Tip II diabetes mellituslu hastalarda eritrosit içi süperoksit dismutaz, katalaz ve glutatyon peroksidaz düzeyleri

Abstract

6. ÖZET Bu çalışmada tip II diabetes mellitusu olan hastaların (n=50) eritrositlerinde süperoksit dismutaz (SOD), katalaz (CAT) ve glutatyon peroksidaz (GSH-PX) aktiviteleri ölçüldü. SOD aktivitesi ksantin/ksantin oksidaz sistemi ile belirlendi. Bu sistem tarafından üretilen süperoksitler NBT'yi indirgeyerek koyu mavi bir renk oluşturur. Eğer ortamda enzim varsa renk oluşmaz. Katalaz aktivitesi, ultraviole spektrum sahasında H202'in harcanması üzerinden ölçüldü. Glutatyon peroksidaz aktivitesi, NADPH'm maksimum absorbans verdiği 340nm'de NADPH'm harcanması ile meydana gelen absorbans azalması esasma göre ölçüldü. Bulunan sonuçlar kontrol grubu (n=50) enzim aktivite değerleri ile karşılaştırıldı. Diabetes mellituslu hastaların eritrositlerinde SOD aktivitesi 653,2 ± 215.5 Ü/gr Hb, CAT aktivitesi 196,3 + 53,3 K/g Hb, GSH-Px aktivitesi 1236,5 ± 478.6 U/g Hb olarak bulundu. Bu sonuçlardan SOD ve CAT aktivitesi kontrol grubu ile karşılaştırıldığında istatistiksel olarak anlamlı idi (p< 0,05). Hasta ve kontrol grubunun GSH-Px aktiviteleri arasında anlamlı bir fark bulunamadı. Mevcut bulguların ışığı allında şu sonuca varıldı: İnsüline bağımlı olmayan diabetes mellitus gibi glukoz toleransının bozulduğu durumlar, serbest oksijen radikallerin aşın oluşumu ile ve daha sonra buna cevap olarak serbest radikal süpürücü enzimlerin artışı ile sonuçlanabilir. 587. SUMMARY ERYTHROCYTE GLUTATHIONE PEROXIDASE, SUPEROXIDE DISMUTASE AND CATALASE ACTTVITffiS IN PATIENTS WITH NON -INSULINE DEPENDENT DIABETES MELLITUS In this study, the activities of SOD, CAT and GSH-Px were measured in the erythrocyte of the patients with type II diabetes mellitus (n=50). SOD activity was determined with xanthme/xanthine oxidase system. The superoxides produced via this system form a dark blue colour reducing NBT, if the enzyme is present in the reaction mixture, the colour does not appear. The catalase activity was measured considering the consumption of H202 in the ultraviolet spectrum area. The glutathione peroxidase activity was measured upon the diminishing in the absorbance of NADPH consumption at 340 nm, in which NADPH gives a maximal absorbance. All the results obtained from patient groups were compared with the results of control groups. The erythrocyte enzyme activities in the patients with NIDDM were found to be following: SOD, 653, 2 ± 215,5 U/g Hb; CAT, 196,3 ± 53,3 K/g Hb; GSH-Px, 1236 + 478,6 U/g Hb. The SOD and CAT activities were found to be statistically significant comparing with control groups (p< 0,05). There was no significant difference between the activities of GSH-Px in the patient and control groups. Considering these results, we conclude that the conditions where the glucose tolerance impaired such as insulin independent diabetes mellitus results in excessive production of the oxygen radicals and then increase in the radical scavenging enzymes. 59

7. SUMMARY ERYTHROCYTE GLUTATHIONE PEROXIDASE, SUPEROXIDE DISMUTASE AND CATALASE ACTTVITffiS IN PATIENTS WITH NON -INSULINE DEPENDENT DIABETES MELLITUS In this study, the activities of SOD, CAT and GSH-Px were measured in the erythrocyte of the patients with type II diabetes mellitus (n=50). SOD activity was determined with xanthme/xanthine oxidase system. The superoxides produced via this system form a dark blue colour reducing NBT, if the enzyme is present in the reaction mixture, the colour does not appear. The catalase activity was measured considering the consumption of H202 in the ultraviolet spectrum area. The glutathione peroxidase activity was measured upon the diminishing in the absorbance of NADPH consumption at 340 nm, in which NADPH gives a maximal absorbance. All the results obtained from patient groups were compared with the results of control groups. The erythrocyte enzyme activities in the patients with NIDDM were found to be following: SOD, 653, 2 ± 215,5 U/g Hb; CAT, 196,3 ± 53,3 K/g Hb; GSH-Px, 1236 + 478,6 U/g Hb. The SOD and CAT activities were found to be statistically significant comparing with control groups (p< 0,05). There was no significant difference between the activities of GSH-Px in the patient and control groups. Considering these results, we conclude that the conditions where the glucose tolerance impaired such as insulin independent diabetes mellitus results in excessive production of the oxygen radicals and then increase in the radical scavenging enzymes. 598. KAYNAKLAR 1. Akkuş î.: Serbest Radikaller ve Fizyopatolojik Etkileri. Mimoza yayıncılık, Konya, 1995 2. Van L.F.: Free radicals, Analytical Chemistry. 1993, 65: 12-15. 3. Cheeseman KH, Slater TF. An introduction to free radical biochemistry. Br Med Bull, 1993, 49 (3): 479-480. 4. Lunec J, Blake D. Oxygen free radicals: Their relevance to disease processes. In: Cohen RD, Lewis B, Alberti KGMM. The Metabolic and Moleculer Basis of Acquired Disease. Balliere Tindall, London. 1990, 189-212. 5. Deby C, Pincemail J. Oxygen toxicity, free radicals and defense machanisms. In Fiinfgeld EW. Rokan (Ginkgo Biloba). Recent result in pharmacology and clinic. Springer- Verlag, Berlin, Heidelberg, New York. 1988, 56-70. 6. Guemori L, Artur Y, Herberth B, Jeandel C, Cuny G, Siest G. Biological variability of superoxide dismutase, glutathione peroxidase and catalase in blood. ClinChem. 1991, 37-11, 1932-1937. 7. Kozumbo WJ, Trash MA, Kensler TW. Are free radicals involved in tumor promotion. Chem. Biol. 1985, 54: 199-207. 8. Niwa Y, Kanoh T, Sakane T, et al. The ratio of lipidperoxides to superoxide dismutase by tumor necrosis factor: Possible protective mechanism. Science. 1988, 242: 941-943. 9. Halliwell B. Reactive oxygen species in living system: source, biochemistry and role in human. Am J Med. 1991, 91: 3 14-322. 10. Evans PH. Free radicals in brain metabolism and pathology, Br. Med Bull. 1993, 49 (3), 577-587. 11. Klebanoff SJ. Oxygen metabolism and toxic properties of phagocytes. Ann Int Med, 1980, 93:480-489. 12. Fremann BA, Crapo JD. Free radicals and tissue injury. Lab Invest. 1982, 47: 412-426. 13. Weiss S J, Lobuglio AF. Phagocyte-generated oxygen metabolites and cellular injury. Lab Invest. 1991, 47: 5-18.