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ISSN 2007-2783 (Print)
Órgano Oficial del Instituto Científico Pfizer

2016, Number 2

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Residente 2016; 11 (2)

Folic acid a true cell keeper

Navarro-Pérez SF, Mayorquín-Galván EE, Petarra-Del Río S, Casas-Castañeda M, Romero-Robles GBM, Torres-Bugarín O, Lozano-de la Rosa C, Zavala-Cerna MG

Language: Spanish
References: 30
Page: 51-59
PDF size: 265.84 Kb.


ABSTRACT

Folic acid, which pharmaceutical form is the pteroylglutamic acid, is the fully oxidized monoglutamic form of vitamin B9, it is a synthetic compound with similar folate structure but with higher bioavailability, found in vitamin supplements and fortified foods; It has no biological activity unless being converted into folates. Folic acid metabolism is complex and is associated with various metabolic pathways, all of them confer protection to the cell and allow its survival. The purpose of this review is to provide information about what is known about the metabolism of folic acid and how is it that deficiencies in this nutrient can trigger the presence of oxidative stress and genetic instability, which can be related to various diseases. Also, a review was made about specific situations where folic acid is administered as a supplement and the benefits of its administration.


REFERENCES

  1. Mahmood L. The metabolic processes of folic acid and Vitamin B12 deficiency. J Health Res Rev. 2014; 1: 5-9.

  2. Coppedè F. The genetics of folate metabolism and maternal risk of birth of a child with Down syndrome and associated congenital heart defects. Front Genet. 2015; 6: 223.

  3. Brito A, Hertrampf E, Olivares M, Gaitán D, Sánchez H, Allen LH et al. Folate, vitamin B12 and human health. Rev Med Chil. 2012; 140 (11): 1464-1475.

  4. Pita-Rodríguez G, Pineda D, Martín I, Monterrey-Gutiérrez P, Serrano-Sintes G, Macías-Matos C. Ingesta de macronutrientes y vitaminas en embarazadas durante un año. Rev Cubana Salud Pública. 2003; 29: 220-227.

  5. Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, D.C.: National Academy Press; 1998. pp. 196-305.

  6. Suárez de Ronderos M. Ácido fólico: nutriente redescubierto. Acta Médica Costarricense. 2003; 45 (1): 5-9.

  7. Fenech M. Folate (vitamin B9) and vitamin B12 and their function in the maintenance of nuclear and mitochondrial genome integrity. Mutat Res. 2012; 733 (1-2): 21-33.

  8. Kandi V, Vadakedath S. Effect of DNA methylation in various diseases and the probable protective role of nutrition: a mini-review. Cureus. 2015; 7 (8): e309.

  9. de Paz R, Hernandez-Navarro F. Management, prevention and control of megaloblastic anemia, secondary to folic acid deficiency. Nutr Hosp. 2006; 21 (1): 113-119.

  10. Lumley J, Watson L, Watson M, Bower C. Periconceptional supplementation with folate and/or multivitamins for preventing neural tube defects. Cochrane Database Syst Rev. 2001; (3): CD001056.

  11. Barua S, Kuizon S, Junaid MA. Folic acid supplementation in pregnancy and implications in health and disease. J Biomed Sci. 2014; 21: 77.

  12. Li Z, Ye R, Zhang L, Li H, Liu J, Ren A. Folic acid supplementation during early pregnancy and the risk of gestational hypertension and preeclampsia. Hypertension. 2013; 61 (4): 873-879.

  13. Kim MW, Ahn KH, Ryu KJ, Hong SC, Lee JS, Nava-Ocampo AA et al. Preventive effects of folic acid supplementation on adverse maternal and fetal outcomes. PLoS One. 2014; 9 (5): e97273.

  14. Barco-Tavares B, Neves-Finochio Sabino AM, Lima JC, Tozzo-Garcia C. Knowledge of folic acid supplementation during pregnancy. Invest Educ Enferm. 2015; 33 (3): 456-464.

