The aim of this thesis is to develop empirical models of the stable catch of brook trout in the Laurentian lakes of Quebec. Current estimators of fish yield are biased and predict poorly. / A model resulting from this study shows that catch increases with fishing effort, but that the rate of increase is smaller at higher effort. For a given effort, the catch-per-unit of effort (CPUE) is greater in larger lakes. Catch is also greater in phosphorus rich lakes and smaller in acid lakes. Catch of bigger fish is associated with a lower CPUE. / No dome-shaped relationship between catch and effort, standardized for the effects of lakes characteristics, could be established. Thus the maximum sustainable yield (MSY) concept provides no guidelines for management of the fishery. However, an early warning of overexploitation is an exceptionally high rate of fishing success. In addition logistic regression based on easily obtained variables can predict the likelihood of stability of the fisheries.

Municipal wastewater effluent (MWWE) is an important source of pollution in the aquatic environment impacting fish. MWWE is a complex mixture of chemicals including pharmaceuticals, personal care products, industrial chemicals and pesticides. A link between reproductive endocrine disruption and MWWE exposure has been established in fish, but less is known about the effects of MWWE on non-reproductive endocrine disruption. The overall objective of this thesis was to examine the impacts of MWWE exposure on the stress response and intermediary metabolism in rainbow trout (Oncorhynchus mykiss). In fish, the primary adaptive organismal stress response involves the activation of hypothalamic-sympathetic-chromaffin axis to produce catecholamines, predominantly epinephrine, and the hypothalamic-pituitary-interrenal (HPI) axis to produce cortisol. Both of these hormones play a key role in elevating plasma glucose levels that is essential to fuel the increased energy demand associated with stress. Along with the organismal stress response, the cellular stress response, involving the synthesis of a suite of heat shock proteins (hsps), also plays an important role in protecting cellular protein homeostasis in response to stressors, including toxicants. The impact of MWWE on stress-related pathways were identified using a low-density trout cDNA microarray enriched with genes encoding for proteins involved in endocrine-, stress- and metabolism-related processes. This was further confirmed by assessing plasma hormone and metabolite levels and stress-related targeted genes and proteins expression and enzyme activities in select tissues in rainbow trout. Studies were carried out in controlled field (caging) and laboratory experiments to examine the impacts of MWWE on stress and tissue-specific metabolic responses in rainbow trout. Further in vitro studies using rainbow trout hepatocytes in primary cultures were carried out to investigate the mechanism of action of two pharmaceuticals, atenolol and venlafaxine, found in relatively high concentrations in MWWE in impacting the stress-mediated glucose response. In caged fish, MWWE exposure significantly elevated plasma cortisol and glucose concentrations, and altered the mRNA abundance of a number of stress-related genes, hormone receptors, glucose transporter 2 and genes related to immune function. When fish were exposed to an acute handling stress following a 14 d exposure to MWWE, the cortisol response was abolished and the glucose response was attenuated. The effects on cortisol did not correlate with changes in the expression of genes involved in cortisol biosynthesis, but were associated with an increase in hepatic glucocorticoid receptor (GR) protein expression. Upon further investigation in controlled laboratory studies, MWWE exposure elevated constitutive hsp 70 and hsp90 expression after 8 d exposure, which correlated with a decrease in glycogen levels in the liver in fish exposed to a high concentration of MWWE compared to control fish, pointing to a MWWE-induced increase in liver energy demand. By 14 d, glycogen stores were replenished, and this was commensurate with increases in liver gluconeogenic capacity, including increases in the activities of phosphoenolpyruvate carboxykinase (PEPCK) and alanine aminotransferase (AlaAT), along with a decrease in liver GR expression. In the heart, GR protein expression increased in treated fish, and the activity of pyruvate kinase increased, indicating an increase in glycolytic capacity. Subjecting the MWWE exposed fish to a secondary handling disturbance (acute stress) led to an attenuated plasma cortisol and glucose response compared to the control group. This corresponded with a reduced liver gluconeogenic capacity and a lower liver and heart glycolytic capacities, reflecting a disturbance in the energy substrate repartitioning that is essential to cope with stress. While it is difficult to establish causative agents from a complex mixture such as MWWE, the two pharmaceutical that were tested impacted glucose production. Specifically, atenolol and venlafaxine disrupted the epinephrine-induced glucose production, but did not modify cortisol-mediated glucose production in trout hepatocytes. The suppression of epinephrine-mediated glucose production by atenolol and venlafaxine was abolished by cAMP analogue (8-bromo cAMP) or glucagon (a metabolic hormone that increases glucose production). This suggests that both drugs disrupt β-adrenoceptor signaling, while it remains to be determined if the response is receptor isoform-specific. Altogether MWWE exposure disrupts the organismal and cellular stress responses in trout. Key targets for MWWE impact leading to the impaired cortisol and metabolic responses to stress include liver and heart GR expression, liver gluconeogenic capacity, and liver, heart and gill glycolytic capacities. Most significantly, MWWE impairs the ability to metabolically adjust to a secondary acute stressor, which is an important adaptive process that is integral to successful stress performance. From an environmental stand-point, long-term exposure to MWWE will lead to reduced fitness and will compromise the capacity of fish to cope with additional stressor, including escape from predators.

