Feeding behaviour, growth performance and toxicological responses in rainbow trout (Oncorhynchus mykiss (Walbaum)) fed on normal and medicated diets
This thesis was focused on the study of (i) individual feeding behaviour and growth performance of juvenile rainbow trout fed on normal and medicated diets and (ii) the responses of hepatic detoxification mechanisms in rainbow trout to dietary oxolinic acid and flumequine. During the first experiment, the development of dorsal and caudal fin damage over time was compared between 4 groups of rainbow trout fed on different ration levels (0.25, 0.5, 1.0 and 1.5% B.W. day-1) and between individuals of different feeding rank within each group. The feeding and growth data indicated that the strength of the social hierarchy became more relaxed within increasing ration. The severity of both dorsal and caudal fin damage was significantly dependent on the ration size fed to the group, with lower ration groups sustaining more fin damage, whereas subordinate fish suffered the most dorsal fin damage within the two lower ration groups. Subsequently, the inter-individual variability in consumption and growth was studied in two groups of rainbow trout fed diets containing flumequine in different concentrations. Flumequine, at either concentration, had a deleterious effect on growth performance, even when palatability problems were not apparent, and resulted in dose-related increases in inter-individual variability in consumption and growth and changes in the pre-established feeding hierarchies. Cytochrome P450 biomarkers and ultrastructural alterations in hepatocytes were used to assess the toxicological responses to rainbow trout following oral administration of oxolinic acid or flumequine. Both antibiotics induced and/or activated CYP1A isoforms of P450 as measured using immunoblotting for P450 protein and a combination of selective substrates and inhibitors for P450 activity. The increase in the P450 activity was correlated with a significant increase, almost 2.5-fold, in the volume of rough endoplasmic reticulum. In addition, severe depletion of glycogen deposits, formation of lipid droplets, increased lysosomal activity as well as mitochondrial hyperplasia and high nuclear-cytoplasmic ratio in flumequine- and oxolinic acid-treated individuals respectively, were considered compensatory rather than degenerative phenomena, indicative of increased biotransformation activity.