No description available.

A literature review shows that qualitative dichotomies describing interspecific differences in the movement patterns of foraging animals are widely-used and biologically important, but fraught with ambiguity. Consistent use of the terminology from foraging theory and stronger quantification are proposed to increase clarity and facilitate more rigorous tests of hypotheses. Greater consideration of intraspecific variation is also needed. In forest bird and lizard communities, move-frequency distributions are bimodal, supporting a dichotomous view, but there is important variation within the statistical modes. Fish species with more red muscle are more mobile than species with less red muscle, but the frequency distribution of the proportion of red muscle does not match subjective, dichotomous classifications. A quantitative field investigation of foraging young-of-the-year brook charr (Salvelinus fontinalis) reveals significant individual differences in movement patterns that are more strongly related to microhabitat use and diet, than to morphological and environmental parameters thought to influence swimming capability.

1,2-Dibromo-4-(1,2 dibromoethyl)cyclohexane or tetrabromoethylcyclohexane (TBECH) is an additive bromine based flame retardant used primarily in expandable polystyrene beads that are used mainly to produce thermal insulation for housing. Secondary uses include extrusion into polystyrene foam, adhesive in fabric and vinyl lamination, electrical cable coatings and construction materials. The technical formulation contains two diastereoisomers, α- and β-, which are present in equimolar amounts. Under elevated temperatures two other isomers, γ- and δ-, can be formed. The recent detection of TBECH in the environment and suggestions that all four isomers are androgenic prompted me to examine the bioaccumulation and biochemical effects of one of the isomers, β-, in a controlled laboratory environment. I purposely chose to examine this isomer as it has been detected in biota. Juvenile brown trout (Salmo trutta) were exposed to three different amounts of the β-isomer via their to three different amounts of the β-isomer via their food for 56 days (uptake phase). This was followed by a depuration phase in which all fish were exposed to unfortified food for 77 days. A fourth group of fish were exposed to unfortified food for the duration of the experiment. On days 0, 7, 14, 35, 49, 56, 63, 77, 91, 105, and 133 eight fish from each treatment group were sacrificed and liver, plasma, thyroid and gonad gland were collected and whole-fish (carcass minus tissues above) were collected. Residues of β-isomer were analyzed in the whole-fish and in liver extracts by gas chromatography mass spectrometry in the electron ionization while estradiol (E2), 11-ketotestosterone (11-KT) and testosterone (T) were extracted from plasma and analysed by liquid chromatography tandem mass spectrometry. The bioaccumulation of β-isomer was similar in fish from all treatment groups with steady-state occurring before the end of the uptake phase. Depuration of the β-isomer from fish obeyed first order kinetics and there were no statistically significant differences in the depuration half life (t1/2) among the treatment groups: 22.5 ± 10.4 (low), 13.5 ± 5.9 (med) and 13.8 ± 2.2 (high) days. Steady-state biomagnification factors were much smaller than 1 for fish in all treatment groups. I was unable to detect debrominated metabolites in liver or whole-fish extracts and I also found no evidence of isomerization of the β-isomer to other isoforms in vivo. While there were some differences in E2, T and 11-KT levels in plasma of fish from the treated groups relative to plasma in fish from the control group there were no clear, consistent, discerning trends.

