMed1991

Nitrous oxide and formiminoglutamic acid: excretion in surgical patients and anaesthetists.

We have investigated the possible toxicity of nitrous oxide on vitamin B12 and its sequelae upon folic acid metabolism using the urine formiminoglutamic acid excretion test, an index of the functional state of folate metabolism. Ten control subjects not exposed to nitrous oxide and five patients receiving limb surgery under local anaesthesia excreted normal amounts of formiminoglutamic acid in urine for 6 days. Fifty patients received nitrous oxide anaesthesia for similar surgery and, of these, 22 had a dose-dependent increase in excretion on the first 2 days after operation. There were large individual variations. Exposure to 70% nitrous oxide appeared to cause abnormal metabolism of folate when exposure was greater than 90 min. Ten anaesthetists demonstrated normal excretion of formiminoglutamic acid; their exposure to nitrous oxide was typical of that in other studies of theatre environmental pollution.

Adult↗