Sublethal effects of dietary selenium exposure on juvenile fishes
Selenium (Se) is known to cause chronic toxicity in aquatic species. In particular, dietary exposure of fish to selenomethionine (SeMet), the primary form of Se in the diet, is of concern. Previous studies reported that chronic exposure to elevated dietary SeMet altered swimming performance, aerobic metabolism, and energy and endocrine homeostasis in adult fish. However, little is known about the direct effects of dietary SeMet exposure in juvenile fish. Therefore, the overall objective of this thesis was to investigate sublethal pathophysiological effects of subchronic dietary SeMet exposure in two juvenile fish species, fathead minnow (Pimephales promelas) and rainbow trout (Oncorhynchus mykiss). In the first experiment, 20 days post hatch (dph) juvenile fathead minnow were exposed to different measured concentrations (2.8, 5.4, 9.9, 26.5 µg Se/g dry mass [dm]) of Se in food in the form of SeMet for 60 days. In the second experiment, 14 dph juvenile rainbow trout were exposed for 37 days to different measured concentrations (1.0, 4.1, 11.2, 26.1 µg Se/g dm) of Se in food in the form of SeMet. Following exposure, samples were collected for Se analysis and fish were subjected to a swimming performance challenge to assess critical swim speed (Ucrit), tail beat frequency and tail beat amplitude, oxygen consumption (MO2), cost of transport (COT), standard metabolic rate (SMR), active metabolic rate (AMR), and factorial aerobic scope (F-AS). Dietary SeMet exposure impaired swimming ability in both fathead minnow and rainbow trout. Juvenile fathead minnow showed alterations in aerobic metabolism with increased MO2, COT and AMR at the 9.9 and 26.5 µg Se/g diets, while dietary SeMet exposure did not appear to affect aerobic metabolism in juvenile rainbow trout. After swim performance experiments, swam fish were considered fatigued and metabolic and energy storage endpoints were compared to non-swam (non-fatigued) fish. Energy storage capacity was measured via whole body (fathead minnow) and liver and muscle (rainbow trout) triglyceride and glycogen concentrations. For fathead minnow, triglyceride concentrations in non-swam fish were significantly elevated in the 5.4 µg Se/g group relative to controls, and swam fish had significantly lower whole body triglycerides than non-swam fish. All non-swam SeMet exposure groups had significantly decreased whole body glycogen concentrations compared to controls while the 5.4 and 26.5 µg Se/g exposure groups had significantly greater whole body glycogen concentrations in swam versus non-swam fish. In juvenile rainbow trout, liver triglyceride concentrations were significantly lower in all SeMet exposed groups compared to controls in non-swam fish. Swimming decreased liver and muscle triglycerides in the control and 11.2 µg Se/g treatment groups. Liver glycogen concentrations were greater in swam trout in the 4.1 µg Se/g dm exposure group. Muscle glycogen concentrations in non-swam fish, were significantly decreased in the 4.1 and 11.2 µg Se/g exposed groups compared to controls, while muscle glycogen in swam fish was unaffected by dietary SeMet exposure. For the swim status factor, muscle glycogen concentrations were significantly greater in swam versus non-swam trout in all treatment groups. Therefore, dietary SeMet exposure caused impaired swimming performance and metabolic alterations in both juvenile fathead minnow and juvenile rainbow trout. Species differences were apparent, especially in the patterns of altered energy status between swam and non-swam fish exposed to Se. Overall, the pathophysiological implications of these sublethal effects are unclear, but suggest that dietary SeMet exposure may negatively influence juvenile fish survivability in natural habitats.
DegreeMaster of Science (M.Sc.)
CommitteeHecker, Markus; Wickstrom, Mark; Olkowski, Andrew
Copyright DateJune 2014