The molecular biology of macrophage activating and deactivating cytokines and their receptors was discussed. Comparison of IFN-γ amino acid sequences of several mammalian species reveals a low conservation of amino acids. The interaction of IFN-γ with its receptor system is complicated and coherent with the species specificity of IFN-γ. Identification by PCR of an IFN-γ-like gene in the trout genome was not possible. In contrast with IFN-γ, TGF-β is very conserved in its amino acid sequence. The PCR-amplification of a TGF-β fragment from amphibian, <I>Xenopus</I>, and rainbow trout cDNA libraries was possible. Two oligonucleotide primers were used in PCRs to amplify a 360 bp fragment of trout Mhc class II β chain. Using these two oligos, this 360 bp fragment could be amplified from trout spleen cDNA library and HK leucocytes. cDNA synthesized from RNA extracted from ConA/PMA stimulated HK leucocytes was used as template DNA in PCR, and a class II specific fragment was amplified. This class II fragment could not be amplified from HK macrophages treated with a MAF containing supernatant, although HK macrophages treated with a control supernatant did express class II molecules. This could suggest that priming or activation of trout macrophages results in a decreased expression of Mhc class II antigens. A novel method for analysing 5'nucleotidase activity of head kidney macrophages was optimised for use with cell monolayers, with respect to the effect of cell numbers, temperature and substrate concentration. Both lysed and whole cells could be used for determination of 5'nucleotidase activity. Maximal 5'nucleotidase activity was found in the range of 27°C to 33°C and using a substrate concentration of ≥ 1 μmol AMP ml^-1 for whole cells and ≥ 1.5 μmol AMP ml^-1 for lysed cells. 5'nucleotidase activity was also correlated with respiratory burst activity in cells treated with a variety of supernatants containing MAF activity. A significant inverse relationship between these two activities was found. MAF-treated cells were also found to lose 5'nucleotidase activity faster than control cells in the presence of cycloheximide, suggesting such cells may have a higher membrane turnover of this enzyme.

Over the recent years, venlafaxine has become the predominant antidepressant drug detected in municipal wastewater effluents (MWWE) and aquatic systems. However, very little is known about the effect of this drug in the aquatic environment on non-target organisms, including fish. Venlafaxine is a pharmaceutical compound designed to inhibit serotonin and norepinephrine reuptake, thereby increasing the synaptic availability of these neurotransmitters. In teleosts, the key aspect of stress adaptation involves the activation of the hypothalamus-pituitary-interrenal (HPI) axis, leading to the production of cortisol. Given that monoamine neurotransmitters (serotonin, norepinephrine, and dopamine) are involved in the regulation of a wide range of neuroendocrine responses, including stress axis function, my primary hypothesis was that venlafaxine acts as a neuroendocrine disruptor impacting the functioning of the corticosteroid stress axis in rainbow trout (Oncorhynchus mykiss). This hypothesis was tested through a series of in vivo exposure studies, as well as in vitro experiments, using environmentally relevant levels of venlafaxine, in order to tease out potential mode of action of this drug on target tissues involved in HPI axis functioning. The results suggest that venlafaxine alters monoamine neurotransmitter levels and their turnover rates in a region-specific manner in trout brain, and that the midbrain is the prime target. The monoamine changes may be responsible for the downstream effects on neuroendocrine responses coordinated in the hypothalamus, as this region receives monoaminergic inputs from the midbrain. The functional relevance of the above finding was confirmed by showing that venlafaxine exposure disrupted the neuroendocrine responses associated with social stress and appetite regulation. Functional downstream effects of HPI axis dysfunction were further confirmed by subjecting the fish to a handling disturbance, which revealed that the highly conserved cortisol and glucose responses to stressors were disrupted by venlafaxine. Also, there were tissue-specific effects of venlafaxine exposure on metabolic capacities, including enhanced gluconeogenesis and amino acid catabolism in the liver (a key glucose producing tissue), and alterations in the glycolytic capacity and sodium potassium ATPase activity in the gill (a key glucose utilizing tissue). The results suggest that the mode of action of venlafaxine may involve disruption of each target tissue involved in the HPI axis functioning. In vitro mechanistic studies indicated that hypothalamus functioning is disrupted by venlafaxine and this may involve effects mediated by serotonergic pathways. The reduced phosphorylation of cAMP response element binding protein (CREB) suggests that venlafaxine may impact downstream signalling cascades that are CREB-dependent. The transcript changes observed with venlafaxine in the hypothalamus include changes in mRNA levels of key genes involved in appetite regulation and stress response, including corticotropin releasing factor (CRF) and neuropeptide Y (NPY). At the pituitary level, venlafaxine impaired adrenocorticotropic hormone (ACTH) production, and this involved disruption of corticotropin releasing factor-receptor type 1 (CRF-R1), which is a key sensor for CRF stimulation. At the interrenal tissue level, the responsiveness of steroidogenic cells to ACTH stimulation was altered by venlafaxine and the mode of action appears to involve pathways upstream of the intracellular cAMP production. Also, cortisol biosynthetic capacity was disrupted by venlafaxine and this was accompanied by changes in transcript abundances of steroidogenic acute regulatory protein and cytochrome P450 side chain cleavage in the interrenal tissue. Taken together, the results demonstrate for the first time that the antidepressant venlafaxine, a human pharmaceutical contaminating aquatic systems, disrupts neuroendocrine responses and affects stress, feeding and metabolic responses in rainbow trout. The mode of action may include disruptions in brain monoamine levels and pathways involved in CREB signalling, while the exact mechanism of action remains to be elucidated. Exposure of fish to this pharmaceutical drug adversely affects the highly conserved adaptive responses that are essential to cope with subsequent stressors, and may translate into reduced fitness over the long-term. The findings underscore the necessity to understand the mechanisms of action of chemicals present in MWWE, and develop and utilize effective risk management strategies aimed at minimizing discharge of pharmaceuticals into the aquatic environment.

