Kronik asetaldehit uygulaması ile uyarılan oksidatif streste sıçan karaciğerinde ve beyin dokularında N-asetilsistein ve taurinin koruyucu etkileri

Öz

Amaç: Asetaldehit (AA), alkol metabolizmasının ana ürünlerinden biridir. AA'e maruz kalma birçok diyet ürününün yenmesi, sigara dumanı/otomobil egzozlarının solunması veya kozmetik ürünlerle temas yoluyla oluşabilir. AA birikimi oksidatif strese neden olur. Bu çalışmanın amacı kronik AA'e maruz kalan sıçanlarda prooksidant/antioksidan durumunu araştırmak ve N-asetil sistein (NAC) ve taurinin (TAU) proksidant/antioksidan dengesi üzerindeki etkilerini değerlendirmektir.

Yöntemler: Sprague Dawley sıçanlar aşağıdaki gruplara ayrıldı (n = 8; her biri): Kontrol, AA, AA+NAC, AA+TAU. Karaciğer ve beyin dokularında reaktif oksijen türleri (ROS), dien konjugatları (DC), malondialdehit (MDA), protein karbonil (PC), ferrik indirgeyici antioksidan güç (FRAP) ve glutatyon (GSH) düzeyleri ve ayrıca süperoksit dismutaz (SOD) ve glutatyon peroksidaz (GSH-Px) aktiviteleri incelendi.

Bulgular: İçme suyu ile AA uygulanan sıçanların karaciğer ve beyin dokularında prooksidan bir durum oluştuğu saptandı. NAC uygulaması her iki dokuda AA’e bağlı prooksidan durumu azalttı. TAU incelenen dokularda ROS oluşumunu azaltmasına rağmen, MDA ve PC düzeyleri değişmedi. NAC and TAU AA uygulanan sıçanların karaciğer ve beyinlerinde GSH düzeylerini arttırdı.

Sonuç: Kronik AA uygulamasının proksidant bir durum yarattığını, NAC/TAU uygulamalarının AA ile uyarılan oksidatif stresin baskılamada yararlı olabildiği görülmektedir.

Anahtar Kelimeler

• Asetaldehit,oksidatif stres,N-asetilsistein,taurin,karaciğer,beyin

Protective effects of N-acetylcysteine and taurine on oxidative stress induced by chronic acetaldehyde administration in rat liver and brain tissues

Abstract

Aim: Acetaldehyde (AA) is one of the main products of alcohol metabolism. Exposure to AA can occur through ingestion of several dietary products, inhalation of cigarette smoke/automobile exhausts, or contact with cosmetics. AA accumulation causes oxidative stress. The aim of this study was to investigate the prooxidant/antioxidant status in rats chronically exposed to AA, and to evaluate the effects of N-acetylcysteine (NAC) and taurine (TAU) on prooxidant/antioxidant balance.

Methods: Sprague Dawley rats were divided in the following groups (n=8; each): Control, AA, AA+NAC, AA+TAU. Reactive oxygen species (ROS), diene conjugate (DC), malondialdehyde (MDA), protein carbonyl (PC), ferric reducing antioxidant power (FRAP) and glutathione (GSH) levels as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined in liver and brain tissues.

Results: AA treatment in drinking water was detected to induce prooxidant state in both liver and brain of rats. NAC treatment decreased AA-induced prooxidant status in both tissues. Although TAU treatment diminished ROS levels, MDA and PC levels remained unchanged in examined tissues of AA-treated rats. NAC and TAU elevated liver and brain GSH levels in AA-treated rats.

Conclusion: Chronic AA administration has created a prooxidant condition, and NAC/TAU appears to be useful in suppression of the developed oxidative stress.

Keywords

• Acetaldehyde,oxidative stress,N-acetylcysteine,taurine,liver,brain

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