Cadmium is a non-essential metal with a wide distribution that has severe toxic effects on aquatic animals. Changes in hematology and muscle physiology were examined in silver carp (Hypophthalmichthys molitrix) exposed to environmentally relevant levels of cadmium (0.01 mg L−1) for 96 h. Cadmium exposure induced significant increases in the red blood cell count, and in the plasma concentrations of cortisol, glucose, and lactate. This suggests that the dose of cadmium was sufficient to cause stress, possibly associated with impaired gas exchange at the gills. There were no changes in hemoglobin concentration or plasma protein concentration. Significant decreases in muscle energy fuels (ATP and glycogen), and increases in muscle lactate persisted until the end of the exposure period, respectively. The changes in muscle lactate and protein in silver carp differed from those observed in response to exposure of fish to cadmium and heavy metals in other studies. The study highlights the importance of selecting unpolluted release sites with suitable water conditions for the survival of newly released individuals for stock enhancement of the Xiangjiang River.

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Exposure of silver carp (Hypophthalmichthys molitrix) to environmentally relevant levels of cadmium: hematology, muscle physiology, and implications for stock enhancement in the Xiangjiang River (Hunan, China)

Abstract The metabolic cost of stress increased with the severity of handling in juvenile coho salmon Oncorhynchus kisutch examined via respirometry. Stressed fish had rates of oxygen consumption 39–98% higher than controls. Elevation in oxygen consumption was largely eliminated within 1 h after stress. Oxygen consumption was significantly correlated to both plasma cortisol and lactate concentration in response to a moderate stressor, but no correlation was found after more severe stressors. Fish given exogenous cortisol did not experience an increase in oxygen consumption, so cortisol alone is unlikely to have a major effect on metabolic rate. Whole-body lactate concentration was significantly elevated following stress, reaching levels almost 500% higher than controls. We suggest that metabolism associated with exercise or hypoxia is the dominant source of elevated oxygen consumption following handling.

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The energetic response to handling stress in juvenile coho salmon (Oncorhynchus kisutch)

COMPUTATIONAL MODELS TO SCALE FROM SUBLETHAL EFFECTS OF STRESSORS TO ADVERSE FISH POPULATION RELEVANT OUTCOMES By Brandon M. Armstrong Obtaining whole-animal or population-level data to evaluate the thousands of anthropogenic chemicals that exist is impractical. The U.S. National Research Council (NRC) recommended that new, predictive approaches be developed to examine toxicant effects ranging from molecular level changes in individuals to impacts on entire populations. One approach that can help meet the goals of the NRC is the adverse outcome pathway (AOP), a conceptual framework linking a single molecular initiating event to an adverse outcome at the level of the population considered relevant for risk assessment. My research is focused on the development of two AOPs; 1) Reduced fecundity in female fish due to an impairment of vitellogenin production following exposure to select neurotoxicants and 2) Reduced survival and growth of early life stage fish as a result of behavioral impairments following neurotoxicant exposure. Much of the AOP focus has been on fish reproduction, specifically the initiation of the hormonal cascade within the hypothalamic-pituitary-gonadal (HPG) axis and the formation of vitellogenin, an egg yolk precursor protein. Previous efforts modeling fish vitellogenin production were driven by gonadotropin production and did not incorporate components that influenced its release. Many end products of this hormonal cascade are controlled by the upstream production of neurotransmitters, such as gamma-aminobutyric acid and dopamine. Inclusion of a neurotransmission compartment can increase the predictive power and accuracy of the fish vitellogenin model. I hypothesized that several environmental toxicants will interact with and disrupt the function of neurotransmitter receptors and enzymes that have critical roles in vertebrate reproduction and could cause population level effects. Specifically, I explored two case studies, methylmercury (MeHg) and pulp and paper mill effluent (PPME) and their potential for neurotoxic effects on subsequent vitellogenin production. My goal was to incorporate a neurotransmission compartment into the existing fish vitellogenesis model using results from cell-free high throughput bioassays to predict adverse reproductive outcomes following exposure to contaminants. This model highlighted the importance of understanding pathway differences between species and showed a proof of principle concept for determining how perturbations to physiological systems could enhance or inhibit fish reproduction. Additionally, there is a current need for developing an AOP for fish early-life-stage toxicity as conducting traditional early-life stage tests are laborand resource-intensive and do not provide essential information regarding a chemical’s mode of action. Toxicants have been shown to cause adverse effects on larval fish behavior well below exposure concentrations that induce mortality. Behavior can be incorporated into an individual-based model (IBM) to predict how adverse effects on an individual’s behavior cause ramifications at the population level. Previous research has shown that MeHg exposure can impair larval fish behavior. I hypothesized that growth rate and survival of a larval fish population will be reduced due to impaired swimming speed and reduced foraging efficiency following MeHg exposure. My approach was to adapt a previously built IBM in order to link these sublethal behavioral effects to population relevant outcomes such as survival and growth. The last chapter uses the IBM to explore several ecological factors that may explain the recent low recruitment of yellow perch in Lake Michigan. This work highlighted the importance of assessing complex mixtures of stress including both abiotic and biotic sources which can interact and adversely affect the pelagic larval fish community. Copyright by BRANDON M. ARMSTRONG 2016