1,2-Dibromo-4-(1,2 dibromoethyl)cyclohexane or tetrabromoethylcyclohexane (TBECH) is an additive bromine based flame retardant used primarily in expandable polystyrene beads that are used mainly to produce thermal insulation for housing. Secondary uses include extrusion into polystyrene foam, adhesive in fabric and vinyl lamination, electrical cable coatings and construction materials. The technical formulation contains two diastereoisomers, α- and β-, which are present in equimolar amounts. Under elevated temperatures two other isomers, γ- and δ-, can be formed. The recent detection of TBECH in the environment and suggestions that all four isomers are androgenic prompted me to examine the bioaccumulation and biochemical effects of one of the isomers, β-, in a controlled laboratory environment. I purposely chose to examine this isomer as it has been detected in biota. Juvenile brown trout (Salmo trutta) were exposed to three different amounts of the β-isomer via their to three different amounts of the β-isomer via their food for 56 days (uptake phase). This was followed by a depuration phase in which all fish were exposed to unfortified food for 77 days. A fourth group of fish were exposed to unfortified food for the duration of the experiment. On days 0, 7, 14, 35, 49, 56, 63, 77, 91, 105, and 133 eight fish from each treatment group were sacrificed and liver, plasma, thyroid and gonad gland were collected and whole-fish (carcass minus tissues above) were collected. Residues of β-isomer were analyzed in the whole-fish and in liver extracts by gas chromatography mass spectrometry in the electron ionization while estradiol (E2), 11-ketotestosterone (11-KT) and testosterone (T) were extracted from plasma and analysed by liquid chromatography tandem mass spectrometry. The bioaccumulation of β-isomer was similar in fish from all treatment groups with steady-state occurring before the end of the uptake phase. Depuration of the β-isomer from fish obeyed first order kinetics and there were no statistically significant differences in the depuration half life (t1/2) among the treatment groups: 22.5 ± 10.4 (low), 13.5 ± 5.9 (med) and 13.8 ± 2.2 (high) days. Steady-state biomagnification factors were much smaller than 1 for fish in all treatment groups. I was unable to detect debrominated metabolites in liver or whole-fish extracts and I also found no evidence of isomerization of the β-isomer to other isoforms in vivo. While there were some differences in E2, T and 11-KT levels in plasma of fish from the treated groups relative to plasma in fish from the control group there were no clear, consistent, discerning trends.

