SEARCH · PubMed Health

Results for “Formiminoglutamic Acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1989

Experimental maternal and neonatal folate status relationships in nonhuman primates.

The influence of maternal dietary folic acid intake on folate status was studied in Cebus albifrons monkeys by feeding 10 or 250 micrograms/100 kcal dietary folic acid during pregnancy and 4 wk postpartum. Maternal, infant, and nonpregnant hematologic indices; blood and liver folate concentrations; and urinary formiminoglutamic acid excretion all varied with dietary folate intake and pregnancy status as did milk folate concentration in lactating dams. Maternal folate status, determined by plasma, red blood cell, and milk folate concentrations, as well as urinary formiminoglutamic acid excretion, all were correlated significantly with liver folate concentrations in neonates (r = 0.740, r = 0.919, r = 0.936, and r = -0.851, respectively). Results in these primates showed that neonatal folate status was related significantly to the dietary folate intake and folate status of the mother during pregnancy and lactation.

Animals↗

PubMed2006

Quantification of urinary zwitterionic organic acids using weak-anion exchange chromatography with tandem MS detection.

A rapid and accurate quantitative method was developed and validated for the analysis of four urinary organic acids with nitrogen containing functional groups, formiminoglutamic acid (FIGLU), pyroglutamic acid (PYRGLU), 5-hydroxyindoleacetic acid (5-HIAA), and 2-methylhippuric acid (2-METHIP) by liquid chromatography tandem mass spectrometry (LC/MS/MS). The chromatography was developed using a weak anion-exchange amino column that provided mixed-mode retention of the analytes. The elution gradient relied on changes in mobile phase pH over a concave gradient, without the use of counter-ions or concentrated salt buffers. A simple sample preparation was used, only requiring the dilution of urine prior to instrumental analysis. The method was validated based on linearity (r2>or=0.995), accuracy (85-115%), precision (C.V.<12%), sample preparation stability (<or=5%, 72 h), and established patient ranges. The method was found to be both efficient and accurate for the analysis of urinary zwitterionic organic acids.

Acids↗

PubMed1990

Hematologic values and plasma and tissue folate concentrations in dogs given phenytoin on a long-term basis.

During earlier investigations of the hepatic effects in dogs of long-term administration of phenytoin alone or in combination with primidone, erythrocytic macrocytosis, neutropenia, neutrophilic hypersegmentation, and thrombocytopenia were observed. Such abnormalities were observed most often in dogs given phenytoin and resembled those known to be attributable to folate deficiency in human beings with epilepsy treated with phenytoin. To pursue the theory that these hematologic aberrations were caused by drug-induced folate deficiency, 12 dogs were given a diet specifically formulated to contain a minimally adequate concentration of folate. After 2 weeks, phenytoin was administered daily (400 mg, PO, q 8 h) to 8 of the 12 dogs for 54 weeks. A CBC, bone marrow aspiration biopsy, and measurement of plasma and RBC folate concentrations were done every 3 weeks. Bone marrow aspirates were examined by transmission electron microscopy after 24 and 36 weeks, and at the end of the treatment period. Hepatic folate concentration was also determined in all dogs before and after treatment. Excretion of formiminoglutamic acid, as a marker of folate deficiency, was measured in all dogs at the end of the study. All dogs remained healthy throughout the treatment phase. Consistent abnormalities were not observed in the blood or bone marrow of treated dogs. Plasma and RBC folate concentrations decreased in control and treated dogs as a result of dietary restriction (P less than or equal to 0.02), and remained stable until the end of the study. The RBC folate content decreased further in treated dogs (P less than or equal to 0.02), although the hepatic folate content was similar in control and treated dogs. Treated dogs did not excrete formiminoglutamic acid more rapidly than did control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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↗

PubMedDate not supplied

Dietary nickel and folic acid interact to affect folate and methionine metabolism in the rat.

