Dietary selenomethionine exposure alters swimming performance, metabolic capacity and energy homeostasis in juvenile fathead minnow

Abstract

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. Recent studies suggest that chronic exposure to elevated dietary SeMet alters energy and endocrine homeostasis in adult fish. However, little is known about the direct effects of dietary SeMet exposure in juvenile fish. The objective of the present study was to investigate sublethal physiological effects of dietary SeMet exposure in juvenile fathead minnow (Pimephales promelas). Twenty days-post-hatch fathead minnow were exposed for 60 days to different measured concentrations (2.8, 5.4, 9.9, 26.5μgSe/g dry mass [dm]) of Se in food in the form of SeMet. After 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). Ucrit was decreased in the 26.5μgSe/gdm exposure group compared to the control group. Tail beat frequency and tail beat amplitude were significantly reduced in fish fed 9.9 and 26.5μgSe/g. An increase in MO2 and COT was observed in the 9.9 and 26.5μgSe/g exposure groups compared to the control group. While the AMR of the high dose group was increased relative to control, there were no significant differences in SMR and F-AS. Energy storage capacity was measured via whole body triglyceride and glycogen concentrations. Triglyceride concentrations in non-swam fish were elevated in the 5.4μgSe/g group relative to controls. Fatigued (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 26.5μgSe/g exposure groups had significantly greater whole body glycogen concentrations in swam versus non-swam fish. A decrease in whole body cortisol was observed in swam fish in the 5.4μgSe/g exposure group compared to control fish. Whole body cortisol was greater in control, 9.9 and 26.5μgSe/g swam fish compared to non-swam fish. These results suggest that exposure to environmentally relevant concentrations of dietary SeMet impairs swimming performance, aerobic capacity, and energy homeostasis, potentially impacting survivability of juvenile fish in Se impacted aquatic ecosystems.