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PubMedDate not supplied

Plasma homocysteine is a sensitive marker for tissue deficiency of both cobalamines and folates in a psychogeriatric population.

The concentration of blood folates was decreased and the concentration of plasma homocysteine was increased in a psychogeriatric population, whereas the concentrations of methylmalonic acid or serum cobalamins were not changed compared with healthy subjects. The highest frequency of abnormal values was shown by plasma homocysteine concentration, which was increased in 88 of 168 patients. In 29 of these 88 patients increased concentration of plasma homocysteine could possibly be attributed to tissue cobalamin deficiency. One patient had only a lowered concentration of blood folate. Thirteen patients had elevated concentrations of serum creatinine which could explain increased plasma homocysteine concentration. Even if the remaining patients (n = 45) had normal vitamin levels in circulation, the increased plasma homocysteine concentration in most cases must be attributed to tissue deficiency of cobalamins and/or folates. Thus, many patients with increased plasma homocysteine concentrations need further vitamin supplementation despite their normal vitamin levels in serum and blood. Copyrightz1999S.KargerAG,Basel

Aged↗
PubMed1994

Effects of ageing on folate metabolism in rats fed a long-term folate deficient diet.

The present study was focused on the effects of feeding to young (2 mo. old) and aged (30 mo. old) rats either a folate repleted or a folate deficient diet for seven weeks on several markers of folate metabolism. Serum and liver folate contents were determined, and hepatic distribution of folates based on glutamic acid chain length and pteridine ring was obtained. In addition, liver s-adenosylmethionine (Ado Met) and s-adenosylhomocysteine (AdoHcy) concentrations, as well as serum homocysteine concentration have been also determined. Ageing itself seems not to be associated with lower hepatic folate content, but in serum a 50% decrease was observed. Feeding the folate deficient diet did result in significant lower (p < 0.001) liver folate content in both age groups, and in marked decreases in serum folates. These quantitative changes in the folate deficient groups were associated with an elongation of the glutamate chain length, mostly represented by a significant decrease in the proportion of pentaglutamyl derivatives, an increase of hexaglutamyl, and appearance of hepta and octaglutamyl folate derivatives. However, there were no important modifications in the pteridine ring distribution regardless of the age and level of dietary folate. In the present study, ageing seems to be associated with a significantly lower AdoMet/AdoHc ratio (65% decrease, p < 0.05), irrespective of the folic acid included in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1997

Folate deficiency in rats induces DNA strand breaks and hypomethylation within the p53 tumor suppressor gene.

Folate is essential for the de novo biosynthesis of purines and thymidylate, and is an important mediator in the transfer of methyl groups for DNA methylation. Folate deficiency, therefore, could contribute to abnormal DNA integrity and methylation patterns. We investigated the effect of isolated folate deficiency in rats on DNA methylation and DNA strand breaks both at the genomic level and within specific sequences of the p53 tumor suppressor gene. Our data indicate that folate deficiency induces DNA strand breaks and hypomethylation within the p53 gene. Such alterations either did not occur or were chronologically delayed when examined on a genome-wide basis, indicating some selectivity for the exons examined within the p53 gene. Folate insufficiency has been implicated in the development of several human and experimental cancers, and aberrations within these regions of the p53 gene that were examined in this study are thought to play an integral role in carcinogenesis. The aforementioned molecular alterations may therefore be a means by which dietary folate deficiency enhances carcinogenesis.

Animals↗
PubMed1976

Serum vitamin B12 levels in the aged.

In an attempt to throw light on the question of age-related variations in the normal blood content of cobalamin and on the frequency of deficiencies of antimegaloblastic nutriments in the elderly, 273 geriatric patients have been investigated. Low serum vitamin B12 values were found in one third of these patients, due to latent pernicious anaemia in five and malabsorption in seven cases, and probably caused by nutritional deficiency of folate or cobalamin in 78 cases. In that part of the series with apparently normal vitamin B12 levels, the mean value (379+/-14 pg/ml) was lower than the mean (456+/-20 pg/ml) for a younger control group. However, this cannot be taken as a sign of a physiological lowering of the cobalamin values with age, as nutritional deficiencies could not be ruled out in this part of the series. It is concluded that serum vitamin B12 assays should be performed rather liberally in the aged. Patients with nutritional deficiency of cobalamin or folate should be treated, even if frank megaloblastic anaemia is not present.

Age Factors↗
PubMed1985

Vitamin B12-folate interrelationships.

The studies discussed in this review support the view that biochemical and clinical symptoms common to both folate and vitamin B12 deficiency are due to the induction of a functional folate deficiency, which in turn is induced by cobalamin deprivation. The interrelationship between these two vitamins is best explained by the methyl trap hypothesis stating that vitamin B12 deficiency can lead to lowered levels of methionine synthetase, which results in a functional folate deficiency by trapping an increased proportion of folate as the 5-methyl derivative. In addition, as 5-methyl-H4PteGlu is a poor substrate for folylpolyglutamate synthetase, there is a decreased synthesis of folylpolyglutamates and consequently a decreased retention of folates by tissues. The real folate deficiency that ensues because of decreased tissue folate levels is probably as important physiologically as the functional deficiency caused by the methyl trap. The sparing effect of methionine can be explained by adenosylmethionine inhibition of methylenetetrahydrofolate reductase, which would prevent the buildup of 5-methyl-H4PteGlun. A deficiency in vitamin B12 would not, in itself, be sufficient to cause a disturbance in folate metabolism. The deficiency would have to result in lowered methyltransferase levels before any such disturbance would be manifest.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1977

The relationship of defective cell-mediated immunity to visceral disease in systemic sclerosis.

Phytohaemagglutinin-induced lymphocyte transformation and circulating thymus-dependent (T) lymphocyte numbers were studied in twenty-eight patients with systemic sclerosis (SS), in fifty normal controls and eleven elderly controls. Patients with SS were found to have impaired lymphocyte transformation responses which showed a positive correlation with both the number of circulating T lymphocytes and the extent of visceral involvement by the disease. This defect of cell-mediated immunity could not be attributed to the effects of increasing age, corticosteroid treatment, iron and folate deficiency or inhibitory serum factors and may have pathogenetic implications for the disorder.

Adult↗
PubMed2005

Autoantibodies to folate receptors in the cerebral folate deficiency syndrome.

In infantile-onset cerebral folate deficiency, 5-methyltetrahydrofolate (5MTHF) levels in the cerebrospinal fluid are low, but folate levels in the serum and erythrocytes are normal. We examined serum specimens from 28 children with cerebral folate deficiency, 5 of their mothers, 28 age-matched control subjects, and 41 patients with an unrelated neurologic disorder. Serum from 25 of the 28 patients and 0 of 28 control subjects contained high-affinity blocking autoantibodies against membrane-bound folate receptors that are present on the choroid plexus. Oral folinic acid normalized 5MTHF levels in the cerebrospinal fluid and led to clinical improvement. Cerebral folate deficiency is a disorder in which autoantibodies can prevent the transfer of folate from the plasma to the cerebrospinal fluid.

Adolescent↗
PubMed1977

Applicability of an enzymatic quantitation of methylmalonic, propionic, and acetic acids in normal and megaloblastic states.

A rapid sensitive spectrophotometric assay for the measurement of methylmalonic and propionic acids in urine is described. The assay is based upon the quantitation of propionic acid using acetyl coenzyme A synthetase isolated from baker's yeast. This enzyme is highly specific for acetate and propionate, and acetate interference is eliminated by conversion to citrate. Methylmalonic acid was assayed by converting it to propionate by heat decarboxylation and then measuring the propionate increment over the endogenous amount in the noncarboxylated sample. Studies of urine obtained from normal subjects (by isolation, partial purification, and then assay by the isotope dilution technique) demonstrated urinary excretion of less than 1 mg of propionic acid and 1-5 mg of methylmalonic acid per day. In 22 consecutive patients with documented vitamin B12 deficiency, methylmalonic acid excretion in excess of 30 mg/24 hr was found. In four other patients, with only neurologic involvement methylmalonic aciduria aided in identifying B12 deficiency as an etiologic factor. Methylmalonic acid excretion was measured by direct assay of an aliquot of urine, requiring neither a valine load nor special extraction procedures. Propionic aciduria was variably increased in B12 deficiency and did not correlate either with the severity of the deficit or degree of methylmalonic aciduria. The assay was performed on urine, but it is potentially applicable to tissue extracts. In addition, this assay method can be utilized for the quantification of urine acetate levels as well.

Acetates↗
PubMed1978

[Biochemical and hematological measures for determination of folate status in humans. 1. Relation between serum folate and segmentation of neutrophil granulocytes].

In a study on 130 student volunteers the segmentation of neutrophil granulocytes was measured. The serum folate concentration was used as biochemical reference. Both parameters indicate the state of folate supply or the degree of folate deficiency, respectively. Considering the haematologic response as an objective criterion only 71% of the examines showed an adequate folate status. 11% were found "deficient" and 18% were in a marginal state of folate supply. This result was confirmed by repeating the experiment. Further studies are to include folate concentration of erythrocytes and urine concentration of formiminoglutamic acid.

Adult↗
PubMed1999

Folate deficiency beyond megaloblastic anemia: hyperhomocysteinemia and other manifestations of dysfunctional folate status.

Folate plays a key role in nucleic acid synthesis. As a consequence, the most conspicuous complication of folate deficiency or of derangements of folate metabolism is megaloblastic macrocytic anemia caused by interdiction of normal proliferation of rapidly dividing bone marrow cells. Other rapidly dividing cells, including those in the gastrointestinal tract, may also be affected by the megaloblastic process. This may result in malabsorption. However, there is mounting evidence to indicate that there are other earlier manifestations of folate deficiency or of longstanding suboptimal folate nutrition. Chief among these manifestations of folate deficiency are an increased predisposition to occlusive vascular disease and thrombosis, which have been linked to increased levels of homocysteine found in folate deficiency and abnormal states of folate metabolism. In addition, folate deficiency, previously considered free of neurological consequences, is now known to be associated with disturbances of mood, and even spinal cord syndromes similar to those seen in vitamin B12 deficiency. Finally, there is both experimental and clinical evidence to suggest that folate deficiency may interfere with immunologic status and may be associated with an increased predisposition to neoplasia. Nutritional as well as genetic factors may contribute to these various nonhematological manifestations of folate insufficiency.

