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

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TOPAL A., ATAMANALP M., Oruc E., HALICI M. B., ŞİŞECİOĞLU M., Erol H. S., ...Daha Fazla

FISH PHYSIOLOGY AND BIOCHEMISTRY, cilt.41, sa.3, ss.625-634, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 41 Sayı: 3
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1007/s10695-015-0033-1
  • Dergi Adı: FISH PHYSIOLOGY AND BIOCHEMISTRY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.625-634
  • Anahtar Kelimeler: Nickel, Fish, Brain, c-Fos, Toxicity, Oxidative stress, OXIDATIVE STRESS BIOMARKERS, MESSENGER-RNA EXPRESSION, ALPHA-LIPOIC ACID, FRESH-WATER FISH, HEMATOLOGICAL PARAMETERS, LIPID-PEROXIDATION, TERM EXPOSURE, IN-VITRO, LIVER, TOXICITY
  • Atatürk Üniversitesi Adresli: Evet

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.