  15. Navarrete-Muñoz EM, Valera-Gran D, García de la Hera M, Gimenez-Monzo D, Morales E, Julvez J et al. Use of high doses of folic acid supplements in pregnant women in Spain: an INMA cohort study. BMJ Open. 2015; 5 (11): e009202.

  16. deRosset L, Mullenix A, Flores A, Mattia-Dewey D, Mai CT. Promotora de salud: promoting folic acid use among Hispanic women. J Womens Health (Larchmt). 2014; 23 (6): 525-531.

  17. Funk RS, van Haandel L, Leeder JS, Becker ML. Folate depletion and increased glutamation in juvenile idiopathic arthritis patients treated with methotrexate. Arthritis Rheumatol. 2014; 66 (12): 3476-3485.

  18. Ortiz Z, Shea B, Suarez-Almazor M, Moher D, Wells G, Tugwell P. Folic acid and folinic acid for reducing side effects in patients receiving methotrexate for rheumatoid arthritis. Cochrane Database Syst Rev. 2000; (2): CD000951.

  19. van den Bemt BJ, den Broeder AA, Van der Burgt M, Fransen J, van Ede AE, van den Hoogen FH. (Bi)Weekly folic acid supplementation might be inferior to a daily folic acid dosing schedule in the prevention of methotrexate-related toxicity in patients with rheumatoid arthritis. Clin Exp Rheumatol. 2015; 33 (5): 767-768.

  20. Sánchez-Valle V, Méndez-Sánchez N. Estrés oxidativo, antioxidantes y enfermedad. Rev Invest Med Sur Mex. 2013; 20 (3): 161-168.

  21. Perozo-Romero J, Guerra-Velásquez M, Reyna-Villasmil E, Mejia-Montilla J, Reyna-Villasmil N, Torres-Cepeda D et al. Homocisteína sérica en neonatos de preeclámpticas y de embarazadas normotensas. Prog Obstet Ginecol. 2011; 54 (8): 408-412.

  22. Sánchez-Cuevas M, Jiménez-Reséndiz S, Morgado-Vázquez J. La homocisteína: un aminoácido neurotóxico. REB. 2009; 28 (1): 3-8.

  23. Brenner G, Stevens C. Pharmacology. 4th ed. Philadelphia, USA: Lippincott Williams & Wilkins; 2013.

  24. Petras M, Tatarkova Z, Kovalska M, Mokra D, Dobrota D, Lehotsky J et al. Hyperhomocysteinemia as a risk factor for the neuronal system disorders. J Physiol Pharmacol. 2014; 65 (1): 15-23.

  25. Zou CG, Banerjee R. Homocysteine and redox signaling. Antioxid Redox Signal. 2005; 7 (5-6): 547-559.

  26. Faraci FM, Lentz SR. Hyperhomocysteinemia, oxidative stress, and cerebral vascular dysfunction. Stroke. 2004; 35 (2): 345-347.

  27. Fenech M. Micronutrients and genomic stability: a new paradigm for recommended dietary allowances (RDAs). Food Chem Toxicol. 2002; 40 (8): 1113-1117.

  28. Kimura M, Umegaki K, Higuchi M, Thomas P, Fenech M. Methylenetetrahydrofolate reductase C677T polymorphism, folic acid and riboflavin are important determinants of genome stability in cultured human lymphocytes. J Nutr. 2004; 134 (1): 48-56.

  29. Wang Y, Xu S, Cao Y, Xie Z, Lai C, Ji X et al. Folate deficiency exacerbates apoptosis by inducing hypomethylation and resultant overexpression of DR4 together with altering DNMTs in Alzheimer’s disease. Int J Clin Exp Med. 2014; 7 (8): 1945-1957.

  30. Duthie SJ, Narayanan S, Brand GM, Pirie L, Grant G. Impact of folate deficiency on DNA stability. J Nutr. 2002; 132 (8 Suppl): 2444S-2449S.




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