A previous experiment using rats indicated that dietary nickel (Ni), folic acid, and their interaction affected variables associated with one-carbon metabolism. That study used diets that produced only mild folate deficiency. Thus, an experiment was performed to determine the effect of a severe folate deficiency on nickel deprivation in rats. A 2 x 2 factorially arranged experiment used groups of six weanling Sprague-Dawley rats. Dietary variables were nickel, as NiCl2-6H2O, 0 or 1 microgram/g and folic acid, 0 or 4 mg/kg. All diets contained 10 g succinylsulfathiazole/kg to suppress microbial folate synthesis. The basal diet contained < 20 ng Ni/g. After 58 d, an interaction between nickel and folate affected the urinary excretion of formiminoglutamic acid (FIGLU) and the liver concentration of S-adenosylmethionine (SAM). Because of this, it is proposed that the physiological function of nickel is related to the common metabolism shared by SAM and FIGLU. Possibly the physiological function of nickel could be related to the tissue concentration of 5-methyltetrahydrofolate (MTHF) or tetrahydrofolate (THF).

Animals↗

PubMed1977

Anemia in the elderly patients with special reference to folic acid status.

To investigate the role of folic acid deficiency in the pathogenesis of anemia in the elderly, hematological examinationa and assays of serum iron, vitamin B12 and folate were carried out on the 86 elderly patients admitted to a home for the aged. Means of red blood cell counts, hemoglobin levels and hematocrit were 385.3 x 10(4)/mm3, 12g/dl and 36%, respectively. These levels were lower than any other report in Japan. Anemia was detected in 23 out of 86 patients. Judging from mean corposcular volume and mean corposcular hemoglobin, most of them were normocytic and normochromic. Although low serum levels of iron and folate were rather frequently observed, the results on hematological examinations suggest that deficiency of these factors alone is not the cause of the anemia in the elderly patients. Rapid clearance of 5-methyl-tetrahydrofolic acid and increased excretion of formiminoglutamic acid after histidine loading were revealed in some of those who had subnormal serum folate levels. Therefore, supplementation of folic acid is recommended to those who had poor dietary intake.

Aged↗

PubMed1977

Effect of folic acid deficiency on pregnant rats and their offspring.

Two groups of 63-day-old female Wistar rats were fed a folic acid deficient diet, based on 20% of vitamin-free casein and containing 1% of succinylsulfathiazole, for 5 weeks (group A) and 9 weeks (group B) before being bred, and the same diet was continued through pregnancy and lactation. Three out of eleven (21.3%) and three out of seven (42.9%) rats in groups A and B, respectively, resorbed completely, while no control rat resorbed. No pups from group B survived to weaning. Both groups (A and B) showed depressed feed consumption (although the effect in group A rats was small) and weight gains and increased formiminoglutamic acid excretion in the urine during gestation, and low serum folic acid by the end of lactation. A study of blood components in group A rats revealed leucopenia, granulocytopenia, and increased reticulocyte count. While no congenital deformities were observed in pups from deficient dams, group A and group B dams in contrast to controls produced smaller sized litters with lower birth weights and poor survival rate. Surviving pups from group A dams had decreased weaning weights with significantly lower brain weights and brain DNA per gram of tissue.

Animals↗

PubMed1986

Perturbation of methionine metabolism in sheep with nitrous-oxide-induced inactivation of cobalamin.

Exposure of sheep to 36% nitrous oxide for 8 days (2-hr per day) led to 90%, 82% and 74% inhibition of 5-methyltetrahydrofolate-homocysteine methyltransferase in the liver, heart and brain, respectively, while there was no significant decrease in the activity of methylmalonyl-CoA mutase. There was also no change of betaine-homocysteine methyltransferase activity. The level of plasma methionine in nitrous-oxide-exposed sheep fell to 30% of its initial value. S-Adenosylmethionine level was reduced to 50% of the control value in the liver, and was also significantly decreased in the heart, but not in the brain. Excretion of formiminoglutamic acid and homocystine was also observed in the urine of sheep exposed to nitrous oxide. These results demonstrate that inhibition of 5-methyltetrahydrofolate-homocysteine methyltransferase causes a pronounced perturbation of methionine metabolism in sheep, suggesting that dietary methionine plus methionine synthesized from the methyl groups of betaine are not sufficient to meet the methyl needs for biological methylation reactions in this species and, in turn, emphasizing the role of 5-methyltetrahydrofolate-homocysteine methyltransferase in methionine synthesis in the sheep.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

