Folic acid.
Folic acid is an essential nutrient from the B complex group of vitamins. Folate, as a cofactor, is involved in numerous intracellular reactions, and this is reflected in the various derivatives that have been isolated from biological sources. Folic acid is involved in single carbon transfer reactions and serves as a source of single carbon units in different oxidative states. The processes involved in the absorption, transport, and intracellular metabolism of this cofactor are complex. Much of folate is bound tightly to enzymes, indicating that there is not excess of this cofactor and that its cellular availability is protected as well as being strictly regulated. In animals, the liver controls the supply of folate through first pass metabolism, biliary secretion, enterohepatic recirculation, as well as through senescent erythrocyte recycling. Deficiencies of folate can occur for many reasons, including reduced intake, increased metabolism, and/or increased requirements as well as through genetic defects. The effects of folate deficiency include hyperhomocysteinemia, megaloblastic anemia, and mood disorders. Folate deficiency has also been implicated in disorders associated with neural tube defects. Supplementation of grain products such as cereals has been undertaken in several countries as a cost-effective means of reducing the prevelance of neural tube defects. Recently, common polymorphisms have been discovered in several genes associated with folate pathways that may play a role in diseases associated with folate deficiency, particularly mild folate deficiency.
Donnelly
J G
JG
Department of Pathology, the Ottawa Hospital and the University of Ottawa, Ontario, Canada.
D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D005287:Ferredoxin-NADP Reductase / Q000378:metabolism; D005492:Folic Acid / Q000502:physiology*; D005494:Folic Acid Deficiency / Q000150:complications; D006801:Humans; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D009436:Neural Tube Defects / Q000209:etiology; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000378:metabolism; D014018:Tissue Distribution
D005492:Folic Acid; C111241:methionine synthase reductase; D005287:Ferredoxin-NADP Reductase; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase