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Results for “FOLIC ACID DEFICIENCY”

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PubMed2005

Folic acid deficiency increases chromosomal instability, chromosome 21 aneuploidy and sensitivity to radiation-induced micronuclei.

Folic acid deficiency can lead to uracil incorporation into DNA, hypomethylation of DNA, inefficient DNA repair and increase chromosome malsegregation and breakage. Because ionising radiation increases demand for efficient DNA repair and also causes chromosome breaks we hypothesised that folic acid deficiency may increase sensitivity to radiation-induced chromosome breakage. We tested this hypothesis by using the cytokinesis-block micronucleus assay in 10 day WIL2-NS cell cultures at four different folic acid concentrations (0.2, 2, 20, and 200 nM) that span the "normal" physiological range in humans. The study showed a significant dose-dependent increase in frequency of binucleated cells with micronuclei and/or nucleoplasmic bridges with decreasing folic acid concentration (P<0.0001, P=0.028, respectively). These biomarkers of chromosomal instability were also increased in cells irradiated (1.5 Gy gamma-rays) on day 9 relative to un-irradiated controls (P<0.05). Folic acid deficiency and gamma-irradiation were shown to have a significant interactive effect on frequency of cells containing micronuclei (two-way ANOVA, interaction P=0.0039) such that the frequency of radiation-induced micronucleated cells (i.e. after subtracting base-line frequency of un-irradiated controls) increased with decreasing folic acid concentration (P-trend<0.0001). Aneuploidy of chromosome 21, apoptosis and necrosis were increased by folic acid deficiency but not by ionising radiation. The results of this study show that folate status has an important impact on chromosomal stability and is an important modifying factor of cellular sensitivity to radiation-induced genome damage.

Aneuploidy↗
PubMed1990

Anaemia in rheumatoid arthritis: the role of iron, vitamin B12, and folic acid deficiency, and erythropoietin responsiveness.

Thirty six patients with rheumatoid arthritis (RA) (25 with anaemia) were studied to establish the role of iron, vitamin B12, and folic acid deficiency, erythropoietin responsiveness, and iron absorption in the diagnosis and pathogenesis of anaemia in RA. Iron deficiency, assessed by stainable bone marrow iron content, occurred in 13/25 (52%), vitamin B12 deficiency in 7/24 (29%), and folic acid deficiency in 5/24 (21%) of the anaemic patients. Only 8/25 (32%) had just one type of anaemia. The iron deficiency of anaemia of chronic disease (ACD) was distinguished by ferritin concentration, which was higher in that group. Mean cell volume (MCV) and mean cell haemoglobin (MCH) were lower in both anaemic groups, but most pronounced in iron deficient patients. Folic acid, and especially vitamin B12 deficiency, masked iron deficiency by increasing the MCV and MCH. Iron absorption tended to be highest in iron deficiency and lowest in ACD, suggesting that decreased iron absorption is not a cause of ACD in RA. No specific causes were found for vitamin B12 or folic acid deficiency. Haemoglobin concentration was negatively correlated with erythrocyte sedimentation rate in the group with ACD. Erythropoietin response was lower in ACD than in iron deficient patients. It was concluded that generally more than one type of anaemia is present simultaneously in anaemic patients with RA. The diagnosis of each type may be masked by another. Studies on pathogenesis of the anaemia are difficult as deficiencies generally coexist with ACD. Disease activity and, possibly, erythropoietin responsiveness are major factors in ACD pathogenesis.

Aged↗
PubMed1992

Disturbed reproductive performance in extreme folic acid deficient golden hamsters.

We studied the effects of folic acid-deficient diets on maternal red blood cell folate level and reproductive performance in golden hamsters (Mesocricetus auratus, Waterhouse). Animals on the same day of oestrous cycle were put together and finally divided into three groups. Each group comprised at least 12 mature female hamsters. The animals were given three different diets, which were commenced before mating. The feeding regimens comprised a standard diet (group 1), or a folic acid-deficient diet which started either 2 weeks (group 2) or 16 weeks (group 3) prior to mating. The regimens were continued until sacrifice of the animals on day 9 of pregnancy. Pregnancy was realized by caging a male with a selected female during the night of ovulation. Just prior to sacrifice, blood samples were drawn to measure maternal folic acid levels in red blood cells. The pregnant uteri were removed and the embryonic sacs were carefully dissected away from the uterus. The number of sacs per pregnant animal was noted. Extreme folic acid deficiencies were confirmed in the pregnant golden hamsters on a folic acid-deficient diet which started 16 weeks prior to mating as compared to those on a standard diet and on a folic acid-deficient diet which started 2 weeks prior to mating. This deficiency appears to interfere with normal reproductive performance. It caused early embryonic loss several days after mating and resulted, finally, in restoration of the oestrous cycle.