PubMed1983

Effect of methionine on in vivo histidine metabolism in rats.

Experiments were conducted to examine the effects of methionine supplementation on histidine metabolism in rats. All animals were fed 10% casein diets with a methionine content of either 0.6 or 1.1%. Experiments in which the animals were fed their diets containing an additional 1% histidine ad libitum for at least 10 days revealed that methionine-supplemented animals had a 49% reduction of plasma histidine and an 80% reduction in urinary excretion of formiminoglutamic acid (FIGLU) on day 10. This effect was not observed on day 5. In subsequent experiments rats were fed the control or test diet ad libitum prior to receiving their diets, containing a histidine load, by force-feeding. When a 100-mg histidine load was given on day 5, 24-hour urinary FIGLU excretion was 83% lower in methionine-supplemented animals. When rats were force-fed a 75-mg [ring-2-14C]histidine load on day 10, those receiving supplemental methionine oxidized 21% more of the histidine label to 14CO2 and excreted 61% less of the dose as urinary FIGLU in 24 hours. The activities of histidase and urocanase were unaffected by the methionine supplement. The results suggest that dietary methionine supplementation enhances the in vivo catabolism of histidine by stimulating one-carbon metabolism. Delivery of the methionine supplement by ad libitum feeding requires at least 5 days for this effect to be achieved.

Animals↗

PubMed1994

Inter-relationships between single carbon units' metabolism and resting energy expenditure in weight-losing patients with small cell lung cancer. Effects of methionine supply and chemotherapy.

The one-carbon unit metabolism was investigated in 8 weight-losing patients with small cell carcinoma of the lung (SCLC). At diagnosis, 6 of the 8 patients had elevated formiminoglutamic acid (FIGLU) excretion after a histidine load, suggesting a lack of one-carbon units. In accordance, a significant decrease of FIGLU excretion was observed in the patients after oral administration of DL-methionine for 4 days. The elevated FIGLU excretion was positively correlated to weight loss prior to diagnosis and negatively correlated to serum albumin at time of diagnosis. After 3 months of combination chemotherapy, FIGLU excretion was reduced in all patients except 1, who had progressive disease. Despite the elevated FIGLU excretions, all patients had normal blood folate levels. The resting energy expenditure (REE) was recorded in 7 patients, and a significant, positive correlation was observed between pretreatment FIGLU excretion and REE, although the REE measured in this group of patients was within the normal range. These data demonstrate an increased demand of "active" one-carbon units in energy consumption in a group of weight-losing cancer patients. The one-carbon unit deficit was reconditioned by oral administration of the one-carbon unit donor DL-methionine.

Aged↗

PubMed1966

The incidence and prevention of folate deficiency in a pregnant clinic population.

Non-anemic women attending a public antenatal clinic were given, daily, a multivitamin tablet containing 78 mg. of elemental iron. The follow-up studies included an analysis of their diets. A total of 311 patients were included, of which one group received a supplement of 0.5 mg. folic acid and 0.005 mg. vitamin B(12). The incidence of megaloblastic bone marrow change in the unsupplemented group was 26% and of low blood folates approximately 50%. The incidence of megaloblastic changes was sharply reduced in the supplemented group and the blood folates were elevated to supranormal levels, indicating that the dose of folic acid used may have been above the minimal requirement. Formiminoglutamic acid (FIGLU) excretion could not be correlated with other parameters of folate deficiency. Neutrophil lobe counts did not relate to megaloblastic changes or low folate levels unless there was more than 5% hypersegmentation. The dietary intake was suboptimal in total calories, iron and food folate.

