Buradasınız

KRONİK HEMODİYALİZ HASTALARINDA SERUM PARAOKSANAZ AKTİVİTESİ

SERUM PARAOXONASE ACTIVITY IN CHRONIC HEMODIALYSIS PATIENTS

Journal Name:

Publication Year:

Keywords (Original Language):

Abstract (2. Language): 
High-density lipoprotein (HDL) has been shown to prevent the oxidation of low-density lipoprotein (LDL). The antioxidant activity of HDL is believed to reside in its enzymes, particularly paraoxonase. Recently, paraoxonase (PON) has been implicated in the pathogenesis of atherosclerosis. We have examined the activity, and phenotype distribution of serum PON in 76 patients with chronic renalfailure undergoing maintenance hemodialysis as patient group and 66 healthy subjects as control group. The serum paroxonase activity in this patient group were significantly reduced when compared to the control group (p<0.0001). The levels of HDL and apolipoprotein A1 (Apo-A 1) in the patient group were also lowest when compared to the control group (p<0.0001 and p<0.0001, respectively). The PON activity for HDL (PON/HDL ratio) and apoAl (PON/ Apo-Al ratio) levels in the patient group were significantly reduced when compared to the control (p<0.0001) and p<0.0001, respectively). The phenotypic distribution of PON (AA,AB,BB) was not significantly different between patient and the control groups. We conclude that serum paraoxonase activity was significantly lower in the chronic hemodialysis patients as independent of paraoxonase phenotypic
Abstract (Original Language): 
Yüksek dansiteli lipoproteinin (HDL) düşük dansiteli lipoproteinin (LDL) oksidasyonunu önlediği gösterilmiştir. HDL 'nin antioksidan etkisini özellikle paraoksanaz (PON) enzimi olmak üzere, taşıdıkları enzimler aracılığıyla yaptığına inanılmaktadır. Son zamanlarda, PON'un aterosklerozım patogenezinde rol oynadığı düşünülmektedir. Biz 76 kronik hemodiyaliz hastası ve 66 sağlıklı kişide serum PON aktivitesi ve fenotip dağılımını araştırdık. Serum PON aktivitesi, HDL ve apolipoprotein Al (Apo-Al) seviyeleri hasta grubunda kontrol grubuna göre önemli derecede azdı (sırasıyla, p<0.0001, p<0.0001 ve p<0.0001). PON/HDL ve PON/Apo-Al oranlan hasta grubunda kontrol grubuna göre önemli derecede düşük idi (sırasıyla, p<0.0001 ve p<0.0001). PON'un fenotipik dağılım (AA, AB, BB) farkı hasta ve kontrol gruplarında arasında önemli değildi. Biz, kronik hemodiyaliz hastalarında PON aktivitesinin PON'in fenotip inden bağımsız olarak, kontrol grubuna göre düşük olduğu sonucuna vardık.
FULL TEXT (PDF): 
176-179

REFERENCES

References: 

1. Ruiz J, Blanche H, James RW, Blatter-Garin MC, Vaisse C, Charpentier G, et al. Gln-Argl92 polymorphism of paraoxonase and coronary heart disease in type 2 diabetes. Lancet 1995;346:869-872.
2. Paragh G, Asztalos L, Seres I, Balogh Z, Löcsey L, Kârpâti I, et al. Serum paraoxonase activity changes in uremic and kidney-transplanted patients. Nephron 1999:83:126-131.
3. Paragh G, Sers I, Balogh Z, Varga Z, Kârpâti I, Mâtyus J, et al. The serum paraoxonase activity patients with chronic renal failure and hyperlipidemia. Nepron 1998;80:166-170.
4. Ayub A, Mackness MI, Arrol S, Mackness B, Patel J, Durrington PN. Serum paraoxonase after myocardial infarction. Arterioscler Thromb Vase Biol 1999;19:330-335.
5. Blatter-Garin MC, James RW, Dussoix P, Blanche H, Passa P, Froguel P. Paraoxonase polymorphism Met-Leu54 is associated with modified serum concentrations
of the enzyme. J Clin Invest 1997;99:62-66.
6. Aviram M, Rosenblat M, Bisgaiger CL, Newton RS, Primo-Parma SL, La Du BN. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase.
J Clin Invest 1998;101:1581-1590.
7. Karakaya
A
, İbiş S, Kural T, Köse SK, Karakaya AE. Serum paraoxonase activity and phenotype distribution in Turkish subjects with coronary heart disease and its relationship to serum lipids and lipoproteins. Chem-Biol Interact 1999;118:193-200.
8. Mackness MI, Harty D, Bhatnagar D, Winocour PH, Arrol S, Ishola M, et al. Serum paraoxonase activity in familial hypercholesterolemia and insulin-dependent diabetes mellitus. Atherosclerosis 1991;86:193-199.
9. Suehiro T, Nakauchi Y, Yamamoto M, Arii K, Itoh H. Hamashige N, et al. Paraoxonase gene polymorhism in Japanese subjects with coronary heart disease. In J
Cardiol 1996;57:69-73.
10. Mackness B, Mackness MI, Arrol S, Turkie W, Durrington PN. Effect of the molecular polymorphisms of human paraoxanase (PON1) on the rate of hydrolysis
of paraoxon. Br J Pharmacol 1997;122:265-268.
11. La Du BN, Eckerson HW. The polymorphic paraoxonase/arylesterase isozymes of human serum.
Fed Proc 1984;43:2338-2341.
12. Eckerson HW, Wythe CM, La Du BN. The human
serum paraoxonase/aryesterase polymorphism. Am J
Hum Genet 1983;35:1126-1138.
13. Witztum JL, Daniel S. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest 1995;88:1785-1792.
14. Odawara M, Tachi Y, Yamashita K. Paraoxonase polymorphism (Glnl92-Arg) associated with coronary heart disease in Japanes noninsulin dependent diabetes
mellitus. J Clin Endocrinol Metabol 1997;82:2257-
2260.
15. Krauss RD, Berkeley MD. The tangled web of coronary
risk factors. Am J Med 1991 ;90 (suppl 2A):36-41.
16. Serrato M, Marian AJ. A variant of human paraoxonase/arylesterase (HUMPONA) gene is a risk factor for coronary artery disease. J Clin Invest 1995;96:30005-30008.
179

Thank you for copying data from http://www.arastirmax.com