Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOLIC ACID”

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 217 records · Page 12Linked to original sources

Folate deaminase and cyclic AMP phosphodiesterase in Dictyostelium discoideum: their regulation by extracellular cyclic AMP and folic acid.

Cyclic AMP and folic acid act as chemotactic factors in Dictyostelium discoideum. Both agents, when applied extracellularly, also control cell development from the growth stage to the acquisition of aggregation competence. Cyclic AMP phosphodiesterase and folate deaminase are extracellular enzymes whose activity is regulated during early differentiation of D. discoideum cells. The two enzymes help control the extracellular levels of cyclic AMP and folic acid. The substrates cyclic AMP and folic acid each increase the extracellular activity of folate deaminase as well as phosphodiesterase. The specificity of extracellular phosphodiesterase regulation by cyclic AMP indicates that the effect is mediated by specific cyclic AMP receptors rather than the catalytic site of cell surface phosphodiesterase. To some extent cyclic AMP and folic acid are interchangeable with respect to regulating differentiation and enhancing enzymatic inactivation of intercellular signals. Thus the two extracellular signals may share a common cellular pathway of signal transduction. The regulation of folate deaminase and phosphodiesterase by folic acid does not always parallel the folic acid effects on development. Pulses of folic acid stimulate development of aggregation competence, whereas a continuous flux inhibits. In contrast, either continuous flux or pulses of folic acid increase the deaminase and phosphodiesterase activities.

3',5'-Cyclic-AMP Phosphodiesterases↗

Neural tube defects: prevention by folic acid and other vitamins.

Folic acid has been demonstrated in clinical trials to reduce significantly the recurrence (and probably occurrence) of neural tube defects (NTD). In the U.K., there has been no decline in prevalence of NTD since the publication of the findings with folic acid. This article examines a series of questions relating to the action of folic acid, with emphasis on the use of mouse models as a source of experimental information which cannot easily be obtained by direct study of humans. Several mouse genetic NTD models exhibit sensitivity to prevention by folic acid, whereas other mice which develop morphologically similar NTD are resistant. Folic acid normalises neurulation in the sensitive mouse strains, providing evidence for a direct effect on the developing embryo, not on the pregnant female: Mouse studies do not support the proposed action of folic acid in encouraging the in utero demise of affected fetuses (i.e. terathanasia). Polymorphic variants of several folate-related enzymes have been shown to influence risk of NTD in humans and an inherited abnormality of folate metabolism has been demonstrated in one mouse NTD model. However, the biochemical basis of the action of folic acid in preventing NTD remains to be determined in detail. NTD in one folate-resistant mouse strain can be prevented by myo-inositol, both in utero and in vitro, raising the possibility of a therapeutic role also in humans. Gene-gene interactions seem likely to underlie the majority of NTD, suggesting that poly-therapy involving folic acid and other agents, such as myo-inositol, may prove more effective in preventing NTD than folic acid treatment alone.

Animals↗

Serum folates in gestating swine after folic acid addition to diet.

Folic acid was added to the diet as a simple means to increase serum folates in gestating sows. At weaning, 95 multiparous sows were randomly assigned to five treatments. Of these sows, 67 farrowed and were used for this trial. Three supplementation levels of folic acid added to a commercial diet at 3, 9 and 27 mg per kg were studied. A commercial diet without any supplementation of folic acid was used as a control treatment. A fifth treatment consisted of eight im injections of 15 mg of folic acid each, according to a predetermined schedule that was previously effective in improving the reproductive performance of sows when combined with flushing. Each sow was kept in an individual cage and received 2 kg of feed daily. Serum folates were measured at weaning, mating and on d 14, 28, 42 and 56 after mating. The time-response curve of serum folates in sows injected with folic acid was higher than that of sows fed the unsupplemented diet (P = .057). Adding folic acid to diet may be as efficient as folic acid injections to elevate serum folates when compared with sows fed the control diet. The mean supplementary level of folic acid sufficient to maintain the serum folate concentration at approximately the same levels as those observed in sows injected with folic acid was estimated to be near 4.3 mg per kg of feed.

Animals↗

Methanol-induced neurotoxicity in pups exposed during lactation through mother: role of folic acid.

