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Results for “FOLIC ACID”

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At least 73 records · Page 4Linked to original sources
PubMed1984

Substantia nigra cell death from kainic acid or folic acid injections into the pontine tegmentum.

Injections of kainic acid into the rostral pontine tegmentum in rats caused not only local lesions but destruction of GABAergic and dopaminergic cells in the substantia nigra (SN), as indicated histologically and by measurements of tyrosine hydroxylase (TH) and glutamate decarboxylase (GAD). Injections of folic acid caused the nigral damage without local lesions. Pretreatment with scopolamine prevented the losses in GAD without affecting those in TH. The destruction of nigral cells is attributed to pathological stimulation of afferent pathways to the SN, some of which are cholinergic, and it is possible that a similar mechanism may be involved in some forms of Parkinsonism.

Afferent Pathways↗
PubMed1976

[Folic acid substitution in hemodialyzed patients. Folic acid levels in plasma and erythrocytes].

Investigations of folic acid levels in plasma and erythrocytes. In 20 patients on hemodialysis with and without folic acid substitution the concentration of folic acid in plasma and in red cells was estimated by radioassay. In patients, who were substituted with folic acid concomitantly with elevated folic acid concentrations hematocrit values were higher than those of patients who were not substituted. Folic acid concentrations in patients not substituted. Folic acid concentrations in patients not substituted were subnormal and further decreased on dialysis. Results of folic acid determinations in plasma were paralleled by concentrations in erythrocytes. It is concluded, that folic acid substitution is necessary in patients on hemodialysis.

Adolescent↗
PubMed1982

Folic acid derivatives do not reproduce the neurotoxic effects of kainic acid on chicken retina.

Methyltetrahydrofolic acid, formyltetrahydrofolic acid, folic acid and dihydrofolic acid were injected intravitreally into the eyes of chickens. No short-term or long-term signs of neurotoxicity were observed, even when doses 100-200 times those at which kainic acid produces clear neurotoxic effects were injected. The folic acid derivatives neither inhibited nor potentiated the neurotoxic effects. Thus no support is given to the suggestion that folic acid and its derivatives may act as kainic acid agonists or antagonists, even though the receptors involved in kainic acid-induced neurotoxicity appear to be of the kainic acid rather than quisqualic acid or N-methyl-D-aspartic acid type.

Animals↗
PubMed1993

Evaluation of egg injection of folic acid and effect of supplemental folic acid on hatchability and poult weight.

Two experiments were conducted with Large White turkey hens housed individually in cages in a conventional house. In Experiment 1, three dietary treatments were used: an unsupplemented practical corn-soybean meal basal diet; the basal diet supplemented with 2.64 mg folic acid/kg of diet; and the basal diet supplemented with 5.51 mg folic acid/kg of diet. Eggs from hens fed 2.64 mg folic acid/kg of diet were injected with folic acid in 20 injection trials over two production cycles. The response data from dietary supplemental folic acid were analyzed on a production period basis using all of the hens, and on a subset of hens producing eggs in each production period, for hatchability of fertile eggs and poult weight. The response patterns in each case were similar. Incremental dietary supplemental folic acid levels produced a positive linear response pattern on the transfer of folic acid in eggs, but did not result in a hatchability increase over the unsupplemented folic acid basal diet. Hatchability increase did not occur for eggs injected at 25 days of incubation with 19.3 micrograms folic acid per egg in 20 injection trials over two cycles of production. The results of the study indicate that hatchability is not increased in turkey eggs from hens fed supplemental folic acid or with egg folic acid injections. However, egg and poult weights were significantly increased (P < .05) in eggs containing 6 to 7 mg folic acid/g of dried egg, from hens fed 5.51 mg folic acid/kg of diet.

Analysis of Variance↗
PubMed1992

Inhibition of the neutrophil NADPH oxidase by folic acid and antagonists of the folic acid metabolism.

The influence of folic acid and several antagonists of the folic acid metabolism on neutrophil superoxide generation was investigated with the cytochrome c reduction assay. The compounds were found to be partial competitive inhibitors of the NADPH oxidase, their activity apparently increasing with larger substituents at the 10 position. There is evidence that compounds with a 4-oxo substituent are taken up more slowly by neutrophils than those with a 4-amino functionality. Scavenging properties could be excluded from control measurements with the xanthine/xanthine oxidase assay.

Adult↗
PubMed1986

Experiments on the biological activities of various fractions of the folic acid antagonist "X-methyl" folic acid.

