Rola homocysteiny jako źródła dysfunkcji sródbłonka naczyń: niezależny czynnik ryzyka miażdżycy

• Autorzy: Wasilewska A , Lysiak-Szydlowska W.
• Języki publikacji: PL

Słowa kluczowe

PL

choroby czlowieka; miazdzyca; ryzyko zachorowan; homocysteina; srodblonek; zywienie czlowieka

• Wydawca: -
• Czasopismo: Żywienie Człowieka i Metabolizm
• Rocznik: 1999
• Tom: 26
• Numer: 3
• Opis fizyczny: s.255-263,tab.,bibliogr.

Twórcy

autor

Wasilewska A

• Akademia medyczna, 80-210 Gdansk, ul.M.Curie-Sklodowskiej 3A

autor

Lysiak-Szydlowska W.

Bibliografia

• 1. Bassenge E.: Endothelial function in different organs. Prog. Cardiovasc. Dis., 1996, 39, 209.
• 2. Boers G.H.J.: Hyperhomocysteinemia: A newly recognized risk factor for vascular disease. Neth. J. Med., 1994, 45, 34.
• 3. Bostom A.G., et al.: High dose B-vitamin treatment of hyperhomocysteinemia in dialysis patients. Kidney Int., 1996, 49, 147.
• 4. Brattstrom L., et al.: Impaired homocysteine metabolism in early onset cerebral and peripheral occlusive disease - effects of piridoxine and folic acid. Atherosclerosis 1990, 81, 51.
• 5. Cichocka A., Cybulska B.: Homocysteina - mniej poznany czynnik ryzyka chorób sercowo-naczyniowych. Med. Metabol., 1999, 2, 42.
• 6. Clark R.: Lowering blood homocysteine with folic acid based supplements: Meta-analysis of randomised trials. Br. Med. J., 1998, 16, 894.
• 7. Cravo M.L., et al.: Hyperhomocysteinemia in chronic alcoholism: correlation with folate, vitamin B12, and vitamin B6 status. Am. J. Clin. Nutr., 1996, 63, 220.
• 8. D’Angelo A., Selhub J.: Homocysteine and thrombotic disease. Blood 1997, 90, 1.
• 9. Demuth K., Myara I., Moatti N.: Biology of the endothelial cell and atherogenesis. Ann. Biol., Clin. Paris, 1995, 53, 171.
• 10. Food and Drug Administration. Food standards of identity for enriched grain products to require addition of folic acid. Final rule. Fed. Regist., 1996, 61, 8781.
• 11. Harpel PC., Zhang X., Borth W: Homocysteine and hemostasis: pathogenic mechanisms predisposing to thrombosis. J. Nutr., 1996, 126, 1285S.
• 12. Jacobsen D.W.: Homocysteine and vitamins in cardiovascular disease. Clin. Chem., 1998, 44, 1833.
• 13. Kang S.S., Wong P.W, Malinow M.R.: Hyperhomocysteinemia as a risk factor for occlusive vascular disease. Ann. Rev. Nutr., 1992, 12, 279.
• 14. Kunachowicz H., Nadolna I., Przygoda B.: Tabele wartości odżywczej produktów spożywczych. Warszawa, Instytut Żywności i Żywienia, 1998.
• 15. Lenz S.R., Sadler J.E.: Inhibition of thrombomodulin surface expression and protein C activation by the thrombogenic agent homocysteine. J. Clin. Invest., 1991, 88, 1906.
• 16. Liao J.K.: Inhibition of Gi proteins by low-density-lipoprotein attenuates bradykinin-stimulated release of endothelial-derived nitric oxide. J. Biol. Chem., 1994, 269, 19528.
• 17. Liao J.K., Shin W.S., Lee W.Y., et al.: Oxidized low-density-lipoprotein decreases the expression of endothelial-derived nitric oxide synthase. J. Biol. Chem., 1995, 270, 319.
• 18. Liao J.K.: Endothelium and acute coronary syndromes. Clin. Chem., 1998, 44, 1799.
• 19. Luscher T.F., Barton M.: Biology of the endothelium. Clin. Cardiol., 1997, 20, 3.
• 20. Makoff R., Dwyer J., Rocco M.: Folic acid, pyridoxine, cobalamin and homocysteine and their relathionship to cardiovascular disease in end-stage renal disease. J. Ren. Nutr., 1996, 6, 2.
• 21. Malinow M.R., Bostom A.G., Krauss R.M.: Homocysteine, diet and cardiovascular disease. A statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation 1999, 99, 178.
• 22. Mansoor M.A., Svardal A.M., Schneede J., et al.: Dynamic relation between reduced, oxidized and protein-bound homocysteine and other thiol components in plasma during methionine loading in healthy men. Clin. Chem., 1992, 38, 1316.
• 23. McCully K.S.: Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am. J. Pathol., 1969, 56111.
• 24. McCully K.S., Wilson R.B.: Homocysteine theory of arteriosclerosis. Atherosclerosis 1975, 22, 215.
• 25. Mudd S.H., et al.: The natural history of homocysteinuria due to cystathione β-synthase deficiency. Am. J. Hum. Genet., 1985, 37, 1.
• 26. Mudd S.H., Levy H.L.: Disorders in transsulfuration. In: The metabolic basis of inherited disease. Scriver C., Beaudet A., Sly W., New York, McGraw Hill, 1989, 693.
• 27. Mudd S.H., Levy H.L., Skovby F.: Disorders of transsulfuration. In: The metabolic and molecular basis of inherited disease. Scriver C.R., Beaudet A.L., Sly W.S., New York, 7th ed. McGraw Hill, 1995, 1279.
• 28. Nygard O., et al.: Total plasma homocysteine and cardiovascular risk profile-the Hordaland homocysteine study. J. Amer. Med. Assoc., 1995, 274, 1526.
• 29. Oemar B.S., Yang Z., Luscher T.F.: Molecular and cellular mechanisms of atherosclerosis. Curr. Opin. Nephrol. Hepertens., 1995, 4, 82.
• 30. Ohara Y., Peterson T.E., Harrison D.G.: Hypercholesterolemia increases endothelial superoxide anion production. J. Clin. Investig., 1993, 91, 2546.
• 31. Olszewski A.J., McCully K.S.: Fish oil decreases serum homocysteine in hyperlipemic men. Coron. Art. Dis., 1993, 4, 52.
• 32. Reddy K.G., Nair R.N., Sheehan H.M., et al.: Evidence that selective endothelial dysfunction may occur in the absence of angiographic or ultrasound atherosclerosis in patients with risk factors of atherosclerosis. J. Am. Coll. Cardiol., 1994, 23, 833.
• 33. Rimm E.B., et al.: Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. J. Amer. Med. Assoc., 1998, 279, 359.
• 34. Sacks T., Moldow C.F., Craddoxk P.R., et al.: Oxygen radical mediated endothelial cell damage by complement stimulated granulocytes: An in vitro model of immune vascular damage. J. Clin. Invest., 1978, 6, 1161.
• 35. Seidel D.: Risk factors of atherosclerosis. Differential profile - various mechanisms? Z. Kardiol., 1993, 82, 33.
• 36. Strydom A.J.C., et al.: A. Comparative study in human of their plasma homocysteine and cholesterol levels in relation to diet. Clin. Chem., 1990, 36, 954.
• 37. Tsai J.C., et al.: Promotion of vascular smooth muscle growth by homocysteine: a link to atherosclerosis. Proc. Natal. Acad. Sci. USA 1994, 91, 6369.
• 38. Ubbink J.B., Van der Merwe A., Vermaak W.J.K., et al.: Hyperhomocysteinemia and the response to vitamin suplementation. Clin. Investig., 1993, 71, 993.
• 39. Ubbink J.B.: Effective homocysteine metabolism may protect South African blacks against coronary heart disease. Am. J. Clin. Nutr., 1995, 62, 802.
• 40. Ubbink J.B., Delport R., Vermaak W.J.H.: Plasma homocysteine concentrations in a population with a low coronary heart disease prevalence. J. Nutr., 1996, 126, 1254.
• 41. Ueland P.M., et al.: Total homocysteine in plasma or serum: methods and clinical applications. Clin. Chem., 1993, 39, 1764.
• 42. Verhoef P., Stampfer M.J., et al.: Homocysteine metabolism and risk of myocardial infarction: relation with vitamins B6, B12 and folate. Am. J. Epidemiol., 1996, 143, 845.
• 43. Zeiher A.M., Drexler H., Saurbier B., et al.: Endothelium-mediated coronary blood flow modulation in humans: effects of age, atherosclerosis, hypercholesterolemia and hypertension. J. Clin. Investig., 1993, 92, 652.