Animals↗
PubMed1975

Folic acid deficiency in the United States: folate assays in a prenatal clinic.

Tissue deficiency of folic acid, as measured by a red cell folate level below 150 ng. per milliliter, was present in 16 per cent of 110 sequential pregnant women at the time of their first prenatal visit to a municipal clinic. A further 14 per cent of subjects had red cell folate levels in the range "suggestive but not conclusive for tissue folate depletion" (150 to 199 ng. per milliliter). All of the subjects were from low-income families in New York City and most were black or of Puerto Rican origin. Serum folate levels showed good general correlation with red cell folate but were of less value as a diagnostic test, since they were below the lower limit of normal in 64 per cent of subjects, including many subjects who did not yet have low tissue folate. In contrast to their value in other folate deficiency states, neutrophil lobe counts showed no correlation with serum or red cell folate levels in pregnancy and thus appeared of little diagnostic value in pregnancy. It is suggested that surveys of folate deficiency in other pregnant population groups in the United States be carried out. These results support the recommendations of the Committee on Maternal Nutrition and the Committee on Dietary Allowances of the Food and Nutrition Board, National Research Council (U.S.A.) that folic acid supplements (200 to 400 mug per day) should be taken throughout pregnancy.

Black or African American↗
PubMed2005

Folic acid deficiency modifies the haematopoietic response to recombinant human erythropoietin in maintenance dialysis patients.

BACKGROUND: While folic acid deficiency causes macrocytic anaemia in non-renal patients, the relevance of altered folate metabolism in anaemia of end-stage renal disease and its response to rHu-EPO is less clear. METHODS: Ten haemodialysis patients with macrocytic anaemia due to dietary folic acid deficiency were compared to 10 matched (age, duration of dialysis, degree of anaemia) patients with normocytic normochromic anaemia. Nineteen patients received erythropoietin-alpha intravenously thrice weekly. The study design was a prospective crossover (ABA) comparison of the effects of intravenously administered high doses of folic acid on haemoglobin levels and EPO doses, with 6 months active supplementation (B) and two periods of 6 months duration each without folic acid supplementation (A). RESULTS: The two patient groups did not differ at recruitment. Red blood cell folate levels were normal in patients with normocytic anaemia, but they were subnormal in all patients with macrocytic anaemia. Compared to the first period without folic acid supplementation, patients with macrocytic anaemia had significantly higher haemoglobin levels despite lower EPO doses after 6 months high-dose folic acid, and red cells had become normocytic. The removal of folic acid supplementation resulted in re-occurrence of macrocytosis and in a significantly lower response to rHu-EPO. In contrast, high-dose folic acid supplementation had no effect on response to rHu-EPO in patients with normocytic anaemia. CONCLUSIONS: Folic acid deficiency may occur in elderly haemodialysis patients with poor dietary folate intake without regular oral supplementation and may cause hyporesponsiveness to rHu-EPO. Macrocytosis is a simple and cheap indicator for folate deficiency in end-stage renal disease patients on maintenance dialysis.

Adult↗
PubMedDate not supplied

[Folic acid deficiency and its association with neural tube defects in northern Mexico].

OBJECTIVE: To evaluate folic acid deficiency and other risk factors and their relationship with the occurrence of neural tube defects (NTD), in the rural population of northern Mexico (Chihuahua, Durango and Zacatecas). MATERIAL AND METHODS: A multicentric case-control study was performed. Cases were both live and stillborn with NTD, and controls were healthy newborns without congenital malformations. Exposure to known risk factors was determined, establishing its association with NTD using multiple logistic regression analysis. RESULTS: Risk factors associated to NTD were: folic acid deficiency (OR 11.1; CI 95% 1.2-106.2, p = 0.04); the antecedents of previous NTD pregnancies (OR 3.3; CI 95% 1.1-18.8, p = 0.05) and stillbirths (OR 7.1; CI 95% 1.1-46.3, p = 0.04). CONCLUSIONS: Folic acid deficiency is one of the major risk factors associated to NTD among the rural population of northern Medico. Further investigations are necessary to determine the role of involved risk factors and implement adequate preventive measures.

Adolescent↗
PubMed1984

Severe thrombocytopenia associated with acute folic acid deficiency and severe hemorrhage in two patients.

Severe thrombocytopenia associated with acute folic acid deficiency in two inpatients is described. Both patients had severe hemorrhagic manifestations. A similar syndrome has previously been described in patients who have undergone extensive surgery or dialysis or both. The present cases show that acute folic acid deficiency can occur in other circumstances and may go unrecognized because other signs in the peripheral blood of a megaloblastic process may be minimal. A good response was obtained with folic acid therapy.

Acute Disease↗
PubMed1977

Folate-responsive neurological and mental disorders: report of 16 cases. Neuropsychological correlates of computerized transaxial tomography and radionuclide cisternography in folic acid deficiencies.

Two groups of patients with folic acid responsive neurological and psychiatric disorders are reported. The first group (7 patients) had well-established acquired folate deficiency due either to defective absorption (4 cases with atrophy of jejunal mucosa) or to a deficient diet (3 cases). One patient had a subacute combined degeneration of the spinal cord while others were depressed and had weight loss, permanent muscular and intellectual fatigue, restless legs syndrome, depressed ankle jerks, diminution of the sense of vibration in the knees and a stocking-type tactile hypoesthesia. The second group (9 patients) comprised idiopathic cases of folic acid deficiency. Their main subjective complaints were chronic fatigability and familial restless legs syndrome. The neurological findings were similar to those of the patients with acquired disorders. Neuropsychological testing procedures revealed an abnormal intellectual functioning in all 16 patients. Abnormal patterns of radionuclide cisternograms and computerized transaxial tomography (CTT) were found in 11 patients. After 6-12 months of folic acid therapy a striking improvement regarding their intellectual functioning was noticed: the IQ, Kohs Block Design and Category tests were significantly improved. The correlation of neuropsychological findings with CTT and radionuclide cisternograms led to the conclusion that chronic folate deficiency could induce cerebral atrophy.

Adult↗
PubMed1989

Homocysteinemia in rats induced by folic acid deficiency.

The effect of folate deficiency on homocysteine metabolism was examined in rats given a folate-deficient diet. Total homocysteine was determined in serum stored at -22 degrees C for 3 wk. All animals in the control group had more than 20 ng.ml-1 of serum folate and more than 1000 pg.ml-1 of serum cyanocobalamin throughout the experimental period. In contrast, serum folate in animals given the folate-deficient diet decreased to less than 3 ng.ml-1 after 4 wk and to less than 2 ng.ml-1 (a subnormal level) after 10 wk of the experiment while serum cyanocobalamin remained at more than 1000 pg.ml-1 throughout the experiment. In the control group, mean serum total homocysteine +/- SD was 4.04 +/- 1.07 nmol.ml-1 during the 20 wk of experiment. At the 10th wk before serum folate reached subnormal levels, the animals given the folate-deficient diet had a mean serum total homocysteine of 7.67 +/- 1.53 nmol.ml-1, demonstrating a significant increase (P less than 0.001). No further significant increase of mean serum total homocysteine concentrations was observed after serum folate became subnormal. This study demonstrated for the first time that a selective deficiency of folic acid caused a 2-4 fold increase in serum total homocysteine when serum folate was at low normal and at subnormal levels in rats.

Animals↗
PubMed1986

A pregnant woman with severe epistaxis--a rare manifestation of folic acid deficiency.

The case-history of a pregnant woman with a life-threatening thrombocytopenia, due to folic acid deficiency, caused by an extremely low dietary intake is described. As folic acid deficiency manifests itself in a variety of ways, its clinical features are not always easily recognized. Timely recognition is important because of the rapid progressive nature of the disorder, especially in pregnancy, and because rapid improvement is achieved by simple treatment: supplementation of the deficiency. This is well illustrated in the patient described in this case report. A short review of the literature is presented.

Adult↗
PubMed2006

The prevalence of folic acid deficiency among adolescent girls living in Edirne, Turkey.

PURPOSE: A high incidence of iron-deficiency is a common observation among adolescent girls, whereas only limited data are available regarding the folic acid status of this group. This study was designed to determine the prevalence of biochemical folic acid deficiency in a group of Turkish adolescent girls. METHODS: We surveyed the serum folic acid, complete blood count, and dietary folic acid intake of Turkish adolescent girls after using three-day self-reported food intakes in urban and rural areas of Edirne, Turkey. RESULTS: A sample population was composed of 704 adolescent girls; their serum folic acid levels were found to be adequate for 37.6% (> or = 6 ng/mL), marginal for 46% (3 to 5.9 ng/mL), and at deficient levels for 16.3% (< 3 ng/mL). Folic acid deficiencies were found in 20.1% (36 of 179) and 14.7 % (61 of 416) of adolescent girls from rural and urban areas, respectively. Self-reported three-day folic acid intakes were correlated with the corresponding blood values for this nutrient. In the logistic regression analysis, three factors emerged as significant independent predictors of folic acid deficiency: low income (odds ratio [OR]: 2.4, 95% confidence interval [CI]: 1.3-4.2, p < .001), low vitamin C (OR: 1.9, 95% CI: 1.1-3.5, p < .05), and folic acid intake (OR: 4.8, 95% CI: 2.8-8.1, p < .001). CONCLUSION: Data from the present study may indicate that serum folic acid is low in a group of Turkish adolescent girls. These low values appear to be associated with low income, and low dietary intakes of folic acid and vitamin C.

