ELEVATED BLOOD LEVEL OF HOMOCYSTEINE AS INDICATOR OF HEALTH HAZARD
DOI:
https://doi.org/10.56782/pps.54Keywords:
homocysteine, hyperhomocysteinemia, folic acid, cardiovascular diseasesAbstract
Elevated plasma level of homocysteine (hyperhomocysteinemia) is considered as an independent risk factor for cardiovascular diseases (vascular thrombosis, myocardial infarctions, strokes), neurodegenerative diseases (Alzheimer and Parkinson disease), neural tube defects, danger of spontaneous abortion and carcinomas (especially colon carcinoma). It has been observed that one in ten inhabitants of Europe shows increased plasma homocysteine concentration which is connected with higher risk of cardiovascular diseases development, as myocardial infarction or ischaemic strokes. Pregnant women with hyperhomocysteinemia are exposed to hypertension and neural tube defects of fetus. Elevated plasma levels of homocysteine were found in patients with chronic renal failure, hypothyroidism, several types of carcinomas, pernicious anemia, liver disfunctions and in patients with hypovitaminosis, especially folic acid deficiencies. It has been established that 25% reduction of plasma homocysteine concentration can decrease the risk of myocardial infarction of about 11%, stroke of about 19% and can essentially lower the frequency fetal defects. Authorities still quarrel over the best method of treatement, however it is suggested that witamins B12, B6 as well as the supplementation with folic acid are generally effective in reducing homocysteine level. Recently, dieticians campaign for flours’ supplementation with folic acid. This article aims at stressing the role of hyperhomocysteinemia in etiology of several dangerous civilization diseases.
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Chen P., Poddar R., Tipa E.V., Dibello P.M., Moravec C.D., Robinson K., Green R.,Kruger W.D., Garrow T.A., Jacobsen D.W. : Homocysteine metabolism in cardiovascular cells and tissues: implications for hyperhomocysteinemia and cardiovascular disease. Adv Enzyme Regul, 1999, 39, 93-109. DOI: https://doi.org/10.1016/S0065-2571(98)00029-6
Irizarry M.C., Gurol M.E., Raju S., Diaz-Arrastia R., Locascio J.J., Tennis M., Hyman B.T., Growdon J.H., Greenberg S.M., Bottiglieri T.: Association of homocysteine with plasma amyloid beta protein in aging and neurodegenerative disease. Neur, 2005, 65(9),1402-8. DOI: https://doi.org/10.1212/01.wnl.0000183063.99107.5c
Rosenquist T.H., Ratashak S.A., Selhub J.: Homocysteine induces congenital defects of the heart and neural tube: effect of folic acid. Proc Natl Acad Sci, 1996, 93, 15227-15232. DOI: https://doi.org/10.1073/pnas.93.26.15227
Akoglu B., Milovic V., Caspary W.F., Faust D.: Hyperproliferation of homocysteine-treated colon cancer cells is reversed by folate and 5-methyltetrahydrofolate. Eur J Nutr, 2004, 43,93-9. DOI: https://doi.org/10.1007/s00394-004-0446-6
Mitchell T.: Methylation a little-known but essential process. Life Extension sierpień 1998, dostępna pod adresem: www.lef.org/magazine/mag98/aug98-report2.html
Medina M., Urdiales J.L., Amores-Sanchez M.L.: Roles of homocysteine in cell metabolism: old and new functions. Eur J. Biochem. 2001, 268,3871-82. DOI: https://doi.org/10.1046/j.1432-1327.2001.02278.x
Bailey L.B., Gregory J.F.: Polymorphisms of methylenetetrahydrofolate reductase and other enzymes: metabolic significance, risks and impact on folate requirement. J Nutr, 1999, 129, 919-922. DOI: https://doi.org/10.1093/jn/129.5.919
Brattström L., Wilcken DE., Ohrvik J., Brudin L.: Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: The result of a meta-analysis. Circulation, 1998, 98, 2520-2526. DOI: https://doi.org/10.1161/01.CIR.98.23.2520
Bilwani F., Syed N.A., Usman M., Khurshid M.: Familial homocystinuria. J Coll Physicians Surg Pak, 2005,15, 106-7.
Jakubowski H.: Protein homocysteinylation: possible mechanism underlying pathological consequences of elevated homocysteine levels. FASEB J, 1999, 13, 2277-2283. DOI: https://doi.org/10.1096/fasebj.13.15.2277
Jakubowski H.: Protein N-homocysteinylation: implications for atherosclerosis, Biomed Pharmacother, 2001, 55, 443-447. DOI: https://doi.org/10.1016/S0753-3322(01)00085-3
Hoogeveen E.K., Kostense P.J., Jakobs C., Dekker J.M., Nijpels G., Heine R.J., Bouter L.M., Stehouwer C.D.: Hyperhomocysteinemia increases risk of death, especially in type 2 diabetes: 5-year follow-up of the Hoorn Study. Circulation 2000, 101, 1506-1511. DOI: https://doi.org/10.1161/01.CIR.101.13.1506
Wang H., Yoshizumi M., Lai K., Tsai J.C., Perrella M.A., Haber E., Lee M.E. Inhibition of growth and p21ras methylation in vascular endothelial cells by homocysteine but not cysteine. J Biol Chem, 1997, 272, 25380-25385. DOI: https://doi.org/10.1074/jbc.272.40.25380
Tsai J.T., Wang H., Perrella M.A., Yoshizumi M., Sibinga N.E.S., Tan L.C., Haber E., Chang T.H.T., Schlegel R., Lee M.E.: Induction of cyclin A gene expression by homocysteine in vascular smooth muscle cells. J Clin Invest, 1996, 97, 146-153. DOI: https://doi.org/10.1172/JCI118383
Gaciong Z.: Nadciśnienie tętnicze, hiperhomocysteinemia i kwas foliowy. Czynniki Ryzyka, 2005, supl.11, 11.
Szczeklik A.,Undas A.: Homocysteina w żylnej chorobie zakrzepowo-zatorowej. Czynniki Ryzyka, 2005, supl. 11, 14-15.
Jakubowski H.: Metabolism of homocysteine thiolactone in human cell cultures: possible mechasmism for pathological consequences of elevated homocysteine levels. J Biol Chem,1997, 272, 1935-1942. DOI: https://doi.org/10.1016/S0021-9258(19)67504-6
Ryglewicz D.,Graban A.: Zaburzenia metabolizmu homocysteiny w chorobach zwyrodnieniowych ośrodkowego układu nerwowego.Czynniki Ryzyka, 2005, supl.11,20-22.
Zhu B.T.: Medical hypothesis: hyperhomocysteinemia is a risk factor for estrogen-induced hormonal cancer. Int J Oncol, 2003 Mar;22(3):499-508.
Kozłowska-Wojciechowska M.: Jak zapobiegać hiperhomocysteinemii? Naturalne źródła folianów i witamin z grupy B w polskiej diecie. Czynniki Ryzyka, 2005,supl.11,25-26.
Zalecenia Polskiego Towarzystwa Badań Nad Miażdżycą, http://www.dach-liga-homocystein.org.
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