Folate Metabolism and Requirements

Bailey, Lynn B.; Gregory, Jesse F.

doi:10.1093/jn/129.4.779

Cited by 511 publications

(402 citation statements)

References 26 publications

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“…21 A healthy person requires 200-400 μg folic acid per day, however, during pregnancy and lactation, its daily requirements become 500-600 μg. 22 Defi ciency of folic acid in body may lead to pathogenesis of megaloblastic anemia and macrocytosis of erythrocytes. 23 Diet low in folic acid may increase risk of breast, pancreatic, and colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Beetroot Extract against Phenyl Hydrazine Induced Anemia in Rats

Jaiswal¹,

Ganeshpurkar²,

Awasthi³

et al. 2014

Phcog J.

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Background: Anemia can be regarded as one of the oldest blood malformation known over a century. Megaloblastic anemia arises due to curtailed formation of erythrocytes, which leads to formation of a large number of underdeveloped erythrocytes. Proper nutritional supplementation may be useful in such condition. Beta vulgaris or beetroot is one of the important vegetables consumed worldwide. The aim of the present work was to evaluate anti-anemic potential of beetroot. Methods: Beetroot was extracted with ethanol. Phytochemical and phytoanalytical studies were performed on extract. Anemia was induced by phenyl-hydrazine. Animals were treated with extract throughout the study for 24 days. The red blood cell (RBC) number and hemoglobin concentration were determined every 3 days for 24 days. Results: Extract was found to be rich in folic acid, ascorbic acid, and iron. Following the induction of anemia, the number of erythrocytes and the hemoglobin concentration decreased by 62.51% and 69.64%, respectively. Administration of standard hematinic preparation and extract (200 mg/kg) resulted in signifi cant increase (P < 0.001; P < 0.01) in the number of RBCs as well as hemoglobin concentration when compared to the untreated phenyl hydrazine-induced anemic rats. Conclusion: Extract effectively raised the level of hemoglobin and erythrocyte count at dose 200 mg/kg. Vitamin and minerals found in beetroot are most likely active ingredients responsible for its hematinic effects. Still, methodical studies are obligatory to derive its effects on humans.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Beetroot Extract against Phenyl Hydrazine Induced Anemia in Rats

Jaiswal¹,

Ganeshpurkar²,

Awasthi³

et al. 2014

Phcog J.

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“…MTHFR catalyzes the biologically irreversible reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, which provides the methyl group for the remethylation of homocysteine to methionine (Bailey et al, 1999). In the MTHFR enzyme, several single nucleotide polymorphisms including the two most important, C677T and A1298C, can affect folate and total homocysteine (tHcy) status.…”

Section: Introductionmentioning

confidence: 99%

The MTHFR C677T Polymorphism and Risk of Acute Lymphoblastic Leukemia: an Updated Meta-analysis Based on 37 Case-control Studies

Jiang

Hou²,

Zhang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Chronic nutritional deficiencies in folate, choline, methionine, vitamin B 6 , and/or vitamin B 12 can perturb the complex regulatory network that maintains normal one-carbon metabolism and homocysteine homeostasis (3)(4)(5)(6)(7). Genetic polymorphisms in these pathways can act synergistically with nutritional deficiencies to accelerate the metabolic pathology associated with chronic disease states (8).…”

mentioning

confidence: 99%

Increase in Plasma Homocysteine Associated with Parallel Increases in Plasma S-Adenosylhomocysteine and Lymphocyte DNA Hypomethylation

Melnyk

Pogribna

et al. 2000

Journal of Biological Chemistry

588

381

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An elevation in plasma homocysteine is a sensitive but nonspecific biomarker for an imbalance in the integrated pathways of one-carbon metabolism (1, 2). Chronic nutritional deficiencies in folate, choline, methionine, vitamin B 6 , and/or vitamin B 12 can perturb the complex regulatory network that maintains normal one-carbon metabolism and homocysteine homeostasis (3-7). Genetic polymorphisms in these pathways can act synergistically with nutritional deficiencies to accelerate the metabolic pathology associated with chronic disease states (8). Although several hypotheses have been proposed to explain the association between hyperhomocysteinemia and the thrombotic/atherosclerotic process occurring with occlusive cardiovascular disease, as yet none has been definitive (9 -12). Similarly, increases in plasma homocysteine concentrations have been associated with increased risk of certain birth defects (13-16), but the underlying mechanism remains elusive. A major unanswered question is whether direct cellular toxicity of homocysteine is causally involved in pathogenesis or whether homocysteinemia is simply a passive and indirect indicator of a more complex mechanism.Homocysteine is derived solely from methionine metabolism and is significantly recycled to conserve sufficient methionine for protein and S-adenosylmethionine synthesis. The interactive and interdependent pathways of the methionine/homocysteine cycle are diagrammed in Fig. 1 to emphasize the indirect effects of pathway perturbations on cellular methyltransferase reactions. The metabolic generation of homocysteine from methionine is initiated by the ATP-dependent transfer of adenosine to methionine via methionine adenosyltransferase. The product, S-adenosylmethionine (SAM), 1 is a priority for onecarbon metabolism because it is the methyl donor for most cellular methyltransferase reactions. In addition to DNA methylation, SAM-dependent methyltransferase activity is essential for hundreds of other cellular methylation reactions including synthesis of creatine in the liver, membrane phosphatidylcholine synthesis, central nervous system neurotransmittor synthesis, methylation/detoxification, and RNA and protein methylation (17). After transfer of the methyl group, SAM is converted to S-adenosylhomocysteine (SAH) within the active site of the methyltransferase enzyme. Because most methyltransferases bind SAH with higher affinity than SAM, they are subject to potent product inhibition by SAH (18). Thus, the efficiency of methyltransferase reactions is absolutely dependent on efficient product removal of SAH. This is effectively accomplished by SAH hydrolase (SAHH), an enzyme that appears to act in close proximity to the methyltransferases, at least in the nucleus (19). The crystal structure of SAHH has been recently reported, and interestingly, the polypeptide folding pattern at the catalytic domain of SAHH is almost identical to that reported for the DNA methyltransferases and suggests that SAH molecules can travel easily between the catalytic pockets of th...

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Folate Metabolism and Requirements

Cited by 511 publications

References 26 publications

Protective Effects of Beetroot Extract against Phenyl Hydrazine Induced Anemia in Rats

Protective Effects of Beetroot Extract against Phenyl Hydrazine Induced Anemia in Rats

The MTHFR C677T Polymorphism and Risk of Acute Lymphoblastic Leukemia: an Updated Meta-analysis Based on 37 Case-control Studies

Increase in Plasma Homocysteine Associated with Parallel Increases in Plasma S-Adenosylhomocysteine and Lymphocyte DNA Hypomethylation

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