Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOLIC ACID DEFICIENCY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed2000

DNA stability and genomic methylation status in colonocytes isolated from methyl-donor-deficient rats.

BACKGROUND: Epidemiological studies report an inverse relationship between intake of the B vitamin folic acid and colon cancer. Folate is important for DNA synthesis and repair. Moreover, the production of S-adenosylmethionine (SAM), essential for normal DNA methylation and gene expression, is dependent on folic acid. Folate deficiency may increase the risk of malignant transformation by perturbing these pathways. AIMS OF THE STUDY: The principal aim of this study was to determine the effects of folate deficiency on DNA stability and DNA methylation in rat colonocytes in vivo. As the metabolic pathways of folate and other dietary methyl donors are closely linked, the effects of methionine and choline deficiency were also evaluated. METHODS: Male Hooded-Lister rats were fed a diet deficient in folic acid, or in methionine and choline, or in folate, methionine and choline for 10 weeks. DNA strand breakage and misincorporated uracil were determined in isolated colonocytes using alkaline single cell gel electrophoresis. Global DNA methylation was measured in colonic scrapings. Folate was measured in plasma, erythrocyte and liver samples. RESULTS: Methyl donor deficiency induced DNA strand breakage in colonocytes isolated from all experimental groups. Uracil levels in colonocyte DNA remained unchanged compared with controls. DNA methylation was unaffected either by folate and/or methionine and choline depletion. Rats fed a folate-deficient diet had less folate in plasma, red blood cells and liver than controls. CONCLUSIONS: Folate and methyl deficiency in vivo primarily affects DNA stability in isolated colonocytes of rats, without affecting overall DNA methylation.

Animals↗
PubMed1984

Effects of folic acid malnutrition on rotaviral infection in mice.

A study was undertaken to determine if dietary deficiencies of folic acid would influence rotaviral diarrheal disease in infant mice. Female mice were fed diets containing essentially no folic acid, 25% of a normal quantity of folic acid, or a normally recommended quantity of folic acid, beginning at time of breeding and continuing through periods of gestation and lactation. Two-day-old infants from these dams were exposed to purified murine rotavirus or to sterile virus diluent and the severity of the rotaviral infection monitored. Infants from the low folic acid group had significantly lower folate levels in their livers, indicating a deficiency was achieved, and developed more severe disease manifestations than those infants from the dams receiving the normal folic acid levels in their diet. The infection enhancement was seen as increased incidences of diarrhea and a significantly greater number of mice exhibiting high intestinal rotaviral antigen titers. Serum rotavirus antibody titers were below detectable levels in a significant number of these same infants.

Animals↗
PubMed1982

[Iron-deficiency anemia. Hematologist's viewpoint].

Enlarged spleen, fever, increased susceptibility to infections, and thrombocytosis, are manifestations of iron deficiency which are relatively specific of pediatric patients. Iron deficiency anemia is part of everyday pediatrics. Patients are referred to the hematologist in the following situations: 1) Therapy is ineffective for one of the following reasons: the hypochromic anemia is not caused by iron deficiency (hemoglobinopathies); iron is less efficiently used because of transferrin deficiency or infectious, inflammatory or cancerous disease; iron therapy is inadequate either because of insufficient dosage or of suboptimal duration. 2) A relapse occurs in spite of adequate therapy. Before investigating the digestive tract, abnormal hemostasis. Osler-Weber-Rendu syndrome and pulmonary hemosiderosis should be considered. 3) Iron deficiency anemia is less common in adolescents. This condition, known as chlorosis, results mainly from increased needs, unbalanced diet, and onset of menses. In some cases no explanation is found but iron therapy leads to recovery. 4) Difficult problems arise in patients with complex anemias: iron deficiency with folic acid or vitamin B12 deficiency; hyposideremia complicating one of the hemoglobinopathies.

Adolescent↗
PubMed1977

The effects of a marginally lipotrope-deficient diet on the hepatic levels of S-adenosylmethionine and on the urinary metabolites of 2-acetylaminofluorene in rats.

Hepatic levels of S-adenosylmethionine (AdoMet), of glutathione, and of the microsomal enzymes p-nitroanisole demethylase and benzo(a)pyrene hydroxylase were measured in male and female rats fed a diet marginally deficient in choline and methionine and void of folic acid (lipotrope deficient) or an adequate diet for 0 to 14 weeks with and without added 2-acetylaminofluorene (AAF). The urinary metabolites of AAF were determined throughout the experimental period. After 2 to 4 weeks of dietary administration, the hepatic AdoMet levels were 43% lower in male rats fed the lipotrope-deficient diet than in male rats fed the lipotrope-adequate diet; no differences were found in hepatic AdoMet of females fed the lipotrope-deficient or lipotrope-adequate diets for 2 to 14 weeks. Administration of AAF to lipotrope-deficient female rats for 2 weeks led to a transient decrease in hepatic levels of AdoMet. The administration of AAF for 2 to 14 weeks did not significantly affect hepatic AdoMet in female rats fed the lipotrope-adequate diet or in male rats fed either diet. Female rats fed the lipotrope-deficient diet and treated with AAF excreted decreased proportions of N-hydroxy-2-acetylaminofluorene and increased proportions of 5-hydroxy-2-acetylaminofluorene in their urine. However, the urine of lipotrope-deficient male rats treated with AAF contained increased proportions of N-hydroxy-2-acetylaminofluorene and decreased levels of 5-hydroxy-2-acetylaminofluorene. The urinary excretion of 7-hydroxy-2-acetylaminofluorene by male and female lipotrope-deficient rats treated with AAF was generally similar to that in lipotrope-adequate rats. The lipotrope-deficient diet did not appear to alter the hepatic levels of glutathione, p-nitroanisole demethylase, or benzo(a)pyrene hydroxylase activity was lower in the livers of lipotrope-deficient male rats treated with AAF for 8 to 14 weeks than in the livers of lipotrope-deficient rats not receiving the carcinogen. The altered metabolism of AAF correlated well with the previously reported effects of a marginal lipotrope deficiency on AAF carcinogenesis.

2-Acetylaminofluorene↗
PubMed1988

Effect of high levels of dietary folic acid on folate metabolism in vitamin B12 deficiency.

The effect of administering high levels of folic acid to vitamin B12-deficient animals was studied. In B12 deficiency histidine oxidation is decreased. This is the result of both decreased liver folate levels and increases in the proportion of methyltetrahydrofolates. The purpose of this study was to determine if the addition of very high levels of folic acid to B12-deficient diets could increase liver folates and thereby restore histidine oxidation. Rats were fed a soy protein B12-deficient diet containing 10% pectin which has been shown previously to accelerate B12 depletion. When this diet was supplemented with B12 and folic acid, histidine oxidation was 5.4% in 2 h and the livers contained 3.49 micrograms of folate/g. In the absence of B12, the histidine oxidation rate was 0.34% and the liver folate level was 1.33 micrograms/g. When 200 mg/kg of folic acid was added to the B12-deficient diet there was no increase in histidine oxidation (0.35%) but the liver folates were increased to 3.68 micrograms which is about the same as that with B12 supplementation. The percentage tetrahydrofolate of the total liver folates was the same with and without a high level of dietary folic acid. Thus there was an increase in the absolute level of tetrahydrofolate without any increase in folate function as measured by histidine oxidation. Red cell folate levels were the same with and without B12, which is in contrast to the markedly lower liver folate levels in B12 deficiency. These data suggest a difference between B12 regulation of folate metabolism in the liver and in the bone marrow.

Animals↗
PubMed1964

MICROBIOLOGICAL ASSAY OF FOLIC ACID ACTIVITY IN HUMAN SERUM.

A method is described for the microbiological assay of folic acid activity in serum with Lactobacillus casei as test organism and a modified medium in which the organism gives a greater growth response than in media previously detailed. The results of experiments carried out to validate the use of this medium are shown. In 94 control subjects levels of folic acid activity in the serum ranged from 2. to 28 mmug./ml. (mean 7.8). The values in nine out of 10 patients with megaloblastic anaemia due to deficiency of folic acid were 1.0 mmug./ml. or less and one result was 2.0 mmug./ml. In six patients with megaloblastic anaemia associated with pregnancy the results ranged from 0.7 to 4.0 mmug./ml., and in untreated pernicious anaemia 28 out of 31 results were within or above the control range and three values were just below the lower limit of normal.

Anemia↗