Adolescent↗
PubMed2006

Effects of folic acid deficiency and MTHFR C677T polymorphism on spontaneous and radiation-induced micronuclei in human lymphocytes.

Folic acid plays a key role in the maintenance of genomic stability, providing methyl groups for the conversion of uracil to thymine and for DNA methylation. Besides dietary habits, folic acid metabolism is influenced by genetic polymorphism. The C677T polymorphism of the methylene-tetrahydrofolate reductase (MTHFR) gene is associated with a reduction of catalytic activity and is suggested to modify cancer risk differently depending on folate status. In this work the effect of folic acid deficiency on genome stability and radiosensitivity has been investigated in cultured lymphocytes of 12 subjects with different MTHFR genotype (four for each genotype). Cells were grown for 9 days with 12, 24 and 120 nM folic acid and analyzed in a comprehensive micronucleus test coupled with centromere characterization by CREST immunostaining. In other experiments, cells were grown with various folic acid concentrations, irradiated with 0.5 Gy of gamma rays and analyzed in the micronucleus test. The results obtained indicate that folic acid deficiency induces to a comparable extent chromosome loss and breakage, irrespective of the MTHFR genotype. The effect of folic acid was highly significant (P < 0.001) and explained >50% of variance of both types of micronuclei. Also nucleoplasmic bridges and buds were significantly increased under low folate supply; the increase in bridges was mainly observed in TT cells, highlighting a significant effect of the MTHFR genotype (P = 0.006) on this biomarker. Folic acid concentration significantly affected radiation-induced micronuclei (P < 0.001): the increased incidence of radiation-induced micronuclei with low folic acid was mainly accounted for by carriers of the variant MTHFR allele (both homozygotes and heterozygotes), but the overall effect of genotype did not attain statistical significance. Treatment with ionizing radiations also increased the frequency of nucleoplasmic bridges. The effect of folic acid level on this end-point was modulated by the MTHFR genotype (P for interaction = 0.02), with TT cells grown at low folic acid concentration apparently resistant to the induction of radiation-induced bridges. Finally, the effect of in vitro folate deprivation on global DNA methylation was evaluated in lymphocytes of six homozygous subjects (three CC and three TT). The results obtained suggest that, under the conditions of this work, folic acid deprivation is associated with global DNA hypermethylation.

Adult↗
PubMed1983

Growth of Trichinella spiralis larvae in rats receiving folic-acid-deficient diet.

A study of the effect of growth of Trichinella spiralis in rats fed a folic-acid-deficient diet is described. Trichinella spiralis larvae encysted in the diaphragms of two groups-rats fed a folic acid-deficient diet and rats fed a complete (normal) diet-were examined. In rats fed a folic-acid-deficient diet, the number of the encysted larvae was larger than that in the controls. However, the encysted larvae were substantially longer in the control group of rats fed complete (normal) diets.

Animals↗
PubMed2001

The effect of folic acid deficiency and MTHFR C677T polymorphism on chromosome damage in human lymphocytes in vitro.

We performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid deficiency on primary human lymphocytes. Lymphocytes were cultured in medium containing 12-120 nM folic acid for 9 days in a novel cytokinesis-block micronucleus (CBMN) assay system (n = 20). Besides identifying optimal folic acid concentrations for in vitro genomic stability, we tested the hypothesis that lymphocytes from individuals homozygous for the C677T methylenetetrahydrofolate reductase (MTHFR) polymorphism (TTs, n = 10) are protected against chromosome damage relative to controls (CCs, n = 10) under conditions of folic acid deficiency. This hypothesis is based on the assumption that reduced MTHFR activity in TT lymphocytes causes a diversion of 5,10-methylene tetrahydrofolate toward thymidine synthesis, which minimizes uracil-induced double-stranded DNA breakage. Cells were scored for micronuclei, apoptosis, necrosis, nucleoplasmic bridges, and nuclear budding. The latter two endpoints are indicative of chromosome rearrangements and gene amplification, respectively, and to the best of our knowledge, this is the first report of their association with folic acid concentration. Folic acid concentration correlated significantly (P < 0.0001) and negatively (r, -0.63 to -0.74) with all markers of chromosome damage, which were minimized at 60-120 nM folic acid, much greater than concentrations assumed "normal," but not necessarily optimal in plasma. Two-way ANOVA revealed no effect of the MTHFR genotype on any of the endpoints. Results show that the C677T polymorphism does not affect the ability of a cell to resist chromosome damage induced by folic acid deficiency in this in vitro system.

Analysis of Variance↗
PubMed1983

Brain atrophy, peripheral neuropathy and folic acid deficiency.

A woman with peripheral neuropathy and cerebral atrophy, both secondary to a selective folic acid deficiency caused by severe gastrointestinal disturbances, was given folic acid replacement therapy, which improved her clinical, blood and neurophysiological status.

Atrophy↗