Deneysel Karbon Tetraklorür Zehirlenmesinde Akciğer Doku Hasarı ve Melatonin Hormonunun Koruyucu Rolü: Işık Mikroskobik ve Biyokimyasal Bir Çalışma
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Tarih
2012
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Bu çalışmada, akciğer dokusu üzerindeki karbon tetraklorür (CCl4) toksisitesine karşı melatonin hormonunun koruyucu etkisinin incelenmesi amaçlandı. 24 adet Wistar-Albino cinsi erkek sıçanlar üç eşit gruba ayrıldı. Grup Ideki sıçanlar kontrol olarak kullanıldı. Grup IIdeki hayvanlara gün aşırı olarak ve derialtı yolla CCl4 uygulandı. Grup IIIdeki sıçanlara ise CCl4 enjeksiyonu ile birlikte yine gün aşırı olarak ve derialtı yolla melatonin verildi. Dört haftalık deney süresi sonunda bütün sıçanlar dekapite edilerek akciğerleri çıkartıldı. Biyokimyasal incelemeler için, akciğer doku örneklerinin bir bölümünde süperoksit dismutaz (SOD), glutatyon peroksidaz (GSH-Px) enzim aktiviteleri ve malondialdehit (MDA) seviyeleri spektrofotometrik olarak belirlendi. Mikroskobik incelemeler için, doku örnekleri rutin histolojik prosedürlerden geçirilerek parafine gömüldü. CCl4 enjeksiyonu yapılan sıçanlara ait akciğer doku örneklerindeki SOD ve GSH-Px enzim aktivitelerinin kontrol grubuna göre istatistiksel olarak anlamlı bir şekilde azaldığı, MDA düzeylerinin ise arttığı tespit edildi. Mikroskobik incelemede ise, CCl4 maruziyetinin akciğerde pulmoner interstisyumda hemorajiye, polimorf çekirdekli lökosit ve makrofaj infiltrasyonuna neden olduğu görüldü. CCl4 enjeksiyonu ile birlikte melatonin uygulanan hayvanlarda, SOD ve GSH-Px enzim aktivitelerinde bir artışın meydana geldiği, MDA değerlerinde ise anlamlı bir düşüşün olduğu gözlendi. Işık mikroskobik incelemelerde, CCl4 toksisitesinin neden olduğu histopatolojik değişikliklerin melatonin uygulamasıyla düzeldiği görüldü. CCl4 toksisitesinin akciğerlerde önemli ölçüde oksidatif doku hasarına yol açtığı ve bu hasarın melatonin uygulamasıyla önlenebildiği tespit edildi.
In this study, it was aimed to investigate the protective effects of melatonin hormone against to carbon tetrachloride (CCl4)-induced toxicity in lung tissue. Twenty-four male Wistar-Albino rats were randomly divided into three equal groups. Rats in group I were used as control. Rats in group II were injected subcutaneously every other day with CCl4. Rats in group III were injected subcutaneously every other day with CCl4 and melatonin. At the end of four weeks of experimental period, all animals were killed by decapitation and their lungs were removed. For biochemical examination, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels were determinated by a spectrophotometer in some of the lung tissue specimens. For light microscopic examination, tissue specimens were embedded in paraffin blocks following routine histological procedures. In lung tissue samples of rats treated with CCl4, SOD and GSH-Px enzyme activities were significantly lower and malondialdehyde (MDA) levels were significantly higher than the control group. Microscopically, interstitial pulmonary hemorrhage, leucocytes with polymorphic nuclei and macrophage infiltration were observed in the lung specimens of rats exposed to CCl4 alone.There is a statistically significant increase in SOD and GSH-Px enzyme activities, and a decrease in MDA levels in rats treated with CCl4 and melatonin. Histopathological changes caused by CCl4 toxicity were not observed in rats treated by melatonin. It is concluded that CCl4 creates oxidative damage in lung tissue and melatonin has protective effects against this CCl4 induced damage
In this study, it was aimed to investigate the protective effects of melatonin hormone against to carbon tetrachloride (CCl4)-induced toxicity in lung tissue. Twenty-four male Wistar-Albino rats were randomly divided into three equal groups. Rats in group I were used as control. Rats in group II were injected subcutaneously every other day with CCl4. Rats in group III were injected subcutaneously every other day with CCl4 and melatonin. At the end of four weeks of experimental period, all animals were killed by decapitation and their lungs were removed. For biochemical examination, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels were determinated by a spectrophotometer in some of the lung tissue specimens. For light microscopic examination, tissue specimens were embedded in paraffin blocks following routine histological procedures. In lung tissue samples of rats treated with CCl4, SOD and GSH-Px enzyme activities were significantly lower and malondialdehyde (MDA) levels were significantly higher than the control group. Microscopically, interstitial pulmonary hemorrhage, leucocytes with polymorphic nuclei and macrophage infiltration were observed in the lung specimens of rats exposed to CCl4 alone.There is a statistically significant increase in SOD and GSH-Px enzyme activities, and a decrease in MDA levels in rats treated with CCl4 and melatonin. Histopathological changes caused by CCl4 toxicity were not observed in rats treated by melatonin. It is concluded that CCl4 creates oxidative damage in lung tissue and melatonin has protective effects against this CCl4 induced damage
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3