Using computational models to scale sublethal effects of stressors to adverse population outcomes in fish

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Energetic Costs of AhR Activation in Rainbow Trout (Oncorhynchus mykiss) Hepatocytes

Abstract The objective of this research was to determine the effect of freshwater acclimation on the swimming performance and plasma osmolarity of gulf killifish Fundulus grandis. Fish were acclimated to either freshwater or brackish water (10‰ salinity) for 10 d before experimentation. Plasma osmolarity was significantly lower in the freshwater-acclimated fish; however, no significant changes occurred in plasma osmolarity in fish recovering from a swim challenge at either salinity. Critical swimming speeds of the fish acclimated to freshwater were significantly lower than those of fish acclimated to brackish water. Furthermore, the swimming challenge caused 40% mortality in the freshwater fish but no mortality in the brackish-water fish. Acclimation of gulf killifish to freshwater environments appears to have a substantial metabolic cost.

Effect of freshwater acclimation on the swimming performance and plasma osmolarity of the euryhaline gulf killirish

Freshwater teleost fish often experience natural and anthropogenic conditions that result in fluctuating energy availability, therefore the ability to acquire, transform and use energy is essential for the survival of these fish. Polychlorinated biphenyls (PCB's) are recognized as physiological sources of stress to fish as they incite defense mechanisms that are generally costly in terms of metabolic resources. Over time, such responses may decrease individual performance and possibly fitness by changes in foraging, migration and escape behaviors, and the population in terms of reproductive capacity due to the alterations in energy allocation following an exposure. The main goal of this study was to determine if a sublethal exposure to PCB-126 affects the energy budget of the fish and can therefore be responsible for functional deficiencies associated with their locomotion. Fish were injected low (100 |ig/kg) and high (400 ng/kg) concentrations of PCB-126 and swimming performance parameters including critical swimming speed, metabolic rate and recovery ratios were evaluated. EROD activity was also measured in the liver as an indication of PCB-126 intoxication while blood and white muscle tissue metabolites were analyzed to quantify the physiological disturbance levels associated with this exposure. A significant decrease was observed in the swimming performance of rainbow trout for the low and high PCB-126 treatments as well as an impaired recovery with increasing level of PCB exposure following exhaustive exercise. This study also showed the occurrence of physiological disturbance by a reduction in the hepatosomatic and spleen somatic indices and elevation of plasma Cortisol and glucose levels, as well as white muscle reductions in glucose and glycogen indicating higher metabolic costs during recovery and muscle restoration for PCB-exposed fish. Overall, this research provides insights into the sublethal effects of toxic organic compounds on fish.

https://www.ruor.uottawa.ca/bitstream/10393/28868/1/MR74201.PDF

Consequences of Sublethal Polychlorinated Biphenyl Exposure on the Swimming Performance of Rainbow Trout Oncorhynchus mykiss

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Karyne M. F. Bellehumeur

Papers

Consequences of Sublethal Polychlorinated Biphenyl Exposure on the Swimming Performance of Rainbow Trout Oncorhynchus mykiss

Swimming Performance of Rainbow Trout Oncorhynchus mykiss