A crude synthetic preparation called crude "X-methyl" folate has previously been shown to function as a folate antagonist for rats and chicks. This product has been shown to contain two folate antagonists: 9-methyl folate, present as 6% by weight of the product and which has low activity as a folate antagonist for Streptococcus faecalis, and pyrrofolic acid, a compound present in small amounts (0.04%), but having high anti-folate biological activity for S. faecalis. These experiments deal with the antifolate activity of these two fractions for the rat as measured by their effects on histidine oxidation. Rats were fed a purified diet based on 20% vitamin-free casein and containing 1.0% sulfasuxidine. When this diet was supplemented with a marginal amount of folic acid (0.3 mg per kg diet), the addition of 4 g of crude antagonist decreased histidine oxidation and decreased liver folate levels. The addition of 240 mg of pure 9-methyl folic acid (amount of 9-methyl folic acid in 4 g of crude) produced similar decreases in histidine oxidation and liver folate levels. A concentrate of pyrrofolic acid (equivalent to 4 g of crude) free of 9-methyl folic acid produced no decrease in histidine oxidation and minimal changes in liver folate. This indicates that the folate antagonist activity observed previously with animals is probably due to the 9-methyl folic acid component rather than to the pyrrofolic acid activity.

Animals↗
PubMed2006

Postprandial serum folic acid response to multiple doses of folic acid in fortified bread.

The benefit of the introduction of mandatory folic acid fortification of all flour products in the USA in 1998 has been amply demonstrated in a reduction of neural tube defect births. Doubt has been cast on the actual level of fortification and recent calculations have shown that the level of folic acid fortification is likely to have been over twice the amount mandated. The implication of this is that a greater proportion of the population are likely to have consumed folic acid at >1 mg/d, the Food and Drug Administration safe upper level of intake. Using the criteria of appearance of synthetic folic acid in serum, the objective of this pilot study was to investigate the consequences of consumption of baked bread preparations containing 1 mg folic acid. Four healthy adult volunteers undertook each dosing schedule 2 weeks apart. This consisted of a single dose of 1000 microg, two doses of 500 microg, three doses of 333 microg, five doses of 200 microg and, finally, ten doses of 100 microg. Serum was collected pre- and postprandially and analysed for synthetic folic acid by a combined HPLC-microbiological assay for folic acid. Folic acid appeared in all subjects at all test doses, with the effect more pronounced as the standard dose was administered in smaller amounts over the test period. Approaches to optimise folic acid intake in target populations as part of a universal fortification strategy should take into consideration the potential hazard of over-exposure in groups consuming high amounts of flour-based products.

Adult↗
PubMed2006

The effect of docosahexaenoic acid and folic acid supplementation on placental apoptosis and proliferation.

The hypothesis was tested that the additional dietary uptake of n-3 fatty acids, in particular of DHA and 5-methyltetrahydrofolate (5-MTHF), during the second half of pregnancy would influence proliferation and apoptosis in the full-term human placenta. The diets of pregnant women from Spain (n 55) were supplemented with modified fish oil and/or 5-MTHF or placebo, and assigned in a random, double-blind manner to one of the four groups. Immunohistochemistry and immunoblotting were used to detect placental proliferation and apoptosis with monoclonal antibodies for key proteins that reflected the extent of both processes: proliferation cell nuclear antigen (PCNA), p53, cytokeratin 18 neoepitope. The PCNA level in the fish oil/5-MTHF-treated group was higher by 66 % (P < 0.05) than that of the placebo group, whereas the levels of p53 and cytokeratin 18 neoepitope were unaffected by treatment. PCNA expression was altered only in the trophoblast compartment (placebo 11.1 (se 0.5) % v. combination 21.5 (se 1.2) %; P < 0.05), whereas the proportion of nuclei stained in endothelial and other stromal cells was similar in the placebo and combined treatment groups. No correlation was found between fish oil or 5-MTHF supplementation and the levels of the proteins. The present data suggest that supplementation with fish oil and/or 5-MTHF had no effect on the parameters reflecting placental proliferation and apoptosis. A defined combination of DHA and 5-MTHF may, however, affect placental proliferation.

Adolescent↗
PubMed1975

Synthesis and biological activity of 10-thia-10-deaza analogs of folic acid, pteroic acid, and related compounds.

The 10-thia analogs of pteroic acid, folic acid, their esters, and their 4-amino analogs were synthesized through a reaction sequence involving, as a key step, the condensation of 2-amino-3-cyano-5-chloromethylpyrazine with appropriately substituted thiols. The abilities of the products to inhibit the growth of methotrexate (MTX)-sensitive and MTX-resistant microorganisms were investigated as were their abilities to inhibit dihydrofolic acid reductase and thymidylic acid synthetase. Several compounds had high activity.

Enterococcus faecalis↗