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Results for “FOLIC ACID DEFICIENCY”

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PubMed1975

Trypanosoma lewisi, Trypanosoma rhodesiense: mitotic activity in normal and folic acid deficient rats.

Ten experiments were performed to compare mitotic activity in livers of rats infected with Trypanosoma rhodesiense and Trypanosoma lewisi. The host dietary groups were: (1) complete of full complement; (2) folic acid deficient, and (3) pair-fed or calorically restricted. Liver mitotic counts of T. lewisi-infected rats fed complete and pair-fed control diets showed a high degree of significance over that of control rats. From days 35 to 55, liver mitotic counts of T. lewisi-infected rats deficient in folic acid showed an average of 16 +/- 2 mitotic phases as compared to 9 +/- 2 for livers of uninfected animals. Liver mitotic counts of T. rhodesiense-infected and non-infected rats fed complete and pair-fed control diets showed that there were essentially no differences in the mitotic counts from that seen in liver from control, uninfected animals. On day 25 (day 5 of infection), folic acid-deficient infected rats showed a significantly higher number of dividing cells than the controls. Folate was measured in isolated, washed T. lewisi and T. rhodesiense cells. T. lewisi and T. rhodesiense contained 9.6 ng folate per 10(8) cells and 6.2 ng of folate per 10(8) cells respectively. Metabolic products of T. lewisi contained an average of 0.51 ng of folate per 10(8) trypanosomes. T. rhodesiense metabolic products contained 0.3 ng of folate per 10(8) trypanosomes.

Animals↗
PubMedDate not supplied

[Role of folic-acid deficiency in deficiency diseases of the nervous system. Apropos of 12 cases including an anatomo-clinical case].

The authors report 12 cases of neurological syndromes due to folic acid deficiency, due in 8 cases to chronic alcoholism. In 5 cases there was polyneuritis, 3 cases had cerebellar atrophy, whilst 4 patients had subacute combined degeneration of the cord. Folic acid deficiency occurred alone in five cases out of twelve, as in 3 cases vitamin B1 deficiency was associated, and in four cases there was malabsorption of vitamin B12. A neuropathological study of these cases showed: 1) moderate involvement of the mamillary tubercles as observed in deficiency encephalopathies. 2) severe peripheral nerve involvement especially of axonal type. 3) involvement of the anterior horns of the spinal cord with appearances of central chromatolysis and a few atrophic neurones.

Adult↗
PubMed2002

Folic acid deficiency and homocysteine impair DNA repair in hippocampal neurons and sensitize them to amyloid toxicity in experimental models of Alzheimer's disease.

Recent epidemiological and clinical data suggest that persons with low folic acid levels and elevated homocysteine levels are at increased risk of Alzheimer's disease (AD), but the underlying mechanism is unknown. We tested the hypothesis that impaired one-carbon metabolism resulting from folic acid deficiency and high homocysteine levels promotes accumulation of DNA damage and sensitizes neurons to amyloid beta-peptide (Abeta) toxicity. Incubation of hippocampal cultures in folic acid-deficient medium or in the presence of methotrexate (an inhibitor of folic acid metabolism) or homocysteine induced cell death and rendered neurons vulnerable to death induced by Abeta. Methyl donor deficiency caused uracil misincorporation and DNA damage and greatly potentiated Abeta toxicity as the result of reduced repair of Abeta-induced oxidative modification of DNA bases. When maintained on a folic acid-deficient diet, amyloid precursor protein (APP) mutant transgenic mice, but not wild-type mice, exhibited increased cellular DNA damage and hippocampal neurodegeneration. Levels of Abeta were unchanged in the brains of folate-deficient APP mutant mice. Our data suggest that folic acid deficiency and homocysteine impair DNA repair in neurons, which sensitizes them to oxidative damage induced by Abeta.

Alzheimer Disease↗
PubMed1989

Growth of 9.5-day rat embryos in folic-acid-deficient serum.

Rat embryos (9.5-day-old) were cultured for 48 hours in serum from diet-induced folic-acid-deficient rats. Resultant embryos were frequently abnormal; many were growth retarded and exhibited a defect in the turning mechanism that inverts the embryo from ventrally to dorsally convex. Affected embryos displayed abnormal twisting or kinking of the neural tube. Gross anaemia was also frequently observed, and the protein content of the embryos was markedly less than that of embryos grown in normal rat serum. Supplementation of the deficient serum with folic acid improved growth and greatly reduced the occurrence of deformities. It virtually eliminated the incidence of gross anaemia but only partially restored the protein content of the embryos to the level observed in those grown in normal rat serum. The effects of the folate deficiency could be eliminated by supplementation with normal rat serum. The data indicate that embryos have a requirement for adequate folate in order for normal growth and differentiation to take place; they also suggest that some of the embryopathic effects of maternal folate deficiency are mediated by secondary effects on maternal metabolism. This may take the form of a disturbance in the production of maternally synthesised growth factors necessary for normal embryonic development.

