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PubMed1961

Studies on the folic acid activity of human serum.

A method for the measurement of serum folic acid activity is described, which is a modification of previous methods. The material in serum with activity for L. casei is made up of a stable and a labile component. The amount of stable component in normal subjects and patients with megaloblastic anaemia is similar. The amount of labile component varies. In patients with folic acid deficiency none is present; in normal subjects it constitutes between 65 and 94% of the total serum L. casei activity. The labile component appears to be an index of folic acid metabolism, and the assay of total serum L. casei activity is therefore a valuable method for differentiating patients requiring treatment with folic acid from normal subjects and patients with primary vitamin B(12) deficiency. Normal subjects had serum folic acid levels from 5.9 to 21.0 mmug./ml. (mean 9.9 mmug./ml. +/- 0.3 mmug./ml. S.E.). In patients with megaloblastic anaemia requiring treatment with folic acid, other than megaloblastic anaemia of pregnancy, the levels were less than 4.0 mmug./ml. Patients with uncomplicated pernicious anaemia had levels from 6.0 to 27.0 mmug./ml. (mean 16.6 mmug./ml. +/- 1.1 mmug./ml. S.E.). The mean level in this group was higher than in normal subjects, and the highest levels of all were found in patients with subacute combined degeneration of the cord with minimal anaemia (range 14.4 to 36.8 mmug./ml.; mean 24.8 mmug./ml. +/- 2.4 mmug./ml. S.E.). The L. casei activity of the labile component is lost during autoclaving or storage at -20 degrees C. This loss can be prevented during autoclaving by using adequate amounts of ascorbic acid in the phosphate buffer used to dilute the serum for assay and by adding ascorbic acid to serum that is to be stored. Moreover, the activity lost during the storage of serum not protected by ascorbic acid could be restored, for periods up to three months, by adding ascorbic acid to this serum before assay.

Anemia↗
PubMed1983

Frequency of fragile X chromosomes, fra(X), in lymphocytes in relation to blood storage time and culture techniques.

The fra(X) frequencies in metaphases of lymphocytes from seven male patients with X-linked mental retardation and macroorchidism were scored after use of different culture techniques and different times of blood storage. No statistically significant differences were found between the fra(X) rates of lymphocytes grown either in folic acid deficient medium (TC 199) or in medium containing folic acid as well as a folic acid antagonist (methotrexate: MTX, aminopterine: AP). With respect to the effect of the time interval between blood sampling and culture set-up, a statistically significant decrease in the fra(X) frequency was observed in all culture types after 4 or 7 days of blood storage.

Blood Preservation↗
PubMedDate not supplied

Macrocytosis as an indicator of human disease.

Adult patients with macrocytosis, defined as a mean corpuscular volume (MCV) greater than 100 femtoliters, were studied to assess the importance of an elevated MCV. After eliminating pregnant and postpartum patients and patients receiving medications known to cause macrocytosis (e.g., phenytoin, zidovudine, and chemotherapeutic agents), 80 patients were identified and studied. Sixty-seven diagnoses were made in 56 patients. These diagnoses were, in descending order: alcoholism, hematological disorders, habitual drinking, B12 deficiency, chronic liver disease, folic acid deficiency, hypothyroidism, anorexia nervosa, and reticulocytosis. While an elevated MCV is neither sensitive nor specific for any one disease state, an elevated MCV should raise suspicions of underlying pathology.

Adolescent↗
PubMed1982

Characteristic abnormality of deoxyribonucleoside triphosphate metabolism in megaloblastic anemia.

To elucidate the biochemical basis of megaloblastic hematopoiesis, the cellular content and metabolism of deoxyribonucleoside triphosphates (dNTPs) were investigated using the bone marrow cells from nine patients with untreated vitamin B12 deficiency and one with folic acid deficiency. The marked imbalance among four dNTPs was noted in all patients. dTTP was invariably elevated rather than depressed. The most striking abnormality, however, was the excessive accumulation of dCTP, which represented the consistent feature exclusive for megaloblastic anemia. Purine nucleotides were also involved to a lesser extent. The apparent turnover pattern of the dTTP pool of megaloblastic anemia marrow cells, in the presence or absence of hydroxyurea, did not differ significantly from that of normoblastic hematopoiesis. The megaloblastic cells assimilated exogenous thymidine into dTTP pool in vitro with enhanced efficiency. It was suggested that the excessive accumulation of dCTP may be related more closely to the pathogenesis of megaloblastic hematopoiesis than to the presumed but not proved deficiency of dTTP.

