Uzun süreli sigara kullanımının eritrosit antioksidan enzim düzeylerine etkisi
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2002
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info:eu-repo/semantics/openAccess
Özet
Öz:Serbest oksijen radikallerinin bir çok dokuda hasar yaptığı bilinmektedir. Bu radikaller lipid peroksidasyonu, enzim aktivasyonu ve inaktivasyonu ve DNA hasarı gibi çok geniş hücresel hasara yol açabilecek, oldukça reaktif bileşiklerdir. Memeli hücreleri enzimatik ve non-enzimatik antioksidan savunma sistemleri ile serbest radikallere karşı korunmaktadırlar. Sigara, hücrelerde lipid peroksidasyonu ve biyolojik hasan başlatabilen serbest radikalleri içerir. Bu çalışmada; Süperoksit Dismutaz (CuZn-SOD), Katalaz (CAT) ve Glutatyon Peroksidaz (GSH-Px) enzim aktiviteleri sağlıklı sigara kullananların eritrositlerinde ölçüldü. Çalışma grubu 52 sağlıklı sigara kullanan ve 59 sağlıklı sigara kullanmayan kişiden oluştu. Cu,Zn-SOD aktivitesi spektrofotometrede 560 nm'de, ksantin/ksantin oksidaz sistemi ile üretilen süperoksit anyonları tarafından nitro blue tetrazolium'un (NBT) indirgenmesinin belirlenmesi ile ölçüldü, CAT aktivitesi spektrofotometrede 240 nm'de hidrojen peroksitin yıkılmasının takibi ile ölçüldü. GSH-Px aktivitesi 340 nm'de redükte nikotin amid adenin dinükleotid fosfat (NADPH)' m oksitlenmesinin izlenmesi ile ölçüldü. Kontrol grubu eritrosit Cu,Zn-SOD, CAT ve GSH-Px aktiviteleri sırasıyla 821,8±229,3 Ü/gHb, 155±42,3 K/gHb, ve 1230±380,5 Ü/gHb bulundu. Sağlıklı sigara kullananlarda aynı enzimlerin aktiviteleri sırasıyla 800,6±250,4 Ü/gHb, 181,6±64 K/gHb, ve 1211,2±392,6 Ü/gHb, idi. Bu sonuçlara göre CAT aktivitesi sigara kullananların eritrositlerinde kullanmayanlara göre daha yüksekti (p<0.05). Sigara kullanan ve kullanmayanların SOD ve GSH-Px enzim aktiviteleri arasında anlamlı bir fark bulunamadı (p>0.05). Bu verilerin ışığında uzun süreli sigara kullanımının oksijen radikallerinin aşırı üretimine neden olabileceği ve eritrositlerdeki oksidan/antioksidan dengeyi bozabileceği kanaatine varıldı.
Abstract:Oxygen free radicals are known to produce damage in many biological tissues. These free radicals are highly reactive compounds that can cause on a variety of cell damage including lipid peroxidation, enzymes inactivation and activation, and DNA damage. Mammalian cells are protected against free radicals by enzymatic and non-enzymatic antioxidant defense systems. Cigarette, contains free radicals which may initiate lipid peroxidation and biological damage in the cells. In this study, the enzyme activities of Superoxide Dismutase (Cu,Zn-SOD), Catalase (CAT) and Glutathione Peroxidase (GSH-Px) were measured in the erythrocyte of the healthy cigarette smokers. The study group included 52 healthy smokers and 59 healthy non-smokers. Superoxide Dismutase (Cu,Zn-SOD) activity was measured by determining the reduction of nitro blue tetrazolium (NBT) by Superoxide anion produced with xanthme/xanthine oxidase system at 560 nm in a spectrophotometer. Catalase (CAT) activity was determined by monitoring the initial rate of disappearance of hydrogen peroxide at 240 nm in a spectrophotometer. Glutathione Peroxidase (GSH-Px) activity was measured by monitoring the oxidation of reduced nicotiriàmide adenine dinucleotid phosphate (NADPH) at 340 nm. The activities of erythrocyte enzymes Cu,Zn-SOD, CAT and GSH-Px from control group were determined as 821,8±229.3 U/gHb, 155±42.3 K/gHb, and 1230.6±380.5 U/gHb respectively. In the healthy smokers activity of the same enzymes were 800.6±250.4 U/gHb, 181.6±64 K/gHb, 1211.2±392.6 U/gHb in that order. As a result it was found that; CAT activity is higher in the erythrocytes of smokers than non-smokers (P<0.05). No significant difference was found in SOD and GSH-Px enzyme activities between the smokers and non-smokers (P>0.05). Considering these results, we conclude that the long term cigarette smoking may cause in excessive production of the oxygen radicals and disturb of the oxidant/antioxidant balance in erythrocytes.
Abstract:Oxygen free radicals are known to produce damage in many biological tissues. These free radicals are highly reactive compounds that can cause on a variety of cell damage including lipid peroxidation, enzymes inactivation and activation, and DNA damage. Mammalian cells are protected against free radicals by enzymatic and non-enzymatic antioxidant defense systems. Cigarette, contains free radicals which may initiate lipid peroxidation and biological damage in the cells. In this study, the enzyme activities of Superoxide Dismutase (Cu,Zn-SOD), Catalase (CAT) and Glutathione Peroxidase (GSH-Px) were measured in the erythrocyte of the healthy cigarette smokers. The study group included 52 healthy smokers and 59 healthy non-smokers. Superoxide Dismutase (Cu,Zn-SOD) activity was measured by determining the reduction of nitro blue tetrazolium (NBT) by Superoxide anion produced with xanthme/xanthine oxidase system at 560 nm in a spectrophotometer. Catalase (CAT) activity was determined by monitoring the initial rate of disappearance of hydrogen peroxide at 240 nm in a spectrophotometer. Glutathione Peroxidase (GSH-Px) activity was measured by monitoring the oxidation of reduced nicotiriàmide adenine dinucleotid phosphate (NADPH) at 340 nm. The activities of erythrocyte enzymes Cu,Zn-SOD, CAT and GSH-Px from control group were determined as 821,8±229.3 U/gHb, 155±42.3 K/gHb, and 1230.6±380.5 U/gHb respectively. In the healthy smokers activity of the same enzymes were 800.6±250.4 U/gHb, 181.6±64 K/gHb, 1211.2±392.6 U/gHb in that order. As a result it was found that; CAT activity is higher in the erythrocytes of smokers than non-smokers (P<0.05). No significant difference was found in SOD and GSH-Px enzyme activities between the smokers and non-smokers (P>0.05). Considering these results, we conclude that the long term cigarette smoking may cause in excessive production of the oxygen radicals and disturb of the oxidant/antioxidant balance in erythrocytes.
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ÇİĞREMİŞ Y,ÖZUĞURLU F,TÜRKÖZ Y,YÜKSEL E,GAFFAROĞLU M,YILMAZ M (2002). Uzun süreli sigara kullanımının eritrosit antioksidan enzim düzeylerine etkisi. Süleyman Demirel Üniversitesi Fen Bilimleri Enstitüsü Dergisi, 6(3), 141 - 147.
