Peroxidation in muscle and liver tissues from fish in a contaminated river due to a petroleum refinery industry
Yükleniyor...
Tarih
2005
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Academic Press Inc Elsevier Science
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
In this study, we aimed to investigate the possible effects of the wastewater water contamination of a petroleum industry on the oxidant/antioxidant status of muscle and liver tissues from fish in the Kizilirmak River, Kirikkale, Turkey. The antioxidant/oxidant parameters were analyzed in the muscle and liver tissues from fish in 10km of the river above and below the industry. Malondialdehyde (MDA) and susceptibility to oxidation (SO) values were measured in the liver and muscle tissues as indexes of oxidation, and antioxidant potential (AOP), superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), and catalase(CAT) activities were measured as indexes of antioxidant status. There was significant oxidation in the muscle tissue of the fish obtained in the river downstream of the industry compared to those obtained upstream of the industry. Although there were no meaningful differences between the SOD and GSH-Px activities, the AOP value and CAT activities were found to be reduced in the muscle tissues from the fish obtained downstream. In the liver tissues, the SOD and GSH-Px activities were found to be increased in the fish obtained downstream but no differences were observed in the MDA, SO, AOP, and CAT values. Our results suggest that some contaminants from the petrochemical industry cause oxidation in fish muscle tissues by impairing the antioxidant system. However, because no peroxidation was observed in the liver tissue from the downstream fish, it is possible that liver tissues have a stronger antioxidant capacity than muscle. (C) 2003 Published by Elsevier Inc.
Açıklama
Anahtar Kelimeler
peroxidation, fish, petroleum industry
Kaynak
Ecotoxicology And Environmental Safety
WoS Q Değeri
Q1
Scopus Q Değeri
Q1
Cilt
60
Sayı
1
Künye
closedAccess
