Relevant bibliographies by topics / Folic acid Metabolism

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Folic acid Metabolism'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Folic acid Metabolism"

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Lucock, Mark. "Folic Acid: Beyond Metabolism." Journal of Evidence-Based Complementary & Alternative Medicine 16, no. 2 (March 24, 2011): 102–13. http://dx.doi.org/10.1177/1533210110392950.

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Mandatory and discretionary fortification with folic acid is eliminating deficiency of this vitamin. Blood levels of the vitamin have never been higher, with hematologic folate values commonly exceeding the upper range of calibration. The synthetic analog (pteroylmonoglutamic acid) prevents neural tube defects and lowers homocysteine, both positive attributes, yet negative correlates of pteroylmonoglutamic acid are increasingly reported. These involve increased risk for common cancers (ie, colon, breast, prostate) and antimetabolite effects on natural killer cells and at dihydrofolate reductase, a critical gatekeeper enzyme. This review, however, takes a different, human ecological perspective, examining novel folate-related phenomena distinct from the classic metabolic role of the vitamin in maintaining health and well-being. An argument is developed that at molecular, cellular, and organism levels, folate is crucial to some important events that link light to life.
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Khaitovich, M. V. "Folates: Modern Pregnant Health Support." HEALTH OF WOMAN, no. 4(150) (May 30, 2020): 37–42. http://dx.doi.org/10.15574/hw.2020.150.37.

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Folates (folic acid-based chemical compounds) got their name from the Latin “folio” - “leaf”, since they were first synthesized from spinach leaves, in which vitamin B9 is found in maximum quantities. As an important cofactor in carbon metabolism, folates are involved in the most important metabolic processes in the body, in particular, they play a key role in the synthesis of nucleotides and DNA replication. The article provides information on the physiological role of folates, their metabolism and its genetic aspects. The clinical significance of folate deficiency is examined, their sources and doses are described, and the interaction of folic acid and drugs is highlighted. Keywords: folate, metabolism, folic acid deficiency, pregnancy.
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Metz, Jack. "Folic Acid Metabolism and Malaria." Food and Nutrition Bulletin 28, no. 4_suppl4 (December 2007): S540—S549. http://dx.doi.org/10.1177/15648265070284s407.

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Pellis, Linette, Yvonne Dommels, Dini Venema, Ab van Polanen, Esther Lips, Hakan Baykus, Frans Kok, Ellen Kampman, and Jaap Keijer. "High folic acid increases cell turnover and lowers differentiation and iron content in human HT29 colon cancer cells." British Journal of Nutrition 99, no. 4 (September 10, 2007): 703–8. http://dx.doi.org/10.1017/s0007114507824147.

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Folate, a water-soluble B vitamin, is a cofactor in one-carbon metabolism and is essential for DNA synthesis, amino acid interconversion, methylation and, consequently, normal cell growth. In animals with existing pre-neoplastic and neoplastic lesions, folic acid supplementation increases the tumour burden. To identify processes that are affected by increased folic acid levels, we compared HT29 human colon cancer cells exposed to a chronic supplemental (100 ng/ml) level of folic acid to cells exposed to a normal (10 ng/ml) level of folic acid, in the presence of vitamin B12and other micronutrients involved in the folate–methionine cycle. In addition to higher intracellular folate levels, HT29 cells at 100 ng folic acid/ml displayed faster growth and higher metabolic activity. cDNA microarray analysis indicated an effect on cell turnover and Fe metabolism. We fully confirmed these effects at the physiological level. At 100 ng/ml, cell assays showed higher proliferation and apoptosis, while gene expression analysis and a lower E-cadherin protein expression indicated decreased differentiation. These results are in agreement with the promoting effect of folic acid supplementation on established colorectal neoplasms. The lower expression of genes related to Fe metabolism at 100 ng folic acid/ml was confirmed by lower intracellular Fe levels in the cells exposed to folic acid at 100 ng/ml. This suggests an effect of folate on Fe metabolism.
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Sahar, Saniya. "Role of Folate and Folic Acid During Pregnancy." International Journal for Research in Applied Science and Engineering Technology 9, no. 12 (December 31, 2021): 1488–92. http://dx.doi.org/10.22214/ijraset.2021.39295.

