Biología, patobiología y bioclínica de la homocisteína eh la especie humana
Biology, pathobiology and subclinical homocysteine in the human species
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García, G. A. (2010). Biología, patobiología y bioclínica de la homocisteína eh la especie humana. Revista Repertorio De Medicina Y Cirugía, 19(2), 115–134. https://doi.org/10.31260/RepertMedCir.v19.n2.2010.586
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La homocistinuria fue descrita en 19a2 en niños con dificultades de aprendizaje y en 19a9 McCully informó la evidencia en autopsias de trombosis arterial eztensa y aterosclerosis en niños con elevadas concentraciones de homocisteína plasmática y homocistinuria. La homocisteína, un aminoácido de azufre, es un metabolito intermedio de la metionina, y sobre la base de estos hallazgos bioquímicos, ellos propusieron que la homocisteína plasmática elevada puede causar lesión neural y enfermedad vascular aterosclerótica. Hoy se considera un factor de riesgo independiente para esta última. La hiperhomocistinemia leve es bastante prevalente en la población general. Puede deberse a defectos genéticos en las enzimas que participan en el metabolismo de la homocisteína, carencias nutricionales de vitaminas y cofactores, ciertos medicamentos, ingesta rica en metionina o enfermedad renal. La alta concentración puede reducirse con folato, y es así que la suplementación vitamínica ha sido propuesta en individuos con hiperhomocistinemia con el fin de reducir su riesgo de enfermedad cardiovascular. En este artículo hacemos una revisión de la biología, la patobiología y la bioclínica del metabolismo de la homocisteína.
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3. Trabetti E. Homocysteine, MTHFR gene polymorphisms, and cardio-cere- brovascular risk. J Appl Genet. 2008;49:267-82.
4. Obeid R, McCaddon A, Herrmann W. The role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric diseases. Clin Chem Lab Med. 2007;45:1590-606.
5. Deth R, Muratore C, Benzecry J et al. How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis. Neurotoxicology. 2008;29:190-201.
6. Frankenburg FR. The role of one-carbon metabolism in schizophrenia and depression. Harv Rev Psychiatry. 2007;15:146-60.
7. Folstein M, Liu T, Peter I, Buell J et al. The homocysteine hypothesis of depression. Am J Psychiatry. 2007;164:861-7.
8. Almeida OP, McCaul H, Hankey GJ et al. Homocysteine and depression in later life. Arch Gen Psychiatry. 2008;65:1286-94.
9. Dodds L, Fell DB, Dooley HC et al. Effect of homocysteine concentration in early pregnancy on gestational hypertensive disorders and other pregnancy outcomes. Clin Chem. 2008;54:326-34.
10. Forges T, Pellanda H, Diligent C et al. Do folates have an impact on fertility? Gynecol Obstet Fertil. 2008;36:930-9.
11. Devlin TM. Textbook of Biochemistry with Clinical Correlations, 6a. ed., New York. Wiley-Liss. 2006.
12. Nelson DL, Cox MM. Lehninger Principles of Biochemistry, 5a. ed., New York. W. H. Freeman. 2008.
13. Berg JM, Tymoczko JL, Stryer L. Biochemistry, 6a. ed., New York. W. H. Freeman. 2006.
14. Scriver CR, Sly WS, Childs B, et al. The metabolic and molecular basis of inherited disease, 8a. ed., New York. McGraw-Hill Professional. 2001.
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20. Steensholt G. On the methylation of ethanol amine, dimethyl ethanol amine, guanidine acetic acid and homocysteine. Acta Physiol Scand. 1947;14:340-7.
21. Greenberg DM. Biological methylation. Adv Enzymol Relat Areas Mol Biol. 1963;25:395-431.
22. Pasieka AE, Morgan JF. The detection of homocysteine in biological systems. Biochim Biophys Acta. 1955;18:236-40.
23. Bartosinski B. Biosynthesis of methyl group of methionine. Postepy Biochem. 1964;10:463-74.
24. Langemann H, Hensler CJ. Spontaneous increase in the rate of formation of methionine from dimethylthetin and homocysteine in rat liver homogenates. Arch Biochem. 1951;33:344-5.
25. Gibson F, Woods DD. The synthesis of methionine from homocysteine by
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