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CUPROPHAN VE POLİSÜLFON DİALİZÖRLERİNİN OKSİDAN / ANTİOKSİDAN DENGESİ ÜZERİNE ETKİLERİ*

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Abstract (2. Language): 
In chronic renal insufficiency, many toxic metabolites which are normally nontoxic but become toxic when combined improving oxidative metabolism, accumulates in the body fluids. We studied the effect of the most frequently used cuprophan and polysulfone dialysers in hemodialysis treatment on oxidant/ antioxidant status. For this purpose, 26 cases (9 females, 17 males, mean age of 36) that are used cuprophan dialysers (n=15) and polysulfone dialysers (n=11) were examined. The cases with COPD, DM and the ones using vitamin E and C, were excluded. First the plasma and red blood cells of the venous blood taken before and after hemodialyses were separated and than plasma MDA and intraerythrocyter GSH levels, activities of GSH-Px and SOD were measured. Results.- When the groups that are used cuprophan and polisulfone dialysers are compared; It is observed that the cuprophan dialysers increased plasma MDA levels (p<0,05), decreased the intraerythrocyter GSH levels (p<0,01), activities of GSH-Px (p<0,05) and SOD (p<0,05), as polisulfone dialysers did not influence the MDA and GSH levels, activities of GSH-Px and SOD (p>0,05). Conclusion.- Hemodialysis treatment is an oxidant stress for the organism and some of used dialysers is effective on this oxidant stress. As a conclusion, this is important in developing new membranes to control the production of free oxygen radicals.
Abstract (Original Language): 
KRY’li hastaların oksidan stres altında olduğu bilinmektedir. Cuprophan ve polisülfon dializörlerinin organizmanın oksidan sistemi ve antioksidan savunması üzerine ne gibi etkileri olduğunu saptamak amacıyla bu çalışmayı planladık. Çalışma Haydarpaşa Numune Hastanesi Hemodializ ünitesi ve özel bir merkez tarafından takip edilen 26 hasta üzerinde yapılmıştır. Hastaların 15’i Cuprophan dializörü, 11’i ise Polisülfon dializörü ile hemodialize girmiştir. Araştırma projemize göre, hastalardan hemodializ öncesi ve hemodializ sonrası, Cubital venden heparinli tüpe 10 ml kan alınmış, kan örnekleri hemen 3000 rpm de 5 dakika santrif üje edilerek plazma ve eritrositlerine ayrılmıştır ve plazma MDA düzeyleri ile, eritrosit içi SOD, GSH-Px enzim aktiviteleri ve GSH düzeyleri ölçülmüştür. Bulgularımıza göre MDA düzeyi hemodializ sonrası istatistiksel olarak anlamlı düzeyde yüksek bulundu (p<0,023). Hemodializ sonrasında, eritrosit-içi SOD ve GSH-Px aktivitesi ile GSH düzeyleri, istatistiksel olarak anlamlı düzeyde azalmış (sırasıyla p<0,018, p<0,026, p<0,007) olarak belirlendi. Cupro-phanla yapılan hemodializ sonrasında MDA düzeyleri artmakta (p<0,037), eritrosit-içi SOD ve GSH-Px aktivitesi ile GSH düzeyleri ise, anlamlı olarak (sırasıyla p<0,032, p<0,05, p<0,007) azalmaktadır. Polisülfonla yapılan hemodializde, saptanan parametreler açısından giriş ile çıkış arasında istatistiksel olarak anlamlılık saptanmamıştır (p>0,05). Sonuç olarak, hemodializin oksidan stresi artırdığı, eritrosit içi (hücre içi) antioksidan enzimlerin aktivitesini azalttığı, Cuprophan dializörünün oksidan stresi artırdığı, antioksidan enzimlerin aktivitesini azalttığı, Polisülfon hemodia- CERRAHPAŞA T 80 IP DERGİSİ Cilt (Sayı) 31 (2) lizörünün oksidan/antioksidan dengeye etkisi olmadığı saptandı. Yeni membranlar geliştirilirken, oksijen radikal üretimi açısından kontrol edilmesinin çok ö- nemli olduğu vurgulandı.
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REFERENCES

References: 

