Antioxidant processes are affected in juvenile rainbow trout (Oncorhynchus mykiss) exposed to ozone and oxygen-supersaturated water

Two groups of juvenile rainbow trout (Oncorhynchus mykiss) were exposed for 4 h to either hyperoxic (>40 mg O₂/l) or ozonised (5.2 μg O₃/l) water containing supersaturated oxygen. Gill, liver, blood cells and plasma were taken 1, 5, 12, 24 and 48 h following the exposure periods and antioxidant responses and oxidative damage studied in terms of, respectively, antioxidant enzyme activities/glutathione status and lipid peroxidation. Observed biochemical changes were significant at p<0.05. Ozonation elevated oxidised glutathione (GSSG) levels, increased lipid peroxidation and decreased reduced glutathione (GSH) levels in gills 1 h following exposure, which indicate oxidative stress. However, the longer-term effects (48 h) following ozone exposure resulted in increased GSH levels in both gills and liver and, measured as oxidative stress index (OSI), were indicative of enhanced potential of tissues to resist oxidative stress. Ozonation also resulted in elevated activity of superoxide dismutase (SOD) at 5–12 h following exposure in gills compared to 24–48 h in liver, indicating either differential regulation and time-courses of response, or an earlier impact of ozonolysis products on gills than liver. In contrast, catalase activity was elevated in both gills and liver at 24 h by the effects of hyperoxia alone. Hyperoxia also decreased GSSG levels in both gills and liver, but had no effect on lipid peroxidation. Increases were seen in the activities of selenium-dependent glutathione peroxidase as a result of ozonation (gills; 5 and 24 h) and hyperoxia (liver; 1 h), and in total GPX (Se-dependent and independent) as a result of ozonation (both tissues; 48 h), but no effects were seen on glutathione reductase (GR) in either tissues. Levels of GSH were increased in blood cells at various times following hyperoxia. Overall, the results show (i) differential antioxidant and pro-oxidant effects of ozonation compared to hyperoxia, (ii) gills and possibly blood as the first line of impact and defence, with later effects on liver, and (iii) that even after 24–48 h following ozone exposure, all antioxidant defences had not returned to pre-exposure values.