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Abstract: Pregnancy represents a period of fast tissue growth of maternal and foetal tissues that's related to enhanced energy and nutrient needs. Maternal nutrition throughout gestation period, has being essential for best offspring development, reducing long unwellness burden and for general health throughout life. Maternal Folate throughout pregnancy might have numerous roles in offspring health, as well as neurodevelopment and psychological feature performance in childhood. Folate is crucial for C1 metabolism, a network of pathways concerned in many biological processes as well as nucleotide synthesis, deoxyribonucleic acid repair and methylation reactions. The periconceptional use of pteroylglutamic acid (Folic Acid ) containing supplements reduces the primary incidence, as well as recurrence of neural tube defects. Folic Acid (FA) are artificial form of a necessary vitamin generically considered Folates or B9. It is concerned in one-carbon metabolism, and it's been connected to lowering neural tube Defect (NTD). National programs to mandate fortification of food with Folic Acid have reduced the prevalence of NTDs worldwide . The indisputable protecting role of Folic Acid in the hindrance of NTD, in addition to the low compliance of women to Folic Acid recommendations, has aroused the choice of mandatory Folic Acid fortification, a policy currently in place in over eighty countries worldwide. Mandatory food fortification needs food makers to feature Folic Acid to certain foods (e.g. starch or grain products), whereas voluntary fortification permits Folic Acid to be added to foods at the discretion of manufacturers. Food fortification with Folic Acid because the intervention is likely to achieve increasing Folic Acid intake among populations throughout the world. The objective of this article is to discuss the Role of Folic Acid and Folate during pregnancy and to review the role of Folate and Folic Acid , metabolism , absorption and Folic Acid effects on maternal on the basis of recent findings that are important for implementation of fortified food to design future studies. Keywords: Neurodevelopment, Methylation Reactions, Pteroylglutamic Acid, Bioavailability, Monoglutamates.
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Ratajczak, Alicja Ewa, Aleksandra Szymczak-Tomczak, Anna Maria Rychter, Agnieszka Zawada, Agnieszka Dobrowolska, and Iwona Krela-Kaźmierczak. "Does Folic Acid Protect Patients with Inflammatory Bowel Disease from Complications?" Nutrients 13, no. 11 (November 12, 2021): 4036. http://dx.doi.org/10.3390/nu13114036.

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Folic acid, referred to as vitamin B9, is a water-soluble substance, which participates in the synthesis of nucleic acids, amino acids, and proteins. Similarly to B12 and B6, vitamin B9 is involved in the metabolism of homocysteine, which is associated with the MTHFR gene. The human body is not able to synthesize folic acid; thus, it must be supplemented with diet. The most common consequence of folic acid deficiency is anemia; however, some studies have also demonstrated the correlation between low bone mineral density, hyperhomocysteinemia, and folic acid deficiency. Patients with inflammatory bowel disease (IBD) frequently suffer from malabsorption and avoid certain products, such as fresh fruits and vegetables, which constitute the main sources of vitamin B9. Additionally, the use of sulfasalazine by patients may result in folic acid deficiency. Therefore, IBD patients present a higher risk of folic acid deficiency and require particular supervision with regard to anemia and osteoporosis prevention, which are common consequences of IBD.
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Han, Xuhui, Bingqi Wang, Dongxu Jin, Kuang Liu, Hongjie Wang, Liangbiao Chen, and Yao Zu. "Precise Dose of Folic Acid Supplementation Is Essential for Embryonic Heart Development in Zebrafish." Biology 11, no. 1 (December 26, 2021): 28. http://dx.doi.org/10.3390/biology11010028.

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Folic acid, one of the 13 essential vitamins, plays an important role in cardiovascular development. Mutations in folic acid synthesis gene 5,10-methylenetetrahydrofolate reductase (MTHFR) is associated with the occurrence of congenital heart disease. However, the mechanisms underlying the regulation of cardiac development by mthfr gene are poorly understood. Here, we exposed zebrafish embryos to excessive folate or folate metabolism inhibitors. Moreover, we established a knock-out mutant of mthfr gene in zebrafish by using CRISPR/Cas9. The zebrafish embryos of insufficient or excessive folic acid and mthfr−/− mutant all gave rise to early pericardial edema and cardiac defect at 3 days post fertilization (dpf). Furthermore, the folic acid treated embryos showed abnormal movement at 5 dpf. The expression levels of cardiac marker genes hand2, gata4, and nppa changed in the abnormality of folate metabolism embryos and mthfr−/− mutant, and there is evidence that they are related to the change of methylation level caused by the change of folate metabolism. In conclusion, our study provides a novel model for the in-depth study of MTHFR gene and folate metabolism. Furthermore, our results reveal that folic acid has a dose-dependent effect on early cardiac development. Precise dosage of folic acid supplementation is crucial for the embryonic development of organisms.
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Hagberg, Bengt, and Andreas Killander. "ANTICONVULSIVE DRUGS AND DISTURBED FOLIC ACID METABOLISM." Developmental Medicine & Child Neurology 9, no. 5 (November 12, 2008): 647–48. http://dx.doi.org/10.1111/j.1469-8749.1967.tb02342.x.

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Williams, J. R. B. "Folic Acid Metabolism of Human Marrow Cells." Scandinavian Journal of Haematology 2, no. 2 (April 24, 2009): 155–66. http://dx.doi.org/10.1111/j.1600-0609.1965.tb01291.x.

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Price, John. "Folic acid metabolism in health and disease." Trends in Food Science & Technology 2 (January 1991): 260. http://dx.doi.org/10.1016/0924-2244(91)90712-r.

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Dissertations / Theses on the topic "Folic acid Metabolism"

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Padmanabhan, Nisha. "The biological and molecular effects of abnormal folate metabolism." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708242.

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Bufalino, Andreia 1983. "Analise da suplementação vitaminica e de polimorfismos em genes da via metabolica do acido folico em mães de individuos com fissuras labio-palatinas não-sindromicas." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288724.

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Orientador: Ricardo Della Coletta
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-15T05:46:12Z (GMT). No. of bitstreams: 1 Bufalino_Andreia_M.pdf: 1848465 bytes, checksum: e05d7021dc64d36ed2556bd7fc4b97fd (MD5) Previous issue date: 2010
Resumo: A fissura labial e/ou palatina (FL/P) não-sindrômica é uma malformação congênita do lábio e/ou palato com alta frequência na população brasileira. A etiologia das fissuras é complexa e conta com a participação de fatores genéticos e ambientais. Inúmeros estudos demonstraram que variantes polimórficas das enzimas relacionadas ao metabolismo do ácido fólico podem ser importantes fatores de risco materno para o nascimento de uma criança FL/P não-sindrômica. O objetivo deste estudo foi estudar a influência do consumo de suplementos vitamínicos durante o primeiro trimestre de gravidez e comparar a frequência alélica e genotípica de 4 genes (MTHFR, MTHFD1, MTR e RFC1) que codificam enzimas da via metabólica do ácido fólico entre mães de indivíduos portadores de FL/P não-sindrômicas (grupo experimental) e mães de indivíduos clinicamente normais (grupo controle). Amostras de DNA de 184 mães do grupo controle e de 106 mães do grupo experimental foram genotipadas por reação em cadeia da polimerase associada à análise de polimorfismo de fragmentos de restrição enzimática (PCR-RFLP). A ausência de suplemento vitamínico durante o primeiro trimestre de gravidez aumentou de forma discreta (aproximadamente em 0,4 vezes) o risco de uma mulher ter um filho com FL/P não-sindrômica. Dos 15 polimorfismos analisados neste estudo, 2 apresentaram diferenças entre os grupos. No polimorfismo rs2274976 do gene MTHFR, o alelo A e o genótipo GA ocorreram em uma frequência significantemente maior no grupo experimental que no grupo controle (p<0,000001), aumentando em aproximadamente 6 vezes o risco de uma mãe ter um filho com FL/P não-sindrômica. O genótipo AA no lócus polimórfico rs2236225 do gene MTHFD1 foi significantemente mais prevalente no grupo experimental comparado com o grupo controle (p=0,02). A presença deste genótipo aumentou em aproximadamente 2 vezes o risco de uma mãe ter um filho com FL/P não-sindrômica. Análise multivariada demonstrou que estes fatores contribuíram de maneira independente para a etiologia das FL/P não-sindrômicas. O presente estudo demonstra que os polimorfismos rs2274976 do gene MTHFR e rs2236225 do gene MTHFD1 e a suplementação vitamínica durante o primeiro trimestre de gravidez estão associados ao desenvolvimento de FL/P não-sindrômicas na população brasileira. Este estudo corrobora com evidências prévias que demonstraram a influência de fatores ambientais e genéticos na etiopatogenia das FL/P não-sindrômicas.
Abstract: Nonsyndromic cleft lip with or without cleft palate (CL/P) is a congenital malformation of the lip and/or palate with elevating frequency in the Brazilian population. The etiology of the nonsyndromic CL/P is complex and both environmental and genetic factors play important roles. Several studies demonstrated that polymorphisms in the folic acid metabolic enzymes may be important maternal risk factor for the birth of a child with nonsyndromic CL/P. The aim of this study was to determine the influence of the multivitamin supplements during the first trimester of pregnancy and to compare the allele and genotypic frequencies of 4 genes (MTHFR, MTHFD1, MTR and RFC1) that encode enzymes of the acid folic metabolic pathway between mothers of nonsyndromic CL/P patients (experimental group) and mothers of clinically normal children (control group). DNA samples from 184 mothers of the control group and from 106 mothers of the experimental group were genotyped by polymerase chain reaction associated with reaction fragment length polymorphism (PCR-RFLP). The lack of multivitamin supplementation during the pregnancy first trimester increased in approximately 0.4-fold the maternal risk of a nonsyndromic CL/P child. Two out of 15 polymorphisms showed differences between groups. In rs2274976 MTHFR polymorphism, allele A and genotype GA occurred in a significantly higher frequency on experimental group when compared to control group (p<0.000001), rising in approximately 6 times the risk of a mother giving birth to a nonsyndromic CL/P child. Genotype AA in the rs2236225 MTHFD1 polymorphic locus was significantly more prevalent in experimental group than in control group (p=0.02). This genotype raised in approximately twice the risk of a mother giving birth to a nonsyndromic CL/P child. Multivariate analysis demonstrated that those factors contributed in an independent manner to nonsyndromic CL/P etiology. The present study shows that rs2274976 MTHFR and rs2236225 MTHFD1 polymorphisms, as well as the multivitamin supplementation during the first trimester of pregnancy, are associated with the development of nonsyndromic CL/P in the Brazilian population. This study corroborates with previous evidences demonstrating the influence of environmental and genetic factor on etiopathogenesis of the nonsyndromic CL/P.
Mestrado
Patologia
Mestre em Estomatopatologia
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Chan, Manuel. "Characterization of the 5' region of the human methylenetetrahydrofolate reductase, MTHFR, gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0026/MQ50734.pdf.

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Kapil, Aditya. "Transport and metabolism of pyridoxine and folic acid in the rat small intestine." Thesis, University of York, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284168.

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Weisberg, Ilan S. "Evaluation of common polymorphisms in methylenetetrahydrofolate reductase (MTHFR) and betaine-homocysteine methyltransferase (BHMT)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0032/MQ64479.pdf.

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Crott, Jimmy. "The effects of folic acid deficiency and defects in folate metabolism on chromosome damage in vitro." Title page, table of contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phc9515.pdf.

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Reprints of the author's previously published articles included as an appendix. Bibliography: leaves 165-188. "This thesis describes a series of experiments that aimed to investigate the effects of folic acid deficiency and defects in folate metabolism on chromosome damage rates in human lymphocytes. The accumulation of chromosome damage over time is an important issue because it is thought to contribute to the mechanism of ageing and the aetiology of diseases of age such as cancer and Alzheimer's disease."
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Nimchuk, Anastasia Katherine. "Homocysteine metabolism as a response to aging and folic acid intake in Fisher 344 rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0009/MQ59858.pdf.

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Sibani, Sahar. "Genetic and nutritional folate deficiency : implications for homocystinuria and intestinal neoplasia." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31539.

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Folate deficiency, a prevalent vitamin deficiency in America, can stem from environmental and/or genetic causes. The most common inborn error of folate metabolism is deficiency of methylenetetrahydrofolate reductase (MTHFR), which catalyzes the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Severe MTHFR deficiency results in hyperhomocysteinemia and homocystinuria; patients present with developmental delay, and various neurological and vascular disorders. This thesis describes three mutations identified in the MTHFR locus in patients with severe deficiency: 1025T→C (M→T), 1027T→G (W→G), and 1768G→A (E→K). Genotype-phenotype correlations are described, along with biochemical characterization of three mutations (983A→G (N→S), 1025T→C, 1027T→G). All three mutations exert their effect by decreasing Vmax without changing the enzyme's affinity for its substrate, 5-methyltetrahydrofolate. The 983A→G variant also conferred decreased affinity for FAD, a cofactor.
The more common and mild deficiency observed in the general healthy population is probably due in part to insufficient dietary intake of folate. Folate deficiency has been associated with increased risk for colon cancer. In a pilot study presented here, the impact of altered folate intake on tumor multiplicity in the Min mouse, a model for multiple intestinal neoplasia, was assessed. Folate deficient diets did not produce a consistent change in tumor numbers. However, a linear correlation between S-adenosylmethionine and S-adenosylhomocysteine content of preneoplastic tissue and tumor multiplicity was identified.
This thesis contributes to our understanding of the impact of genetic- and/or dietary-induced folate deficiency on cellular and organismal functions.
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Öhrvik, Veronica. "Folate bioavailability in vitro experiments and human trials /." Uppsala : Dept. of Food Science, Swedish University of Agricultural Sciences, 2009. http://epsilon.slu.se/200963.pdf.

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Lawrance, Andrea Karin. "The impact of genetic and nutritional disturbances of folate metabolism on tumourigenesis in a mouse model of colorectal cancer /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111885.

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The relationship between colorectal cancer (CRC) and folate metabolism is complex. Dietary folate, depending on the timing and dose, may either prevent or enhance tumour initiation and/or growth, and polymorphisms in the genes encoding folate-metabolising enzymes may also modulate risk. In this thesis, the Apcmin/+ mouse model of CRC was used to investigate the effect of nutritional and genetic disturbances in folate metabolism on tumourigenesis and to examine various mechanisms.
The reduced folate carrier I (RFC1) is responsible for the cellular uptake and intestinal absorption of folate, primarily the 5-methyltetrahydrofolate (5-methylTHF) derivative. Methionine synthase (MTR) uses 5-methylTHF to remethylate homocysteine to methionine, which may be activated and used to methylate substrates such as DNA. 5-MethylTHF is also the product of the methylenetetrahydrofolate reductase (MTHFR)-catalysed reduction of 5,10-methyleneTHF, which is also used to convert dUMP to dTMP.
Adenoma number and load were reduced in Rfc1+/-Apc min/+ mice, compared with Rfc1+/+Apc min/+ mice, but were similar in Mtr+/-Apc min/+ and Mtr+/+ Apcmin/+ mice. Neither Rfc1 nor Mtr genotype affected global DNA methylation, apoptosis or plasma homocysteine (tHcy) levels. In the experiments involving Mtr mice, dietary folate deficiency increased adenoma number, plasma tHcy, and apoptosis, and decreased global DNA methylation. Neither Mtr nor Rfc1 genotype affected the dUTP/dTTP ratio in the intestine of mice not predisposed to adenoma formation.
Adenoma number was decreased in Mthfr+/-Apc min/+ mice (compared with Mthfr+/+Apc min/+ mice) and in Mthfr+/+Apc min/+ offspring of Mthfr+/- mothers (compared with Mthfr+/+Apcmin/+ offspring of Mthfr+/+ mothers). A folate-deficient diet, when initiated prior to conception, significantly decreased adenoma number and decreased global DNA methylation. Overall, adenoma number was inversely correlated with plasma tHcy, dUTP/dTTP ratio and apoptosis. When initiated at three weeks of age, a folate-enriched diet significantly increased adenoma number in Apcmin/+ mice. In the intestines of mice not predisposed to adenoma formation, Mthfr deficiency decreased, and folic acid deficiency increased, the dUTP/dTTP ratio.
These results support the evidence that MTHFR polymorphisms are protective in CRC tumourigenesis and that depending on stage or predisposition, folate may inhibit or enhance tumour growth.
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Books on the topic "Folic acid Metabolism"

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Frances, Picciano Mary, Stokstad E. L. Robert, Gregory Jesse F, and American Chemical Society. Food and Nutritional Biochemistry Subdivision., eds. Folic acid metabolism in health and disease. New York: Wiley-Liss, 1990.

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Bailey, Lynn B. Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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1948-, Bailey Lynn B., ed. Folate in health and disease. New York: M. Dekker, 1995.

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Folic acid and the prevention of disease: Report of the Committee on Medical Aspects of Food and Nutrition Policy. London: Stationery Office, 2000.

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Amouzou, Kou'santa Sabiba. Evaluation des marqueurs nutritionnels et génétiques du statut en coenzymes B (cobalamines et folates) et de l'homocystéinemie plasmatique dans une population d'Afrique de l'Ouest (Benin-Togo). Lomé: [s.n., 2003.

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Pristoupilova, Kamila. Role of folates in metabolic pathways (Studie AV CR). Academia, 1997.

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Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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Folate in Health and Disease. 2nd ed. CRC, 2009.

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Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 1994.

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Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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Book chapters on the topic "Folic acid Metabolism"

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Tiwari, Deeksha, Annu Rani, and Hem Chandra Jha. "Homocysteine and Folic Acid Metabolism." In Homocysteine Metabolism in Health and Disease, 3–36. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6867-8_1.

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Huennekens, F. M., and M. J. Osborn. "Folic Acid Coenzymes and One-Carbon Metabolism." In Advances in Enzymology - and Related Areas of Molecular Biology, 369–446. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470122662.ch8.

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Lorenzini, L., A. De Martino, W. Testi, F. Sorbellini, L. Bisozzi, L. Terzuoli, R. Leoncini, et al. "Radioimmunoassay of Folic Acid and its Correlation with Age." In Purine and Pyrimidine Metabolism in Man VIII, 791–93. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_166.

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Scott, J. M., D. G. Weir, A. Molloy, J. Mcpartlin, L. Daly, and P. Kirke. "Folic Acid Metabolism and Mechanisms of Neural Tube Defects." In Ciba Foundation Symposium 181 - Neural Tube Defects, 180–91. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514559.ch11.

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Girdwood, Ronald H. "Some Aspects of Disordered Folic Acid Metabolism in Man." In Ciba Foundation Symposium - Chemistry and Biology of Pteridines, 385–406. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718919.ch28.

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Clifford, Andrew J., Ali Arjomand, Stephen R. Dueker, Philip D. Schneider, Bruce A. Buchholz, and John S. Vogel. "The Dynamics of Folic Acid Metabolism in an Adult Given a Small Tracer Dose of 14C-Folic Acid." In Advances in Experimental Medicine and Biology, 239–51. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1959-5_15.

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Castro, Gerardo Daniel, and José Alberto Castro. "Metabolism of Ethanol to Acetaldehyde in the Rat Mammary Tissue: Inhibitory Effects of Plant Polyphenols and Folic Acid." In Alcohol, Nutrition, and Health Consequences, 145–54. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-047-2_12.

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Zhu, T., R. Koepsel, M. M. Domach, and M. M. Ataai. "Metabolic Engineering of Folic Acid Production." In ACS Symposium Series, 207–19. Washington, DC: American Chemical Society, 2003. http://dx.doi.org/10.1021/bk-2003-0862.ch013.

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Woods, D. D. "Metabolic Relations Between P-Aminobenzoic Acid and Folic Acid in Micro-Organisms." In Ciba Foundation Symposium - Chemistry and Biology of Pteridines, 220–36. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718919.ch18.

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Clemetson, C. Alan B. "Folic Acid Metabolism." In Vitamin C, 43–48. CRC Press, 2018. http://dx.doi.org/10.1201/9781351077583-4.

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Conference papers on the topic "Folic acid Metabolism"

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Akca, Emine Erdağ, Özlem Çağındı, and Ergun Köse. "The Importance of Cereal Based Foods to Prevention of Iron Deficiency." In 6th International Students Science Congress. Izmir International Guest Student Association, 2022. http://dx.doi.org/10.52460/issc.2022.025.

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Abstract:
Iron is vital for almost every organism, due to its role in a wide range of metabolic processes. For the human body, it contributes to crucial activities, especially haemoglobin synthesis and oxygen transport. Iron deficiency anaemia occurs when iron stores release inadequate amount of iron [1; 2; 3]. However, basic strategies can be used effectively in the prevention of iron deficiency and related anaemia. Although the applicability of these strategies mostly depends on the health infrastructure, the economy of the countries and people's access to resources, it is stated that food fortification is one of the most cost-effective methods [3; 4]. Cereals and pulses are often preferred in food fortification studies as they form the basis of daily nutrition. Around the world, 85 countries have already made it mandatory to fortify wheat flour (and corn/rice) with iron or folic acid [4; 5]. In this study, theoretical information and recent developments on the subject were evaluated in detail with a comprehensive literature review about the role of grain-based products in the prevention of iron deficiency and iron deficiency anaemia. Additionally, food fortification, complex food matrix, bioaccessibility/bioavailability, interaction with sensory and organoleptic properties and aimed to gain a current perspective for future studies on the selection of iron forms.
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O'Flanagan, Ciara H., Xuewen Chen, Zahra Ashkavand, Sergey A. Krupenko, and Stephen D. Hursting. "Abstract 247: Nutrient stress via folic acid modulation causes systemic and cancer-specific metabolic reprogramming and differential effects on primary and metastatic mammary tumor growth in lean and obese mice." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-247.

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