Animals↗
PubMed1998

An audit of the investigation and treatment of folic acid deficiency.

On the suspicion that folate deficiency was not being thoroughly investigated we conducted a retrospective study of management in a teaching hospital. Notes from 84 consecutive patients with low red cell folates (mean age 69.5 years, range 21-95, M:F 33:51) were reviewed for haemoglobin, mean cell volume, dietary history, alcohol consumption, drug history, relevant medical history, relevant investigations, treatment, repeat measurement of red cell folate and diagnosis of deficiency. In 52 (61.9%, mean age 72.9 years, range 33-95, M:F 21:51) no diagnosis was reached. In only 32 (38.1%, mean age 63.9 years, range 21-89, M:F 12:20) was a definitive diagnosis established: 5 had coeliac disease, 1 had Crohn's disease, 9 had drug-associated deficiency (4 methotrexate, 3 phenytoin, 1 trimethoprim and 1 valproate), 1 had combined variable immunodeficiency and 16 had dietary deficiency. In most cases of folic acid deficiency no attempt was made to establish aetiology. We recommend that younger patients without an obvious cause are investigated initially by dietary assessment and measurement of anti-endomysial antibody and by duodenal biopsy with small-bowel follow-through if clinically indicated.

Adult↗
PubMed1997

Folic acid deficiency enhances oral contraceptive-induced platelet hyperactivity.

In previous studies conducted in female rats and in women, oral contraceptives (OC) were found to induce a platelet hyperactivity that was related to an oxidative stress. Because cases of megaloblastic anemia have been reported to occur in women taking OC, these treatments are suspected of depleting folate stores. In the study presented herein, which was conducted in rats, we sought to determine the influence of dietary folic acid deficiency (FD) on the thrombogenicity of OC. Animals were fed for 6 weeks with either a folic acid-deficient diet (250 micrograms/kg folic acid) or a control diet (750 micrograms/kg). One-half of the animals in each group were treated with OC (ethinyl estradiol plus lynestrenol). FD and OC individually potentiated platelet aggregation in response to thrombin and ADP and the release and metabolism of arachidonic acid, in particular, the biosynthesis of thromboxane. These platelet activities were further enhanced in animals given both the folic acid-deficient diet and the OC treatment. In addition, FD enhanced the pro-oxidant state in OC-treated rats characterized by (1) a fall in platelet and plasma n-3 fatty acids, (2) an increase in plasma lipid peroxidation products such as conjugated dienes, lipid peroxides, and thiobarbituric reactive substances, (3) a rise in ex vivo erythrocyte susceptibility to free radicals. Moreover, we found that OC treatment led to a reduction of plasma and erythrocyte folate concentrations associated with a moderate hyperhomocysteinemia. Under our experimental conditions, we did not find significant synergistic effects between OC and FD. We propose that, although the untoward effects associated with the OC treatment may not primarily be dependent on FD, the folic acid deficiency magnified OC-induced oxidative stress, which resulted in platelet hyperactivity by elevating the pro-oxidant homocysteine plasma concentration. Despite the limitations of this animal model, the data of the present study suggest that in addition to cigarette smoking, inadequate folic acid intake might predispose those taking OC to vascular thrombosis.

Animals↗
PubMed1975

Depressed cell-mediated immunity in megaloblastic anemia due to folic acid deficiency.

Cell-mediated immunity has been studied in patients with 1) megaloblastic anemia of folic acid deficiency, 2)megaloblastic anemia of pregnancy, or 3) iron-deficiency anemia. Using dinitrochlorobenzene skin tests, phytohemagglutinin-stimulated lymphocyte transformation, and rosette inhibition by antilymphocyte globulin, we have shown that cell-mediated immunity is depressed in megaloblastic anemia due to folate deficiency; this depression was reversed by folate treatment. Cell-mediated immunity was not impaired by iron-deficiency anemia. Suggested interactions between iron deficiency and folate metabolism were not clarified by these studies.

Adolescent↗
PubMedDate not supplied

[Atrophy of the oro-pharyngeal mucosa caused by vitamin B12 and folic acid deficiency. Etiopathologic aspects and clinico-therapeutic problems].