Anemia, Megaloblastic↗
PubMed1997

Epithelial cell folate depletion occurs in neoplastic but not adjacent normal colon mucosa.

BACKGROUND & AIMS: Restricted folate supply is associated with the development of carcinoma, and folate supplements have a protective effect in colorectal carcinoma. This effect may be mediated through correction of local folate deficiency. The aim of this study was to define the folate content of neoplastic colonic epithelial cells and its relation to that of adjacent normal tissue and circulating levels. METHODS: Epithelial cells were isolated from endoscopic biopsy specimens of normal, adenocarcinoma, adenoma, and adjacent normal colonic mucosa by ion chelation. Intracellular folate levels were determined by microbiological assay. RESULTS: Folate levels in carcinoma specimens were lower than in adjacent normal tissue (P < 0.02). Levels in adenoma epithelial cells were lower than in adjacent normal tissue, although this did not reach statistical significance (P < 0.06). Epithelial cells from normal tissue and mucosa adjacent to tumors and adenomata had similar folate contents. Blood folate and vitamin B12 indices for all groups were normal. CONCLUSIONS: Malignant colon epithelial cells show a relative localized folate deficiency. However, there is no evidence for the occurrence of generalized mucosal folate deficiency. This finding suggests that folate supplements do not inhibit carcinogenesis through correction of localized folate depletion.

Adenocarcinoma↗
PubMed1993

Biochemical responses of broiler chicks to folate deficiency.

The effects of folate sufficiency and deficiency in three pathways of folate metabolism were studied in 2-and 3-week-old broiler chicks. Erythrocyte phosphoribosylpyrophosphate concentrations and dihydrofolate reductase (EC 1.5.1.3) activity were significantly elevated in folate deficiency. Percentage incorporation of deoxyuridine into bone marrow DNA was reduced in folate deficiency. There was a trend towards reduced liver dihydrofolate reductase activity in deficient chicks. These studies identify further biochemical criteria that can be used to assess folate status of chicks.

Animals↗
PubMed1979

Folacin and iron status and hematological findings in predominately black elderly persons from urban low-income households.

The folacin and iron status and hemotological parameters of 193 persons 60 years of age and older from urban low-income households were evaluated. Of the serum folacin values 30% were between 3 and 6 ng/ml and 8% were below 3 ng/ml. Of these subjects 60% could be classified as "high risk" (less than 140 ng/ml) and 11% as "medium risk" (140 to 160 ng/ml) based on red blood cell folacin concentrations. Serum iron was normal (greater than 50 micrograms/dl) for all subjects as was transferrin saturation (greater than 15%). Hematological indices showed a 14% incidence of anemia (hemaglobin less than 12 g/dl), and 32% incidence of leukopenia (leukocytes less than 4.8 X 10(3)). These findings demonstrate widespread folacin deficiency and no evidence of iron deficiency in these elderly people.

Aged↗
PubMed1992

Low thyroxine levels in female psychiatric inpatients with riboflavin deficiency: implications for folate-dependent methylation.

Intermediates in the folate-dependent methylation pathways may play a role in the etiology and treatment of such mental disorders as major depression. These pathways include a step dependent on a riboflavin (B2)-derived coenzyme, flavin adenine dinucleotide (FAD), which is reportedly sensitive to thyroid status and to phenothiazine and tricyclic drug exposure. In a sample of 52 male and female acute psychiatric inpatients, 17% (n = 9) showed B2 deficiency (i.e., insufficient FAD activity) on a functional red blood cell enzyme assay, but only one B2-deficient individual showed deficiency in another B-complex vitamin (folate). All patients with B2 deficiency were women, who were also significantly younger than the rest of the sample. The B2-deficient women had significantly lower thyroxine levels, even when controlling for sex and covarying for age. B2-deficient patients exhibited a nonsignificant trend toward more unipolar depression (44% vs 14%), but not toward bipolar or schizophrenic disorders. As in a previous study, drug exposure did not show a relationship to riboflavin deficiency in this sample. The findings suggest that B2 (FAD) activity may serve as a sensitive marker of thyroxine status in certain female psychiatric inpatients and that B2 deficiency may play an etiological role in defects of the methylation pathways in a subset of mentally ill individuals.

Adult↗
PubMed1987

Development of a subacute tetraparesis after disulfiram intoxication. Case report.

A chronic alcoholic was intoxicated with the excessive dose of 25 g of disulfiram and developed a subacute flaccid tetraparesis and an associated encephalopathy. The severity of the clinical picture is partly explained by malnourishment including folate and vitamin B12 deficiency. The clinical, electrophysiological and pathological examinations are in accordance with the concept of a central-peripheral distal axonopathy.

Alcoholism↗