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PERİPORTUM AKUT BÖBREK YETMEZLİĞİ VE PREEKLAMPSİ—EKLAMPSİDE OKSİDATİF SİSTEM

OXIDATIVE -ANTI-OXIDATIVE SYSTEM IN PERIPARTUM ACUTE RENAL FAILURE AND PREECLAMPSIA -ECLAMPSIA

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Abstract (2. Language): 
In this study we aimed to evaluate the oxidative -anti-oxidative systems in peripartum acute renal failure, preeclampsia -eclampsia. The study groups consisted of 17 patients with periparthum acute renal failure (8/17+HELLP Syndrome) (GI), 11 preeclamptic pregnant(GII), 11 pregnant (330 weeks) (Gill) and 11 healthy women (GIV) with aged 18-38 years. Superoxide dismutase (SOD), glutathione peroxidase (GSHPx) in erythrocytes and plasma malondialdehide (MDA) levels were measured in all groups. SOD, GSHPx and MDA levels were also measured at the beginning (GIA), regression of renal dysfunction (GIB) and recovery of renal functions (GIC). MDA levels were 11.95±4.25, 9.22±3.62, 5.10±3.65, 3.40± 1.27, 4.91 ± 2.06, 4.24 ± 1.67 mmol/ml in GIA, GIB, GIC, Gil, GUI and GIV respectively. SOD activitiy in erythrocyte were 3269.23+1437.83, 2641.35 ± 1411.13, 2056.35±l 143.11, 924.±160.04, 1057.91 ±257.03, 861.63+243.28 Ug/Hb in GIA, GIB, GIC, Gil, Gill and GIV respectively. GSHPx activity in erythrocyte were 70.17 ± 23.52, 58.27+23.75, 45.44+17.60, 24.48 + 6.77, 26.28 + 7.27, 32.95 ± 8.24 Ug/Hb in GIA, GIB, GIC, Gil, GUI and GIV respectively. MDA levels and activities of SOD, GSHPx in erythrocytes on the begining, improvement and recovery of acute renal failure (GIA, GIB and GIC) were significantly different from each other and their values decreased while regaining of renal functions. Preeclampsia-eclampsia or normal pregnancy did not cause elevation of plasma MDA levels and GSHPx, SOD in erythrocyte. Although SOD and GSHPx in erythrocytes and plasma MDA level were found similar in healthy women, pregnant women and preeclamptic women. In patients with peripartum acute renal failure SOD, GSHPx and MDA increased at the begining and decreased during recovery of renal functions.
Abstract (Original Language): 
Bu çalışmada, preeklampsi-eklampsi ve peripartum akut böbrek yetmezliğinde oxidatif sistemi değerlendirmeyi amaçladık. Çalışma grubu 18-38 yaş grubundaki ,17 peripartum akut böbrekyetmezlikli (Gl), 11 preeklampsi-eklampsili (GII), 11 sağlıklı gebe (GUI) ve 11 sağlıklı kadın (G1V) dan oluşturuldu.Bütün gruplarda plasma malondialdehid(MDA) ve eritrositlerde glutatyon peroksidaz (GSHPx)- superoxid dismutaz(SOD) düzeylerine bakıldı.GI de MDA, GSHPx ve SOD düzeyleri başlangıç (GIA), toparlanma(GlB) ve düzelme (GIC) dönemlerinde olmak üzere üç kez bakıldı. MDA düzeyleri GIA, GIB, GIC, GII, GUI ve GIVde sırası ile 11.95+4.25, 9.22+3.62, 5.10+3.65, 3.40±1.27, 4.91+2.06, 4.24+1.67 olarak bulundu. Eritrosit SOD aktivitesi GIA, GIB, GIC, GII, GUI ve GIV de sırası ile 3269.23±1437.83, 2641.35±1411.13, 2056.35+1143.11, 924.00+160.04, 1057.91+257.03, 861.63+243.28 Ug/Hb olarak bulundu.Eritrosit GSHPx aktivitesi ise GIA, GIB, GIC.GII, GUI ve GIV de sırası ile 70.17±23.52, 58.27±23.75, 45.44±17.60, 24.48±6.77, 26.28+7.27, 32.95+S.24 Ug/Hb olarak bulundu. GI de başlangıç, toparlanma ve düzelme (GIA,G1B,G1C) dönemlerindekiMDA, SOD ve GSHPx değerleri birbirlerinden istatiksel olarak farklı idi ve böbrek fonksiyonlarının düzelmesine paralel olarak düşüş gösterdi. G ve IV de MDA, SOD ve GSHPx düzeylerinde faklılık yoktu. Preeklampsi, sağlıklı gebe ve sağlıklı kadın gruplarında MDA, SOD ve GSHPx için farklılık olmamasına rağmen, peripartum akut böbrek yetmezliği olan grupta bu değerler yüksekti ve böbrek fonksiyonlanndaki düzelmeye paralel olarak azaldı.
FULL TEXT (PDF): 
141-147

REFERENCES

References: 

1. Isler CM, Martin JN. Preeclampsia: Pathophysiology and practice considerations for the consulting Nephrologist. Seminars in Nephrology 2002; 22: 54-64.
2. McCord JM, Fridovich I. Superoxide dismutase an enzymatic function for erythrocuprein (hemocuprein). .1 Biol Chem 1969; 244: 6049-6055.
3. Beutler E. Red cell metabolism. Grune&Stratton. New York 1975; pp 74-75.
4. Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxidase in animal tissues by thiobarbituric acid reaction. Analytical Biochemistr 1979; 351-358.
5. Michel B. Pregrancy. In: Davison AM, Cameron JS, Grünfeld JP (eds). Textbook of clinical nephrology.
Oxford University Press. Oxford 1998. pp 1704-1713.
6. Schrier RW. Shapiro JI, Chan L, et al. Increased nephron oxygen consumption: Potential role in progression of chronic renal disease. Am J Kidney Dis
1994:23: 176-182.
7. Walker JJ. Antioxidants and inflammatory cell response in preeclampsia. Semin Reprod Endocrinol
1998; 16:47-55.
8. Kharb S, Gulati N, Singh V, et al. Superoxide anion formation and glutathione levels in patients with preeclampsia. Gynecol Obstet Invest 2000; 49: 28-30.
9. Zusterzeel PL, Wanten GJ, Peters WH, Merkus HM,
Steegers EA. Neutrophil oxygen radical production in pre-eclampsia with HELLP Syndrome. Eur J Obstet
Gynecol Reprod Biol 2001; 99:213-218.
10. Knapen MF, Peters WH, Mulder TP, et al. Glutathione
and glutathione-related enzymes in decidua and placenta of controls and women with pre-eclampsia.
Placenta 1999; 20: 541-6.
11. Lopez-Jaramillo P, Casas JP. Serrano N. Preeclampsia: from epidemiological observations to molecular mechanisms. Braz J Med Biol Res 2001; 34: 1227¬1235.
12. Homzova M. Ostro A. Current views on the etiopathogenesis of preeclampsia. Ceska Gynekol
2001;66:276-280.

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