Anemia, Macrocytic↗
PubMed1998

[Macrocytic anemia with anisocytosis due to alcohol abuse and vitamin B6 deficiency].

Megaloblastic anemia due to folic acid deficiency and ringed sideroblastic anemia have been reported in alcohol abusers. It has also been reported that vitamin B6 deficiency causes ringed sideroblastic anemia as well as microcytic anemia that is not associated with ringed sideroblasts. We encountered a case of macrocytic anemia with anisocytosis in a 75-year-old alcohol abuser who suffered vitamin B6 deficiency. Neither megaloblastic changes nor ringed sideroblasts were observed in specimens of the patient's bone marrow. Analyses of porphyrin content and heme biosynthetic enzyme activity suggested a decline in ALA-synthase activity (an enzyme that depends on vitamin B6) as well as decreased ferrochelatase activity or abnormal iron metabolism. Abstention from alcohol led to a reduction in mean corpuscular volume and the disappearance of Pappenheimer bodies commonly observed in the red blood cells of drinkers. Follow-up supplements of vitamin B6 resolved the patient's anisocytosis and anemia.

Aged↗
PubMed1989

Folic acid and psychopathology.

1. The incidence of folic acid deficiency is high in patients with various psychiatric disorders including depression, dementia and schizophrenia. 2. In epileptics on anticonvulsants, folate deficiency often occurs because anticonvulsants inhibit folate absorption. In these patients folate deficiency is often associated with psychiatric symptoms. 3. In medical patients psychiatric symptoms occur more frequently, and in psychiatric patients symptoms are more severe, in those with folate deficiency than in those with normal levels. 4. Many open studies have demonstrated therapeutic effects of folate administration on psychiatric symptoms in folate deficient patients. 5. Several placebo-controlled studies have not demonstrated therapeutic effects, possibly because the doses they used (15-20 mg/day) are known to be toxic and to cause mental symptoms. 6. Two placebo-controlled studies have demonstrated beneficial effects of folic acid administration, one in patients with a syndrome of psychiatric and neuropsychological changes associated with folate deficiency and the other in patients on long-term lithium therapy. In the latter study the dose was only 0.2 mg/day. 7. Folic acid deficiency is known to lower brain S-adenosylmethionine and 5-hydroxytryptamine. S-Adenosylmethionine, which has antidepressant properties, raises brain 5-hydroxytryptamine. Thus, depression associated with folate deficiency is probably related to low brain 5HT. 8. S-Adenosylmethionine is involved in many methylation reactions, including methylation of membrane phospholipids, which influences membrane properties. This may explain the wide variety of symptoms associated with folate deficiency. 9. Because the costs and risks associated with low doses of folic acid (up to 0.5 mg/day) are small, folic acid should be given as an adjunct in the treatment of patients with unipolar or bipolar affective disorders and anorexia, epileptics on anticonvulsants, geriatric patients with mental symptoms and patients with gastrointestinal disorders who exhibit psychiatric symptoms. 10. Although the majority of the patients listed above will probably not be helped by folic acid therapy, a significant minority are likely to have folate-responsive symptoms.

Folic Acid↗
PubMed1995

Megaloblastic anemia in pregnancy.

Megaloblastic anemia is one of the acquired nutritional anemias that may complicate pregnancy. It is most often secondary to folic acid deficiency because folate requirements are increased during gestation. When the diagnosis of megaloblastic anemia is confirmed, appropriate therapy will initiate a rapid reversal of the anemia process. Because of the association between neural tube defects and folate deficiency, it is recommended that women of reproductive age take folic acid supplementation.

Anemia, Megaloblastic↗
PubMed2006

Low folic acid status and its association with anaemia in urban adolescent girls and women of childbearing age in Sri Lanka.

