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Results for “FOLIC ACID DEFICIENCY”

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PubMed1985

[Folic acid deficiency anemia caused by therapy in chronic renal insufficiency].

The turbidimetric determination of folic acid concentration in serum and erythrocytes was made by means of a spectrophotometer multiscan in 35 conservatively treated patients with chronic renal failure with a minimum creatine retention of 309 mumol/l and in 63 hemodialysed patients with terminal renal insufficiency. The result showed a statistically significant diminution of serum folic acid concentration in those patients treated in a conservative manner and a significant diminution of plasmatic and erythrocytic folate++ activity in patients under hemodialysis. There was a correlation between the folic acid concentration and the hemoglobin level in both groups of patients, whereas there was no correlation to the number of leukocytes and thrombocytes. A protein deficiency diet or loss of dialysis through the capillary membrane could be found to be the cause for the loss of folic acid. The possibility of folate++ substitutive therapy and its performance was discussed and recommended for selected indications.

Adult↗
PubMed2002

Micronuclei, nucleoplasmic bridges and nuclear buds induced in folic acid deficient human lymphocytes-evidence for breakage-fusion-bridge cycles in the cytokinesis-block micronucleus assay.

We have validated the analysis of nucleoplasmic bridges (NPBs) and nuclear buds as biomarkers of genomic instability within the cytokinesis-block micronucleus assay in long-term lymphocyte cultures. Lymphocytes from 20 subjects were cultured in medium containing 12-120 nM folic acid for 9 days. Binucleate cells were scored for micronuclei (MN), NPBs and nuclear budding on day nine after 24h incubation in the presence of the cytokinesis inhibitor cytochalasin-B. Folic acid concentration was correlated significantly (P<0.0001) and negatively (r=-0.63 to -0.74) with all these markers of chromosome damage. Chromosome damage was minimised at 60-120 nM folic acid, which is greater than the concentration of folate normally observed in plasma (<30 nM). Current evidence suggests that (a) NPBs originate from dicentric chromosomes in which the centromeres have been pulled to the opposite poles of the cell at anaphase and are therefore, indicative of chromosome rearrangement and (b) that the nuclear budding process is the mechanism by which cells remove amplified DNA and is therefore a marker of gene amplification. The strong correlation between micronucleus formation, nuclear budding and NPBs (r=0.75-0.77, P<0.001) is supportive of the hypothesis that folic acid deficiency causes genomic instability and gene amplification by the initiation of breakage-fusion-bridge (BFB) cycles. These results also suggest that the CBMN assay may be a useful model for the study of the BFB cycle which may be one of the key mechanisms for the hypermutability phenotype required for the rapid evolution of cancer cells.

Cell Division↗
PubMed1984

Assessment of the value of a competitive protein binding radioassay of folic acid in the detection of folic acid deficiency.

The diagnostic value of the Becton Dickinson Radioassay Kit (125I) for the the assay of red cell folate has been investigated. The assay was acceptable with regards to precision but was non-linear with changing packed cell volume. Sensitivity of the assay was satisfactory, with 24 of 25 folate deficient patients giving red cell folate values which fell below the reference range. Specificity of the assay in the detection of folate deficiency was less satisfactory. As with microbiological assays, a considerable proportion of vitamin B12 deficient patients had low red cell folate values. In addition, low concentrations were found in 12% of patients who were unlikely to be deficient in either vitamin B12 or folic acid.

Binding, Competitive↗