No description available.

Proteinase P-II purified from parasitized Pacific whiting muscle was previously identified to be one form of cathepsin L. It appeared to be present in three isozymatic forms on non-denaturing PAGE gel stained for activity. Its autolytic degradation was observed on SDS-PAGE gel under its optimum condition, 55°C and pH 5.5, in the absence of substrate. Amino acid composition analysis revealed that this enzyme had a considerably greater proportion of hydrophobic amino acids than cathepsin L from other fish species, and monosaccharide analysis showed it was not glycosylated. The N-terminal amino acid sequence of the enzyme was 60-65% identical with cathepsin L from chicken and mammalian species, but only 39% identical with mammalian cathepsin B. The moderate identity of the N-terminal amino acid sequence of P-II with other cathepsin L revealed that this cysteine proteinase from Pacific whiting might be encoded by a cathepsin L-related gene. Two degenerate primers were designed to clone cathepsins cDNA from rainbow trout. The 500-bp PCR product from rainbow trout liver cDNA contained at least three different cysteine proteinase sequences, referred to as SFL2, SFL5, and SFL17. SFL5 was the partial cDNA of trout cathepsin L, which was over 80% identical with chicken cathepsin L amino acid sequence. SFL5 was labeled with Dig-11-dUTP and used to screen a trout liver cDNA library. One positive clone referred to as LC was identified and contained a 700-bp insertion overlapping with SFL5. By combining the two overlapping sequences, a 895-bp cDNA sequence was identified, which included 88% of the mature enzyme and a 307-bp 3' end untranslated part. Its deduced amino acid sequences had 83% identity, 91% similarity with chicken cathepsin L and 73% identity, 86% similarity with human cathepsin L. SFL2 might be the partial cDNA of a novel cathepsin L-related cysteine proteinase. SFL17 may be the partial cDNA of trout cathepsin K. It had 70% identity and 89% similarity with rabbit and human cathepsin K at the amino acid level. / Graduation date: 1996

The introduction of trout has been implicated in the declines in native fish fauna in New Zealand and worldwide. Since the introduction of brown (Salmo trutta) and rainbow (Oncorhynchus mykiss) trout to New Zealand in 1867, their distribution has spread and they have been implicated in the fragmentation of native fish distributions, particularly native non-migratory galaxiids. However, in the Upper Waimakariri basin the co-occurrence of trout and galaxiid populations is relatively common, even in streams where trout reach sizes known to be piscivorous. To investigate mechanisms that may regulate trout and galaxiid co-occurrence, I investigated differences in antipredator behaviour and growth rate between stream types with varying levels of trout presence. Using quantitative survey data collected between 1997 and 2006, I found that trout abundance was low and varied annually in frequently disturbed sites compared their high abundance in stable streams. This finding was used to classify streams into three population types, barrier (trout absent), disturbed (trout presence intermittent) and sympatric (constant trout presence). Using this classification, I tested the effects of trout chemical cues on galaxiid activity and refuge use in artificial channels. There were no differences in activity or refuge use between trout odour and there were no effects of population type or galaxiid size during both the day and the night. Using otolith weight-fish length relationships in galaxiids collected from each population type, I found that galaxiid growth rate was higher in disturbed streams than in stable streams either with or without trout. An experiment manipulating trout size and presence, over two months in a natural stream, found galaxiids from treatments without trout grew slower than those with trout. Slow growth rates in galaxiids above trout-migration barriers and in sympatry, combined with low growth rates in treatments without trout suggest that the mechanisms that regulate galaxiid growth are more complex than previously thought.

Thesis (M.S.)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: Alexander V. Zale. Includes bibliographical references (leaves 93-103).

Thesis (M.S.)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: Alexander V. Zale. Includes bibliographical references (leaves 84-96).

Thesis (M.S.)--University of Nevada, Reno, 2007. / "August 2007." Includes bibliographical references (leaves 40-44). Online version available on the World Wide Web.

Thesis (M.S.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains vii, 115 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1994. / Vita. Abstract. Includes bibliographical references (leaves 59-61). Also available via the Internet.