Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes

The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from...

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Veröffentlicht in:	Fish physiology and biochemistry 2015-06, Vol.41 (3), p.625-634
Hauptverfasser:	Topal, Ahmet, Atamanalp, Muhammed, Oruç, Ertan, Halıcı, Mesut Bünyami, Şişecioğlu, Melda, Erol, Hüseyin Serkan, Gergit, Arzu, Yılmaz, Bahar
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylcholinesterase - metabolism Animal Anatomy Animal Biochemistry Animal Physiology Animals Antioxidants Biomarkers Biomedical and Life Sciences Brain Brain - drug effects Brain - metabolism Brain - pathology Catalase - metabolism Chloride Enzymatic activity Enzymes Fish Fisheries Freshwater & Marine Ecology Glutathione - metabolism Heavy metals Histology Immunohistochemistry - veterinary Industrial development Life Sciences Lipid Peroxidation - physiology Morphology Neurotoxicity Neurotoxins - toxicity Nickel Nickel - toxicity Oncorhynchus mykiss Oncorhynchus mykiss - metabolism Oxidative stress Oxidative Stress - drug effects Peroxidation Pollutants Proto-Oncogene Proteins c-fos - metabolism Superoxide Dismutase - metabolism Toxicity Trout Zoology
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Zusammenfassung:	The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels ( p
ISSN:	0920-1742 1573-5168
DOI:	10.1007/s10695-015-0033-1