Anemia, Macrocytic↗

PubMed1983

Folate deficiency in rats fed amino acid diets.

Growth rate, hematological changes, serum, erythrocyte and liver folate levels, and urinary excretion of formiminoglutamic acid (FIGLU) were measured in rats fed p-aminobenzoic acid (PABA)-free, sulfonamide-supplemented purified amino acid diets with and without folic acid and fiber, individually and in combination. Fiber had no effect on growth but was necessary to prevent mortality in the absence of folic acid. Folic acid did not affect growth during the first 40 days, but after this period rats failed to gain weight in the absence of folic acid. Although blood hematocrit was lower when the diet was devoid of fiber and folic acid and leucocyte counts were lower when the diets were devoid of folic acid, the hematological values remained within normal physiological limits for healthy rats of comparable age. FIGLU excretion was increased and serum, erythrocyte and liver folate levels were depressed when rats were fed folic acid-free diets for 28 days. Neutrophil hypersegmentation was clearly evident after 28 days of feeding the folic acid-free diets. The use of an amino acid diet without PABA but containing 5% fiber and 1% succinylsulfathiazole is a useful system to study chronic folic acid deficiency in the rat.

Amino Acids↗

PubMed1979

Megaloblastic anemia as a result of an abnormal transcobalamin II (Cardeza).

A 34-year-old Black woman had severe megaloblastic anemia in childhood. Initially, and over the years, she responded well to massive doses of parenteral cobalamin (Cbl) or oral folic acid. Metabolic reactions involving Cbl and folate enzymes were normal during both relapse and remission except for the absence of thymidylate synthetase in relapse. Amino acid analyses of urine and plasma showed no significant abnormalities. Neither cystathionine, homocystine, formiminoglutamic acid, nor methylmalonic acid was detected in the urine. The serum Cbl level was repeatedly elevated even when the patient was receiving only folic acid therapy. The elevation of the vitamin in the serum was found to be a result of markedly increased levels of transcobalamin II (TC II), as identified by several physicochemical techniques. The patient's TC II-Cbl shared immunologic properties with normal TC II but did not facilitate or impede the uptake of Cbl or Cbl bound to normal TC II, respectively, by human cells.

Anemia, Macrocytic↗

PubMed1965

Detection by paper chromatography of imidazoles, including hydantoin-5-propionic acid, in urine after histidine dosage.

Simple paper chromatography of urine obtained in the Figlu test has been found satisfactory for determining excess excretion of the imidazole metabolites of histidine. It has been confirmed that examination for these in addition to formiminoglutamic acid is necessary for a full assessment of this test. When excretion of the latter is not abnormal in folic-acid and/or vitamin B(12) deficiency, that of urocanic acid, a glycine conjugate of urocanic acid and/or imidazole propionic acid, is usually raised. An abnormally high excretion of hydantoin-5-propionic acid after histidine has also been found in these deficiencies, and its estimation may be of additional use in the evaluation of the Figlu test.

Adult↗

PubMed1978

Megaloblastic erythropoiesis and tissue depletion of folic acid in the cat.

Dietary requirement for folic acid was shown in the cat. Folic acid deficiency was produced by feeding young cats a deficient diet (0.125 mg of total folate/kg of dry weight by analysis) for 22 weeks. The folic acid-deficient cats grew normally, but had reduced plasma, red blood cell, and liver folate concentrations in comparison with those concentrations in cats fed a control diet (1.36 mg of total folate/kg).. Urinary excretion of formiminoglutamic acid was increased in all deficient diet cats 24 hours after L-histidine injection. Erythroblasts in bone marrow smears from folic acid-deficient cats were megaloblastic; they showed abnormal nuclear chromatin patterns and had nuclear-cytoplasmic asynchronism.