Folic acid deficiency is implicated in the aetiology of nutritional anaemia and adverse pregnancy outcomes for the fetus. Data on folic acid status among adolescent girls and non-pregnant, non-lactating young women are limited. We assessed folic acid status in a random sample of 552 subjects (277 adolescent girls aged 15-18.9 years and 275 women aged 19-30 years) living in Colombo, Sri Lanka. The association of low folic acid status with anaemia was evaluated. Socio-economic, food intake and anthropometric data were obtained. Hb, serum folic acid, vitamin B12 and ferritin and plasma homocysteine concentrations were measured. Forty-three per cent of subjects studied had low serum folic acid concentrations (<3 ng/ml) and 47 % had low Fe stores (serum ferritin <20 microg/l). Overall prevalence of anaemia was 12.9 %, and 43.9 % of anaemic subjects had both low folic acid status and depleted Fe stores (serum ferritin <12 microg/l). Both low folate status and depleted Fe stores were significantly associated with anaemia (odds ratio = 2.32; 95 % CI 1.34, 4.01 and odds ratio = 5.98; 95 % CI 3.36, 10.63, respectively). Serum folic acid concentration was associated (r = 0.108, P = 0.015) with folate intake as indicated by a computed folate index. Folate index was associated inversely with household size and positively with economic status and education level. In this study population low folic acid status, besides depleted Fe stores, was associated with anaemia. The high prevalence of low folic acid status observed highlights the need for nutrition education to improve intakes of folate, Fe and other micronutrients among adolescent girls and young women.

Adolescent↗
PubMedDate not supplied

Do Japanese take more folate from traditional Japanese dish than is conventionally estimated?-Actual folate contents in hospital diets and marketed lunch boxes.

Folic acid deficiency is very rare in Japan. However, recent concerns in relation to causal relationships between cancer and low folic acid levels necessitate information on actual folate intake by Japanese, which has hitherto not been well studied. We therefore evaluated folate contents of a hospital diet for 7 consecutive days and of 16 lunch boxes purchased at convenience stores. Dietary intake was assessed for weighed food items after cooking using our previously published data on folate contents of various foods and also by using Standard Tables of Food Composition in Japan (STFCJ). Mean daily folate intake from the hospital diet was 723.9 microg/day using our data but only 359.2 microg/day if calculated using the STFCJ. Twenty-nine % of the total daily folate intake was through rice. Mean folate intake through lunch boxes was 491.7 microg/day by our tabulation and 139.5 microg/day with the STFCJ. Folic acid intake of Japanese is far above the levels taken in other countries and over half of this amount is taken from rice. Levels of folic acid contents (especially in rice) listed in the STFCJ are too low and revision is strongly suggested.

Diet↗
PubMed2004

Methylenetetrahydrofolate reductase C677T polymorphism, folic acid and riboflavin are important determinants of genome stability in cultured human lymphocytes.

We tested the hypothesis that methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism, folic acid deficiency and riboflavin deficiency, independently or interactively, are important determinants of genomic stability, cell death, cell proliferation and homocysteine (Hcy) concentration in 9-d human lymphocyte cultures. Lymphocytes of seven wild-type (CC) and seven mutant (TT) homozygotes were cultured under the four possible combinations of deficiency and sufficiency of riboflavin (0 and 500 nmol/L) and folic acid (20 and 100 nmol/L) at a constant L-methionine concentration of 50 micromol/L. Viable cell growth was 25% greater in TT than in CC cells (P<0.05) and 32% greater at 100 nmol/L folic acid than at 20 nmol/L folic acid (P=0.002). The comprehensive cytokinesis-block micronucleus assay was used to measure micronuclei (MNi; a marker for chromosome breakage and loss), nucleoplasmic bridges (NPB; a marker of chromosome rearrangement) and nuclear buds (NBUD, a marker of gene amplification). The MNi levels were 21% higher in TT cells than in CC cells (P<0.05) and 42% lower in the high folic acid medium than in the low folic acid medium (P<0.0001). The NBUD levels were 27% lower in TT cells than in CC cells (P<0.05) and 45% lower in the high folic acid medium than in the low folic acid medium (P<0.0001). High riboflavin concentration (500 nmol/L) increased NBUD levels by 25% (compared with 0 nmol/L riboflavin) in folate-deficient conditions (20 nmol/L folic acid medium; P<0.05), and there was an interaction between folic acid and riboflavin that affected NBUD levels (P=0.042). This preliminary investigation suggests that MTHFR C677T polymorphism and riboflavin affect genome instability; however, the effect is relatively small compared with that of folic acid.

Adult↗
PubMed2006

Folate deficiency results in alteration in intestinal brush border membrane composition and enzyme activities in weanling rats.

