Neurotoxic effects of nickel chloride in the rainbow trout brain Assessment of c Fos activity antioxidant responses acetylcholinesterase activity and histopathological changes
Yazarlar (8)
Prof. Dr. Ahmet Topal Atatürk Üniversitesi, Türkiye
Prof. Dr. Muhammed Atamanalp Atatürk Üniversitesi, Türkiye
Prof. Dr. Ertan Oruç Selçuk Üniversitesi, Türkiye
Prof. Dr. Mesut Bünyami Halıcı Atatürk Üniversitesi, Türkiye
Melda Şişecioğlu Atatürk Üniversitesi, Türkiye
Doç. Dr. Hüseyin Serkan Erol Atatürk Üniversitesi, Türkiye
Arzu Gergit
Bahar Yılmaz Karamanoğlu Mehmetbey Üniversitesi, Türkiye
| Makale Türü |
Özgün Makale
(SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale)
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| Dergi Adı | FISH PHYSIOLOGY AND BIOCHEMISTRY | ||
| Dergi ISSN | 0920-1742 Wos Dergi Scopus Dergi | ||
| Dergi Tarandığı Indeksler | SCI-Expanded | ||
| Makale Dili | İngilizce | Basım Tarihi | 06-2015 |
| Kabul Tarihi | – | Yayınlanma Tarihi | 10-02-2015 |
| Cilt / Sayı / Sayfa | 41 / 3 / 625–634 | DOI | 10.1007/s10695-015-0033-1 |
| Makale Linki | http://link.springer.com/10.1007/s10695-015-0033-1 | ||
| UAK Araştırma Alanları |
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| Özet |
| 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 < 0.05), but it significantly decreased AChE and CAT enzyme activities (p < 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain. |
| Anahtar Kelimeler |
| Brain | c-Fos | Fish | Nickel | Oxidative stress | Toxicity |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları |