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PubMed1978

[Biochemical and hematological measures for determination of folate status in humans. 2. Comparative determination of folate in blood and in erythrocytes].

Criteria to judge the folate supply have been evaluated in previous studies. The present study is examining parameters to estimate the degree of folate deficiency. Serum folate levels and erythrocyte folate concentrations were measured in 116 volunteers (patients). The erythrocyte folate is to a large extend independent of exterior supply and is lowered only in severe chronic deficiency. Low levels of erythrocyte folate indicate longstanding undersupply. Our experiments show that folate concentration of greater than 250 ng per ml erythrocytes indicate adequate supply. Concentrations below this limit are characteristic for chronic folate deficiency. To confirm this statement further studies will take into account the urine concentration of formiminoglutamic acid.

Adult↗
PubMed1998

Sulfadoxine-pyrimethamine embryopathy in Wistar rats.

Pregnant Wistar rats received a therapeutic dose (0.72 mg/kg body weight) of intramuscular sulfadoxine-pyrimethamine on days 5, 12, and 19 of gestation. The treated animals showed elevated neutrophilic lobe average and increased urinary excretion of formiminoglutamic acid (FIGLU) as compared with controls (p < 0.001), confirming folic acid deficiency due to sulfadoxine-pyrimethamine treatment. Complete embryo resorption occurred in the treatment group, while the control animals littered normally. These findings imply that sulfadoxine-pyrimethamine should be used with utmost caution in early pregnancy as this regimen can lead to folic acid deficiency and consequent pregnancy wastage.

Animals↗
PubMed1966

Relative importance of formiminoglutamic and urocanic acid excretion after a histidine load.

A thin-layer chromatographic method for the simultaneous assessment of formimino-glutamic (Figlu) and urocanic acid excretion after loading with 15 g. histidine has been applied to 15 control subjects and to 49 selected patients. Upper limits of normal excretion were determined for urocanic acid and Figlu alone (15 mg. and 30 mg/8 hr. respectively), and for the combined metabolites (40 mg./8 hr.). Of the 49 patients studied, 27 excreted total metabolites above 40 mg./8 hr.; of these 19 would have been revealed by their abnormal excretion of Figlu and 22 by their abnormal excretion of urocanic acid. Of 74 tests in the 64 subjects, urocanic acid was present in all but 27% of the tests, and in 29.8% of the tests urocanic acid was in excess of the amount of Figlu excreted. In six normal and six abnormal tests urocanic acid was the sole metabolite present. These results re-emphasize the value of estimating both histidine metabolites in tests for folate deficiency in man, and underline the greater relative importance of urocanic acid.

Anemia, Pernicious↗
PubMed1983

Purine synthesis and reutilization in folate-deficient rat hepatocytes.

Although folic acid is known to be involved in the pathways of purine metabolism, the precise changes brought about in purine synthesis, reutilization, pool sizes, and ratios by experimental folate deficiency are not clear. Consequently, these aspects of purine metabolism were measured in hepatocytes from control and folate-deficient rats fed an amino acid diet with and without folic acid, respectively. Purine synthesis and reutilization were measured as the rates of incorporation of [U-14C]glycine and [G-3H]hypoxanthine, respectively, into the adenine and guanine pools of freshly isolated hepatocytes after a 3-hour incubation in folate-free, as well as folate- and/or thymidine-supplemented culture media. Hepatocytes from folate-deficient rats had the same rates of purine synthesis as those from control rats. Purine reutilization, purine pool sizes, and the adenine:guanine ratios were lower in hepatocytes from deficient compared with control rats. Purine synthesis was increased when folic acid or thymidine was added to the culture medium. Although hepatocytes from folate-deficient rats had a lower rate of purine reutilization compared with those from control rats, the reutilization rates did not respond to the addition of folic acid or thymidine to the culture medium. The data suggest that purine synthesis was not impaired but purine reutilization was diminished in folate deficiency. Thymidine was as effective as folic acid in stimulating purine synthesis in both control and folate-deficient hepatocytes.

Animals↗
PubMed1988

Folate deficiency in rats fed diets containing free amino acids or intact proteins.

