Deltamethrin (DMN) exposure causes severe damage to the gill and liver tissues of aquatic organisms, as well as neurotoxic effects and metabolic disorders. The goal of the present study was to assess the impacts of DMN toxicity on blood biochemistry, malondialdehyde (MDA) levels, catalase (CAT) levels, behavior disorder, acetylcholinesterase (AChE) activity, histopathology and 8-hydroxy-2-deoxyguanosine (8 OHdG) of brown trout (Salmo trutta fario). Acute concentrations (1.0 and 2.0μg/L) of DMN caused behavioral disorder such as rapid swimming, loss of balance, aggressiveness and increasing in the surface activity and inactivity in brown trout. A significant increase in malondialdehyde (MDA), aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, and a significant decrease in CAT, AChE, blood albumin, and blood total protein content were observed. Histopathologically, both doses of DMN have caused steatosis, necrosis, and degeneration in hepatocytes and hyperemia in the liver. Also, they led to inflammation, adhesion and fusion depending on severe hyperplasia in secondary lamellae, hyperemia and lamellar edema in gill tissues when compared to control group. Additionally, 8-hydroxy-2-deoxyguanosine (8 OHdG) levels at 2.0 μg/L dose of DMN in liver tissues were more severe according to 1.0 μg/L dose of DMN. Finally, different concentrations of DMN led to changes of the histopathology, 8OHdG, the CAT levels, plasma AChE activity, and the serum metabolites, as well as behavioral disorder in brown trout.
Keywords: Behavioral; Blood biochemistry; Brown trout; Deltamethrin; Histopathology and DNA damage; Oxidative stress.
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