Role of folic acid on methanol-induced neurotoxicity was studied in pups at Postnatal Day (PND) 45 exposed to methanol (1%, 2% and 4%, v/v) during lactation through mothers maintained on folic acid-deficient (FD) and folic acid-sufficient (FS) diet. A gradual loss in the body weight gain was observed in the pups exposed to 2% and 4% methanol in the FD group, while FS group exhibited this alteration only at 4% exposure. The assessment of spontaneous locomotor activity (SLA) showing a significant increase in the distance travelled was observed in the 2% and 4% methanol-exposed groups in both the FS and FD animals when compared with their respective controls, but the effect was more marked in the FD group. A significant decrease in the conditioned avoidance response (CAR) was observed in pups exposed to 2% and 4% methanol in the FD group at PND 45. The results also suggest that disturbances in dopaminergic and cholinergic receptors were more pronounced in the FD group as compared to the FS group. A significant decrease in striatal dopamine levels was also observed in the FD group at 2% and 4% methanol exposure, while in the FS group, a significant decrease was exhibited only at 4% methanol exposure. An aberrant increase in the expression of Growth-Associated Protein (GAP-43), a neuron-specific growth-associated protein was observed in pups in the FD group exposed to 2% and 4% methanol, while an increase in the expression of GAP-43 in the FS group was found only at 4% methanol exposure in the hippocampal region as compared to their respective controls. Results suggests that methanol exposure during growth spurt period adversely affects the developing brain, the effect being more pronounced in FD rats as compared to FS rats, suggesting a possible role of folic acid in methanol-induced neurotoxicity.

Animals↗

Bioavailability of a combination preparation of trimethoprim and folic acid.

The bioavailability of folic acid and trimethoprim was investigated from a combination preparation of folic acid (0.25 mg) and trimethoprim (100 mg) in ten healthy adult volunteers. Peroral administration of the preparation resulted in a mean peak plasma concentration of trimethoprim 1.09 mg/l (SEM 0.06). The AUC values for trimethoprim were 12.42 mg.h/l and 12.77 mg.h/l corresponding to combination preparation and plain trimethoprim, p greater than 0.1. After administration 0.25 mg folic acid in the combination preparation, there was a significant rise in serum folic acid concentrations. The AUC from 0-8 hours was 199.8 nmol.h/l (SEM 8.1) and 166.3 nmol.h/l (SEM 14.2) corresponding to combination preparation and plain trimethoprim, p less than 0.001. A loading dose of folic acid 10 mg was given intramuscularly 24 hours before drug intake. This new type of formulation of trimethoprim and folic acid has been developed in order to prevent in long-term use the adverse haematological effects induced by trimethoprim alone.

Adult↗

[Serum folic acid and vitamin B12 in depressed inpatients. A study of serum folic acid with radioimmunoassay in 121 depressed inpatients].

According to the newer literature on folate deficiencies in depressive patients serum folate and vitamin B12 levels were studied (RIA) in 121 consecutively admitted depressive inpatients (47 male, 74 female depressives; age 17-86 years, mean age 48 years, diagnostic by ICD-9 300.4, 296.1) during the first (1-3) days of admission (normal volumes folate 3-17 ng/ml, vitamin B12 200-900 pg/ml). Only in two patients serum folate below 3 ng/ml were found, low vitamin B12 levels (below 200 pg/ml) showed 14 patients. This result is in contrast to other authors who found folate deficiencies in 10-50% of psychiatric patients.

Adolescent↗

Enterocyte function in progressive systemic sclerosis as estimated by the deconjugation of pteroyltriglutamate to folic acid.

As a measure of enterocyte function, the deconjugation of pteroyl-L-glutamyl-gamma-L-glutamyl-gamma-L-glutamic acid to folic acid and subsequent active absorption was measured in 19 patients with progressive systemic sclerosis and compared with 14 controls. The absorption step of folic acid was identical in the two groups, while deconjugation of pteroyl-L-glutamyl-gamma-L-glutamyl-gamma-L-glutamic acid was significantly decreased in the patients with progressive systemic sclerosis. This observation suggests a primary epithelial defect of the small intestine in patients with progressive systemic sclerosis.

Adult↗

A combined high-performance liquid chromatographic-microbiological assay for serum folic acid.

An assay of folic acid in human serum is described involving HPLC fractionation of deproteinized serum prior to Lactobacillus casei assay. High specific activity [3H]folic acid is added as internal standard to 1 ml serum prior to deproteinization with perchlorate and an aliquot is applied to a C18 reverse-phase HPLC column. The folic acid fraction was assayed by L. casei microtiter plate assay. Intra- and interassay variations (CV) were 5.5 and 7.5% respectively for sera (n = 10) spiked with folic acid. The percentage recovery for folic acid additions of 10 and 20 ng/liter were 105.2 and 103.7%, respectively. The lower limit of detection was 1 ng folic acid/ml serum. Folates other than folic acid and 5-methyltetrahydrofolate were not detected. The assay permitted serial measurements to be made of folates in serum following an oral dose.

Administration, Oral↗