Abstract
The literature data on the etiology and pathogenesis of swim bladder inflammation (SBI) in various fish species have been highlighted in the paper. The main goal of this work was to analyze the impact of the disease on the physiological status of the body of the yearling carp, the state of the antioxidant defense system, and the content of lipid peroxidation products (LPP). The yearling Liubyn scaly carps, with an average weight of 40 g, which were grown in the ponds of the Rivne fish and reclamation station, were selected for experimental research. During control catches and ichthyopathological examination of forty fish, inflammation of the swim bladder was detected with an intensity of 35 %. During the pathological autopsy of this yearling carp, thickening of the walls of the swim bladder with purulent exudate, atrophy of the posterior lobe, and hyperemia of internal organs was found. Data on the content of lipid peroxidation products (LPP) and the state of the antioxidant system (AOS) in the cells of the hepatopancreas and skeletal muscles of this year's carp with SPM have been presented. It was determined that in the hepatopancreas of fish with the swim bladder inflammation, primary and secondary LPP products accumulate, and the activity of AOS enzymes decreases. The increase of diene conjugates in the hepatopancreas of the diseased fish was revealed by 11.8 % compared to the control group, and the content of TBC-active products by 29.8 %. The level of SOD activity is 13.5 % lower in the fish affected by SMP than in the control group. Catalase activity in the hepatopancreas of the diseased fish increases by 11.7 % compared to the control group. There was a 45.5 % decrease in superoxide dismutase activity in the skeletal muscles of fish affected by SBI and a significant increase in the level of catalase (Р < 0.01) compared to the control group. Pathogens that cause diseases of the swim bladder cause also have an inhibitory effect on the activity of enzymes of the antioxidant system, and the content of products of lipid peroxidation increases.
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