1. Hassewander O, Young IS. Oxidative stress in
chronic renal failure. Free Radic Res, 1998; 29:
1-11.
2. Mohora M, Mircescu G, Cirjan C, Mihaliescu I,
Girneata L, Ursea N, Dinu V. Effect of
hemodialysis on lipid peroxidation and
antioxidant system in patients with chronic
renal failure. Rom J Intern Med 1995; 33: 237-
242.
3. Haklar G, Yeğenağa I, Yalçın AS. Evaluation of
oxidant stress in chronic hemodialysis patients:
use of different parameters. Clin Chim Acta
1995; 234: 109-114.
4. Usberti M, Lima G, Arisi M, Bufano G,
D’Avanzo L, Gazzotti RM. Effect of exegenous
reduced glutathione on the survival of red blood
cells in hemodialysed patients. J Nephrol 1997;
10: 261-265.
5. Loughrey CM, Young IS, Lightbody JH,
McMaster D, McNamee PT, Trimble ER.
Oxidative stress in hemodialysis. QJM, 1994;
87: 679-683.
6. Buege JA, Aust SD. Microsomal lipid
peroxidation. Methods Enzymol 1978; 12:302-
310.
7. Sun Y, Oberley LW, Li YA. Simple method for
clinical assay of superoxide dismutase. Clin
Chem.1988: 34: 497-500.
8. Beutler E, Duran O, Kelly BM. Improved
method for the determination of blood
glutathione. J Lab Clin Med 1963; 61:882-888.
9. Seymen O, Seven A, Candan G, Yiğit G, Hatemi
S, Hatemi H. The effect of iron supplementation
on GSH levels, GSH-Px, and SOD activities of
erythrocytes in L-Thyroxine administration.
Acta Med Okayama 1997; 51: 129-133.
10.Paglia DE, Valentine WN. Studies on the
quantitative and qualitative characterization of
erythrocyte glutathione peroxidase. J Lab Clin
Med 1967; 70: 158.
11.Paul JL, Sall ND, Soni T, Poignet JL,
Lindenbaum A, Man NK, Moatti N, Raichvarg
D. Lipid peroxidation abnormalities in
hemodialyzed patients. Nephron, 1993; 64: 106-
109.
12.Durak I, Akyol Ö, Başeşme E, Canbolat O, Kavut
çu M. Reduced erythrocyte defense
mechanisms against free radical toxicity in
patients with chronic renal failure. Nephron,
1994; 66:76-80.
13. Westhuyzen J, Adams CE, Fleming SJ.
Evidence for oxidative stress during in vitro
dialysis. Nephron, 1995; 70: 49-54.
14.Sanaka T, Higuchi C, Shinobe T, Nishimura H,
Omata M, Nihei H, Sugino N. Lipid
peroxidation as an indicater of biocompatibility
in hemodialysis. Nephrol Dial Transplant 1995;
10 [Suppl. 3]: 34-38.
15.Richard MJ, Arnaud J, Jurkovitz C, Hachache
T, Meftahi H, Laporte F, Foret M, Favier A,
Cordonnier D. Trace elements and lipid
peroxidation abnormalities in patients with
chronic renal failure. Nephron 1991; 57:10-15.
16.Delmas-Beauvieux MC, Combe C, Peuchant E,
Carbonneau MA, Dubourg L, de Precigout V,
Aparicio M, Clerc M. Evaluation of red blood cell
lipo-peroxidation in hemodialysed patients
during erythropoietin therapy supplemented or
not with iron. Nephron 1995; 69:404-410.
17.Hosokawa S., Yoshida O.: Effects of
erythropoietin on trace elements in patients
with chronic renal failure undergoing
hemodialysis. Nephron 1993; 65:414-417.
18. Witko-Sarsat V, Friedlander M, Capeillere-
Blandin C, Nguyen-Khoa T, Nguyen AT,
Zingraff J, Jungers P, Descamps-Latscha B.
Advanced oxidation protein products as a novel
marker of oxidative stress in uremia. Kidney
International 1996; 49: 1304-1313.
19. Paskalev D, Tchankova P, Jankova T, Steiner
M, Nenov D. Alteration in red blood cell sodium
and potassium concentrations and increased
lipid peroxidation in patients with chronic renal
failure on maintenance hemodialysis: A
hypothesis. Am J Nephrol 1994; 14: 246-248.
20.Vaziri ND, Oveisi F, Ding Y. Role of increased
oxygen free radical activity in the pathogenesis
of uremic hypertension. Kidney International
1998; 53: 1748-1754.
21.Hagen TM, Aw TY, Jones DP. Glutathione
uptake and protection against oxidative injury
in isolated kidney cells. Kidney International
1988; 34: 74-81.

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