Effects of waterborne copper on gills catalase and blood biochemistry in gilthead seabream (Sparus aurata L.)

Cu is a transition metal essential for every organism, but an excess can lead to toxicity caused by oxidative stress, which can disturb the natural antioxidant defence systems. Since catalase (CAT) is a major enzyme involved in the decomposition of oxygen peroxide, the main goal of this study was to evaluate changes in the concentration and activity of CAT by means of enzymatic and immunohistochemical methods. Modifications in the blood biochemistry profile of Cu-exposed gilthead sea bream (Sparus aurata L.) were also studied. In gills of the exposed fish, Cu significantly increased throughout the study to a maximum of 6.9±4.7 μg g–1 wet weight at the end of the treatment. Immunohistochemistry (IHC) evidenced a brown cytoplasmic stain in the epithelial cells of the primary and secondary lamellae and in pillar cells, while enzyme activity was localized in the epithelium and pillar cells of both primary and secondary lamellae and appeared as a strong cytoplasmic stain particularly at the base of the primary lamellae. IHC and enzymohistochemistry (EHC) quantitative analysis suggested that the main variations in amount and activity of the enzyme were recorded 15 days after exposure (both IHC and EHC expressed a decrease in CAT in exposed fish compared to controls, P<0.0001) and 28 days after exposure (IHC recorded increased CAT in exposed specimens compared to controls, P<0.0001; EHC evidenced a decrease in CAT in exposed subjects compared to controls, P<0.0001). The biochemical blood profile was monitored with a standard blood biochemistry panel. An increase in plasma urea was evident only in exposed fish, while – as a function of time – a decrease of glucose in both exposed and control fish was apparent. The three investigation methods evidenced that CAT was effective against Cu toxicity, and the increase in plasma urea could be considered a suitable metabolic marker of Cu exposure in fish.