BACKGROUND: By atrophy, the decrease in volume of the cell due to loss of cell substances is intended. When a sufficiently high number of cells is involved, the whole tissue or organ decreases in volume or becomes atrophic. The oropharyngeal mucous membrane can be the site of processes of mainly atrophic type whose causes can be found in various pathologies. These pathologies can be caused by alterations in the endocrin-metabolic conditions, such as vitamin deficiencies, especially of vitamin B12 and folic acid. MATERIALS AND METHODS: Twenty-three patients who on objective examination were affected by mucous atrophies, both of the oral cavity and of the oropharyngeal area probably due to vitamin B12 and/or folic acid deficiency have been identified. Indicatively the therapies prescribed consisted of administration of N5calcium methyltetrahydrofolate for 1 month, and of pharmaceutical products containing vitamin B12, again for 1 month. After a month of therapy, the overall clinical situation of all the patients who were included in our protocol was reassessed. RESULTS AND CONCLUSIONS: On clinical examination, 20 patient showed pink oral mucous membrane. The patients also reported disappearance of pyrotic symptoms and the laboratory tests showed values within normal limits. The erethistic ulcers on the lips had disappeared even if the vermilion did not appear fully re-epithelialized in 9 patients. The other 3 patients, who still had values under normal limits, were subjects who had undergone long-term chemotherapy. For these patients the therapy was continued for a further month. At the third check-up and careful objective examination, the lingual mucous membrane appeared pink and re-epitheliated. The patients reported disappearance of the painful oral symptoms. The laboratory tests were repeated again for all the patients and these confirmed values within normal limits for vitamin B12 and folic acid.

Adult↗
PubMed1982

Folic acid deficiency and neutrophil dysfunction.

Polymorphonuclear leukocyte functions were studied in 92 patients with protein-calorie malnutrition. Serum folic acid levels were higher than 3 ng/ml in 38 patients and 3 ng/ml or less in 54 patients. Significant differences were found between these two groups of patients with regard to phagocytosis (81.5 +/- 1.9 versus 69.2 +/- 2.0 percent, p less than 0.001) and bactericidal ability (90.6 +/- 1.1 versus 84.5 +/- 2.3 percent, p less than 0.05). Correction of folic acid deficiency in 22 patients was associated with recovery of normal phagocytosis (p less than 0.001) but not bactericidal function. Adding folic acid to the serum of eight patients also restored normal phagocytic function (p less than 0.001). A correlation was found in vivo and in vitro between changes over time in folic acid levels and in phagocytosis.

Blood Bactericidal Activity↗
PubMed1998

[Folic acid deficiency in chronically hospitalized mental patients].

Studies over the past 30 years have shown a relationship between folic acid deficiency and psychopathology. FA deficiency was observed more often in depressed and in psychotic patients, in alcoholics, in those suffering from organic mental disorders and in the psycho-geriatric population. In a chronic inpatient population of 120 patients, of the 106 in whom FA serum levels were examined, only 1 had a definitely subnormal level. An additional 16 had close to the lower limit of normal (2 ng/ml) and were considered borderline cases. FA-deficient and borderline patients were then compared to matched patients with normal FA levels on the MMSE and PANSS scales by blinded raters. Small differences were found between the 2 groups. The FA-deficient and borderline patients had more organic and psychotic symptoms, but the differences were not statistically significant.

Folic Acid↗
PubMed1975

Folic acid deficiency in sickle cell anaemia.

Megaloblastic anaemia responding to folic acid has been reported in a number fo patients with sickle cell anaemia. The incidence of reduced serum and erythrocyte folate levels in such patients remains unclear, however. Serum and erythrocyte folate contents were measured microbiologically in patients with sickle cell anaemia as well as in two control groups with sickle cell trait or normal haemoglobin pattern. Low serum and erythrocyte folate values were significantly more common in 61 sickle-cell patients than in each of the two socio-economically-matched control groups including 61 subjects with Hb AS and 69 blacks with Hb AA. There was no correlation between serum folate and haematocrit or reticulocyte count. The erythrocyte folate, measured before and after removal of reticulocytes, remains a reliable indicator of deficiency of folic acid in sickle-cell patients despite variable degrees of reticulocytes. Folate therapy resulted in higher haematocrits in three of four sickle-cell patients with low serum and low erythrocyte folate values, but in only one of 12 patients with low serum folate and normal erythrocyte folate. These findings are consistent with other observations that folate requirement may be increased in chronic haemolytic disorders and suggest that erythrocyte folate values should be obtained in sickle-cell patients suspected of having folate deficiency.

Adolescent↗