Development of folate deficiency (FD) was evaluated in weanling rats fed diets containing mixtures of free amino acids or of vitamin-free casein and gelatin as sources of dietary nitrogen. FD could be produced in 21 d with amino acid diets that promoted maximum growth rate, were completely devoid of folate and contained 1% succinylsulfathiazole. Growth retardation and blood dyscrasia associated with FD could not be demonstrated in rats fed diets containing casein and gelatin as nitrogen sources because the vitamin-free casein contained low but measurable levels of folate. The most effective protocol to produce experimental FD in rats is to feed a folate-free diet that otherwise supports maximum growth in young animals. Additional modifications such as use of methotrexate or amino acid-imbalanced or protein-deficient diets are unnecessary.

Animals↗
PubMed1976

Effect of some anticonvulsant drugs on depletion of folate in rats on a vitamin B12-deficient diet.

Rats fed on vitamin B12-deficient or vitamin B12-supplemented diets and treated with phenobarbitone by intraperitoneal injection for 5 d showed significant increases in the activity of glutamate formiminotransferase in liver. The only significant depletion in liver folate activity was in vitamin B12-supplemented rats that were starved for 48 h. When rats were given the same diets, with phenobarbitone and diphenylhydantoin added, for 12 weeks or more in two separate experiments, significant increases in transferase activity were found only in the livers of animals fed on the deficient diet. However, there was significant depletion of liver folate in animals taking the supplemented diet.

Animals↗
PubMed1976

Vitamin B12--folate interrelations.

Megaloblastic anaemia is due to a derangement of DNA synthesis caused by insufficient supply of one or other of the four deoxyribonucleoside triphosphate (dNTP) precursors of DNA synthesis or by direct inhibition of one or other DNA polymerase. Reduced supply of the pyrimidine deoxythymidine triphosphate (dTTP) may be caused by folate or vitamin B12 deficiencies or by the action of dihydrofolate reductase inhibitors (e.g. methotrexate, pyrimethamine or trimethoprim), all of which cause reduced supply of the coenzyme 5, 10 methylene tetrahydrofolate (pentaglutamate) needed for thymidylate synthetase. Reduced dTTP supply may also be caused by direct inhibition of thymidylate synthetase by 5-fluorouracil. Reduced supply of both purines, deoxyadenosine triphosphate (dATP) and deoxyguanosine triphosphate (dGTP), may be caused by hydroxyurea, 6-mercaptopurine (and probably by another purine antagonist azaserine), whilst reduced supply of both pyrimidine DNA precursors, dTTP and dCTP (deoxycytidine triphosphate) may be due to inherited orotic aciduria or to treatment with azauridine. Cytosine arabinoside directly inhibits DNA polymerase. DNA replication is a discontinuous process and a number of enzymes are concerned with different aspects of the process. The parental strands partly unwind and a large number of initiation points or origins are activated on both strands. A primer RNA is first synthesised using the parental strand of DNA as template. Fragments of new DNA are then synthesised on the parental DNA template, starting at the RNA primer, under the action of one or other DNA polymerase (probably gamma). The RNA primer is then removed and the gap left is filled by further DNA synthesis under the action of a different DNA polymerase (probably alpha). The fragments of new DNA are joined to give newly synthesised stretches of DNA (replicons) which are then liigated together to form bulk DNA of enormous molecular weight. It is suggested here that reduced supply of one or other of the four deoxyribonucleoside triphosphate (dNTP) during the 'S' phase of the cell cycle (due to vitamin B12 or folate deficiency, drug treatment or other congenital or acquired abnormality in synthesis of the dNTP) impairs the cell's ability to elongate newly initiated DNA fragments by preventing gap-filling, the polymerase needed for gap-filling requiring substantially greater concentrations of the deoxyribonucleoside triphosphates than the polymerase involved in chain initiation. Cytosine arabinoside, which also may cause megaloblastosis, may affect principally the synthesis of new DNA fragments. Since active protein synthesis is needed for the cell to enter the S phase and RNA synthesis is needed to prime new DNA synthesis, megaloblastic anaemia may be expected to occur only when DNA synthesis is inhibited but protein and RNA synthesis are relatively unimpaired...

Anemia, Megaloblastic↗