Animals↗

PubMed1979

Folacin deficiency and requirement in the squirrel monkey (Saimiri sciuresus).

Acute folacin deficiency was studied in eight young squirrel monkeys (Saimiri sciureus). Half of the animals were fed a semipurified deficient diet (no added folic acid) and half were fed a control diet (0.84 mg of added folic acid per kilogram of dry diet). Monkeys fed the deficient diet lost weight and suffered from diarrhea and dehydration leading to the death of one of the animals after 6 weeks. Folacin deficiency also was studied in six older animals fed diets containing varying levels of added folic acid. Monkeys fed diets containing 0.14 or 0.27 mg of added folic acid per kilogram of dry diet slowly developed alopecia, a scaly dermatitis, and a mild macrocytic anemia. When these animals were fed the deficient diet, they lost weight rapidly, the alopecia and dermatitis worsened, excretion of formiminoglutamic acid in the urine increased, and a severe megaloblastic anemia with profound intramedullary hemolysis developed. Deficient monkeys had low plasma and red blood cell folacin values but maintained normal plasma vitamin B12 values. Repletion of the animals fed the deficient diet with injections of folic acid reversed both the hematological and physical deterioration. The folacin requirement for maintenance of body weight in these animals was 28 micrograms of total folacin per kilogram of body weight per day. More than 75 micrograms of total folacin per kilogram of body weight/day may be needed to assure growth and normal hematological parameters and bone marrow cytology.

Animals↗

PubMed1987

Intestinal absorption, liver uptake, and excretion of 3H-folic acid in folic acid-deficient, alcohol-consuming nonhuman primates.

Nonhuman primates fed folic acid-deficient diets +/- 30% kcal ethanol were used to determine alcohol effects on megaloblastic anemia development and folate bioavailability. Lower hemoglobin (Hb) and red blood cell (RBC) counts and higher mean corpuscular volume (MCV) occurred after 13 wk in alcohol-fed monkeys, later in controls. Plasma, RBC, and liver folate declined and urinary formiminoglutamic acid (FIGLU) was elevated in both groups with FIGLU increasing more among alcohol-fed monkeys at 38 wk. After 40 wk, the bioavailability of oral 3H-folic acid was investigated and showed increased fecal and reduced urinary tritium excretion in alcohol-fed monkeys compared with controls while plasma uptake and liver and whole body tritium retention were similar in both groups. These observations demonstrate that chronic alcohol consumption impairs folate coenzymes, accelerates appearance of hematologic indices of megaloblastic anemia, and causes possible malabsorption of enterohepatically circulated folates in folate deficiency even when other essential nutrients are provided.

Alcohol Drinking↗

PubMed1979

Methylmalonic acid metabolism of germfree and conventional vitamin B-12 deprived rats fed precursors of methylmalonate.

Experiments using germfree (GF), ex-germfree (XGF) and conventional (CONV) rats were conducted to study the relationship of intestinal microorganisms to vitamin B-12 (B-12) status and to methylmalonic acid (MMA) excretion of the host animal, since B-12 depleted GF rats have been found to excrete less than expected level of urinary MMA. The possibility that the GF rat lacks sufficient precursor of MMA was tested by feeding GF, XGF and CONY rats diets low or high in MMA precursors and examining urinary excretion of MMA and formiminoglutamic acid at intervals. The possibility that the GF rat may metabolize propionate and MMA differently from the CONV rat was examined by a MMA loading-recovery study and a CO2 collection study after [14C]propionate injection. Plasma and tissue B-12 levels were determined at the beginning and the end of the study. Results indicate that 1) lack of sufficient precursor of MMA is partly responsible for the failure of GF, B-12 deficient rat to excrete MMA, 2) GF and CONV rats metabolize propionate and MMA by the same pathways and 3) the presence of intestinal microorganism depletes the body B-12 store of the rat.

Animals↗