Folic occurrence

Folic acid, 4-amino-4-deoxy-10-methyl-, 1, 164 3, 325 as anticancer drug, 1, 263 biological activity, 3, 325 Folic acid, 4-amino-10-methyl-toxicity, 1, 141 Folic acid, 7,8-dihydro-biosynthesis, 3, 320 synthesis, 1, 161, 3, 307 Folic acid, 4-dimethylamino-hydrolysis, 3, 294 Folic acid, 5-formiminotetrahydro-biological activity, 3, 325 Folic acid, 5-formyl-5,6,7,8-tetrahydro-biological activity, 3, 325 chirality, 3, 281 occurrence, 3, 325 Folic acid, 10-forfnyltetrahydro-biological activity, 3, 325 Folic acid, 5,10-methenyl-5,6,7,8-tetrahydro-biological activity, 3, 325 chirality, 3, 281 Folic acid, 5-methyl-chirality, 3, 281 Folic acid, 9-methyl-toxicity, 1, 141... 

Cobalamin, 25 803 folic acid and, 25 802 Cobalt (Co), 7 207-228. See also Co-base superalloys 60Co isotope 60Co nucleus Fe-Ni-Co alloys Dicobalt octacarbonyl Tetracobalt dodecacarbonyl analysis, 7 215-216 in ceramic-matrix composites, 5 554t coke formation on, 5 266 colloidal suspensions, 7 275 economic aspects, 7 214-215 effect on copper resistivity, 7 676t environmental concerns, 7 216 health and safety factors, 7 216-218 in M-type ferrites, 11 66, 69 occurrence, 7 208... 

Methotrexate is an antimetabolite of folic acid and has immunosuppressant properties. It inhibits the enzyme dihydrofolate reductase that is required for the synthesis of purines and pyrimidines. It is used in malignant disease, Crohn s disease, rheumatic disease and psoriasis. Folic acid is given with methotrexate to reduce the occurrence of side-effects particularly the risk of mucositis. 

Folate deficiency can be dietary, especially in the eiderly, due to increased demand like in pregnancy, or due to maiabsorption syndromes. Agents which can cause folic acid deficiency with long-term use include phenytoin, oral contraceptives, isoniazid and glucocorticosteroids. In rare instances the use of dihydrofolate reductase inhibitors like trimethoprim, methotrexate or pyrimethamine can contribute to the occurrence of folate deficiency. Folinic acid can circumvent the need for the inhibited dihydrofolate reductase. 

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Patients with alcohol dependence and patients with liver disease can develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Patients who require renal dialysis develop folic acid deficiency because folates are removed from the plasma during the dialysis procedure. 

Werler, M. M., Shapiro, S., and Mitchell, A. A. (1993). Periconceptional folic acid exposure and risk of occurrent neural tube defects. JAMA 269(10), 1257-1261. 

Prevention of fetal neural tube defect (spina bifida). Folic acid supplementation taken before conception and during the early weeks of pregnancy has been shown in an 8-year trial to prevent the condition in pregnancies subsequent to an affected birth. Women hoping to conceive and who have had an affected child are advised to take folic acid 5 mg/day. To prevent a first occurrence 400 micrograms/day should be taken both before conception, or as soon as possible after diagnosis. In both cases folate supplement should be taken for the first 12 weeks of pregnancy. 

Neural tube defects Folic acid RCTs showed reduction in recurrence and occurrence when folic acid was taken preconceptionally MRC study (1991), Czeizel and Dudas (1992)... 

In 1952, Mannheim et al. described the occurrence of megaloblastic anaemia in patients on AEDs. Several reports followed and megaloblastic anaemia was found to occur in less than 1% of patients on PHT, PB and PRD. The anaemia was associated with low levels of folate and could be corrected with the administration of folic acid (Reynolds 1975). 

It appears reasonable to recommend supplementation with several B vitamins in physiological doses to many patients with epilepsy. Patients on inducer AEDs and VPA, and patients with an insufficient diet, are at risk for deficiency of several B vitamins. Moreover, the evidence that folic acid can prevent adverse effects in patients on AEDs is not much higher than the evidence for a protective effect of vitamins B2, Bg, B7 and B12 (Ranganathan and Ramar-atnam 2005). In animal studies, deficiency of vitamins B2 and Bg has been related to the occurrence of foetal malformations. Therefore, women of childbearing potential should supplement their diet with vitamin B2 and Bg, as well as folic acid. 

Fortification with folic acid has produced positive results, reducing the frequency of neural tube defects in the USA, Canada and Chile. In addition to preventing the occurrence of NTDs, folic acid fortification has been associated with reducing the severity of NTDs with potential beneficial effects on health (Hoey et al. 2007). 

The comparisons were intention-to-treat analyses of first events during the scheduled treatment period in all participants allocated to folic acid-based B vitamins or control (irrespective of any other treatment allocated factorially). The main outcomes were coronary heart disease events, stroke, cancer and allcause mortality. Coronary heart disease events were defined as the first occurrence of non-fatal myocardial infarction or coronary death although for several trials the definition of coronary events was restricted to fatal or non-fatal myocardial infarction. Stroke was defined as the first occurrence of either ischemic or hemorrhagic or unspecified strokes. Cancer was defined as any cancer, excluding non-melanoma skin cancers. 

Because of its acidic characteristics and its abundant occurrence in green leaves, the growth factor for S. faecalis R was given the name fohc acid (Latin, folium—Folic acid was isolated in crystalline form from hver and from yeast , and its structure was established by degradation and synthesis . 

It is of interest that folic or folinic polyglutamates are required for the conversion of serine to glycine in a cell-free enzyme preparation from a Clostridium strain which apparently cannot utilize monoglutamates, and evidence for the natural occurrence of M -formyltetrahydropteroyltrigluta-mate has been reported . Other bound forms of folinic acid appear to exist. ... 

The complexity of the relationship between B12 and folic acid function may extend to an interrelation between their biosyntheses. By analogy with the formation of the purine and pyrimidine rings and riboflavin (see earlier sections), one-carbon fragments may enter into the formation of the pteridine group of folic acid and of the benzimidazole group of Bi2. Further complications are the occurrence of labile one-carbon compounds attached to each the formyl group in folinic acid, and the cyano group in cyanocobalamin. There is also the possibility... 

The spontaneous occurrence of megaloblastic anemia in association with infection in infants and in monkeys is described by May ei al. (1952a,b). The low content of folic acid compounds in the liver in both natural and experimental infections and the elimination of megaloblasto-sis from the marrow by folic acid, but not by vitamin Bij or ascorbic acid, led to the conclusion that infection can cause a deficiency of folic acid compounds. 

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