Sıçanlarda 2,3,7,8-Tetraklorodibenzo-P-Dioksin (TCDD) 'nin Neden Olduğu Hepatoksisite ve Nefrotoksisite Üzerine Protokateşik Asitin (PCA) Rolü

En toksik dioksin bileşiklerinden biri olan TCDD'nin insan ve hayvan dokularında serbest radikal oluşturarak oksidatif hasara neden olduğu bilinmektedir. Bu çalışmada, TCDD tarafından toksisite oluşturulan sıçan karaciğeri ve böbreğinde önemli bir fenolik bileşik olan PCA’nın koruyucu etkileri araştırıldı. Bu amaçla 28 adet Wistar Albino cinsi sıçanlar (3-4 aylık ve 280-310 g ağırlığında) kullanıldı. Sıçanlar kontrol, TCDD, PCA ve TCDD + PCA olmak üzere rastgele 4 eşit gruba ayrıldı. TCDD ve PCA mısır yağı içinde çözüldü ve sırasıyla 2 µg / kg ve 100 mg / kg dozunda 45 gün boyunca gavaj yolu ile sıçanlara uygulandı. Çalışmanın sonunda TCDD'nin malondialdehit (MDA) seviyesini arttırdığı, ancak glutatyon (GSH) seviyesini ve süperoksit dismutaz (SOD), katalaz (CAT) ve glutatyon peroksidaz (GSH Px) aktivitelerini azalttığı gözlendi. PCA uygulamasının TCDD'nin aksine enzim aktivitelerini ve GSH seviyelerini arttırdığı ve MDA seviyelerini düşürdüğü tespit edildi. Sonuç olarak, PCA'nın TCDD'nin neden olduğu lipid peroksidasyonunu azalttığı ve antioksidan aktivitesini desteklediği görülmüştür. Bu nedenle PCA’nın, TCDD'nin neden olduğu toksisiteye karşı potansiyel bir indirgeyici madde olduğu öne sürülebilir.

Role of Protocatechuic Acid (PCA) on Hepatoxicity and Nephrotoxicity Induced by 2, 3, 7, 8-Tetracholorodibenzo-P-Dioxin (TCDD) in Rats

It is known that TCDD, one of the most toxic dioxin compounds, causes oxidative damage by forming free radicalin human and animal tissues. In this study, the protective effect of PCA, an important phenolic compound, wasexamined in rat kidney and liver tissues with TCDD-induced toxicity. For this purpose, 28 Wistar Albino rats (3-4 months old and weighing 280-310 g) were used. Rats were randomly divided into 4 equal groups (control, TCDD,PCA and TCDD+PCA). TCDD and PCA were dissolved in corn oil at doses of 2 µg/kg and 100 mg/kg,respectively. Subsequently, the substances were administered to the rats by oral gavage for 45 days. The test resultsshowed that in both kidney and liver tissues, TCDD increased the level of malondialdehyde (MDA) but inhibitedthe level of glutathione (GSH) and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathioneperoxidase (GSH-Px). PCA administration was found to increase the enzyme activities and GSH levels, whereasit decreased the TCDD and MDA levels. In conclusion, it was observed that PCA decreased the TCDD-inducedlipid peroxidation, increasing the antioxidant activity. Therefore, it might be suggested that PCA is a potentialreducing agent for the toxicity caused by TCDD.

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