Folic acid deficiency is the most prevalent vitamin deficiency throughout the world and its effect on brush border membrane composition has not been studied earlier. We investigated the effect of folate deficiency on the structure and function of the intestinal brush border membrane. Various brush border enzyme activities, membrane sugars and lipids were evaluated in two groups of weanling male albino rats after 3 mo of feeding control and folate deficient diets. Except sucrase, all the other three enzymes, viz., alkaline phosphatase, leucine amino peptidase and y-glutamyl transpeptidase showed decrease in activity in rats fed folate-deficient diets. Among sugars, hexoses and hexosamines showed significant decline in amount whereas sialic acid content showed great increase in brush border membrane of folate-deficient rats as compared to controls. Furthermore, there was a significant reduction in cholesterol, phospholipids, triglycerides, cerebrosides and fucolipids in the group fed the folate-deficient diet. Our study suggests that folate deficiency results in altered enzyme activities, lipid and sugar composition of intestinal brush border membrane. Such changes might reflect the underlying cause of the gastrointestinal disturbances observed in folate deficiency.

Amino Sugars↗
PubMed1983

Relationship of alcohol metabolism to folate deficiency produced by ethanol in the rat.

Chronic ethanol use can lead to folic acid deficiency in humans. In rats, acute doses of ethanol produce a marked increase in urinary folate excretion, which precedes a decrease in plasma folate levels. To assess the role of ethanol and its metabolism in these effects, five groups of male Sprague-Dawley rats were treated orally as follows: (1) ethanol in 4 doses of 1 g/kg each at 0, 1, 2 and 3 hr; (2) ethanol, as above, plus the alcohol dehydrogenase inhibitor 4-methylpyrazole (4-MP) at 50 mg/kg IP 15 min prior to 0 hr; (3) glucose in 4 isocaloric doses; (4) glucose plus 4-MP as above; (5) methanol in 4 doses of 1 g/kg. Urinary folate levels (by Lactobacillus casei assay) peaked in both ethanol- and methanol-treated rats at the same time as the urine alcohol levels (6-8 hr) and then declined with a similar time course. Urinary levels of formic acid, which is eliminated by oxidation by a folate-dependent pathway, were significantly increased by ethanol administration, thus indicating another ethanol-folate interaction. Concurrent administration of 4-MP suppressed the increased excretion of formate but had no effect on the increased excretion of folate in ethanol-treated rats. These studies suggest that ethanol has two distinct effects on folate metabolism, one dependent and one independent of ethanol metabolism.

Animals↗
PubMed1979

Demonstration of vitamin B12 deficiency by a simple cytochemical reaction in the peripheral blood smear.

A simple, rapid and inexpensive cytochemical method for the detection of vitamin B 12 deficiency was applied in several types of anemias and matched with the levels of vitamin B12 and folic acid in the serum of the patients. It was found that in patients with low vitamin B12 levels the stained erythrocytes and the erythroid precursors showed a yellowish brown discoloration, which was not detected in folic acid deficiency and all other types of anemias. This test therefore may be used for differentiation between B12 and folate deficiency whenever megaloblastic anemia is diagnosed.

Anemia, Megaloblastic↗
PubMed1994

Analysis of uracil in DNA by gas chromatography-mass spectrometry.

A sensitive method using gas chromatography and negative chemical ionization mass spectrometry for the detection of uracil in DNA is described. Uracil DNA glycosylase is used to specifically cleave uracil from DNA. Once removed, uracil is derivatized with 3,5-bis(trifluoromethyl)benzyl bromide and the sample components are separated with gas chromatography. Negative chemical ionization mass spectrometry is used to quantitatively detect as little as 1 pg of uracil per 100 micrograms DNA. This assay is 10 times more sensitive than previously described quantitative methods for the detection of uracil in DNA. We apply this method as part of a project to determine why folic acid deficiency causes DNA breaks. We demonstrate that inhibition of folic acid metabolism induces an accumulation of uracil in DNA.

Animals↗
PubMed2002

Serum iron, ferritin, folic acid, and vitamin B12 levels in recurrent aphthous stomatitis.

BACKGROUND: The exact aetiology of recurrent aphthous stomatitis (RAS) is still unknown, but different predisposing factors, including iron, vitamin B12 and folic acid deficiencies, have been proposed. MATERIAL AND METHODS: Serum iron, ferritin, folic acid and vitamin B12 levels were investigated in 35 patients with RAS and in 26 healthy controls. RESULTS: Vitamin B12 levels were found significantly lower in subjects with RAS than in controls. No significant differences were found in other parameters. CONCLUSION: We concluded that vitamin B 12 deficiency may be an aetiological factor in recurrent aphthous stomatitis.

Adolescent↗