Carotenoid utilization in rainbow trout (Oncorhynchus mykiss Walbaum) and Atlantic salmon (Salmo salar L.) has been investigated with respect to tissue distribution of carotenoids and the role of the liver on the bioavailability of the lipid soluble carotenoids, astaxanthin and canthaxanthin. Species-specific and tissue-specific accumulations were noted for astaxanthin and canthaxanthin in the rainbow trout and Atlantic salmon, possibly indicating fundamental differences in their utilization in these species. The liver and the kidney were revealed to be the major tissues involved in carotenoid metabolism in both rainbow trout and Atlantic salmon. Apparent digestibilities (-96% and -30% for rainbow trout and Atlantic salmon, respectively) and flesh carotenoid retentions (-12% and -5.4% for rainbow trout and Atlantic salmon, respectively) differed significantly between species, suggesting that rainbow trout are more efficient depositors of carotenoids within the flesh. Isolated rainbow trout liver perfusion experiments revealed small differences in the uptake of astaxanthin and canthaxanthin. Uptake of astaxanthin in both synthetically-derived and serum-derived models showed saturable uptake mechanism that occurred earlier than for canthaxanthin. These results can potentially offer an explanation for the better utilization of astaxanthin in rainbow trout, where the liver reduces the bioavailability of canthaxanthin through continued uptake. Results show a low hepatic extraction ratio (0.03-0.07), in line with published post-prandial elimination rates. Neither astaxanthin nor canthaxanthin significantly induced hepatic or renal xenobiotic-metabolizing enzymes in the rainbow trout, contrary to published reports in rats and mice. This may imply fundamental species-specific differences in the metabolic pathways for these carotenoids. Histochemical investigations revealed that both carotenoids significantly impacted liver structure, resulting in higher levels of total lipids and mucopolysaccharides. This is thought to be due to their antioxidant functions and their provitamin A activity. Carotenoid-treated fish also had higher levels of glycogen phosphorylase in liver sections, providing the first evidence in fish for the possibility of glucuronidation of their metabolites. The present investigations demonstrate the liver to be a major organ in carotenoid metabolism, and consequently affects carotenoid distribution and availability. In addition, carotenoid supplementation significantly affects liver structure and may potentially enhance its function. Furthermore, these investigations have provided new avenues of investigation into the use of isolated organ perfusions for biochemical nutrition research, and expanded the knowledge of liver physiology and biochemistry.

No description available.

Metabolic power budgeting, the regulation of metabolism with respect ot metabolic scope, was studied in the laboratory in zebra fish using respirometry, and in the field on pike using heart-rate telemetry. Increased food consumption by zebra fish resulted in higher growth, mortality and metabolism. The magnitudes of the components of metabolism: maximum metabolism, standard metabolism, routine metabolism and feeding metabolism were measured. Power budgets for zebra fish fed high and low rations were constructed. Fish fed high rations worked harder than fish fed lower rations, but were apparently not working near the upper limit of the metabolic scope. Possible mechanisms for growth-related mortality are considered. Biological information on the populations of pike in Lochs Kinord and Davan (Grampian Highlands) were gathered. The population of L. Kinord was dominated by young, small fish; apparently due to exploitation. L. Davan is unexploited and had a pike population consisting of a much wider range of ages and sizes. Methods for assessing regurgitation by pike were developed. Effects of long and short-term temperature fluctuations, and feeding on heart rate of captive pike were studied. Resting heart rate increased exponentially with increasing temperature; heart rate appeared to accommodate all changes in resting metabolism. Post-prandial heart-rate records could be used to accurately estimate meal size. Gastric evacuation rates corresponded to digestion times estimated from heart-rate records. Heart-rate telemetry was used to study metabolic power budgeting, feeding and activity of wild pike from Lochs Kinord and Davan in June 1988. Pike worked mainly at low power levels relative to metabolic scope. Tachycardias associated with localized movement were frequent, and such movement was accurately recorded by heart-rate telemetry but frequently undetected by conventional means. Feeding events were identified and the metabolic costs of survival estimated. Some unusually energetically-expensive localized movements were recorded; the possible reasons for this are discussed. Intraperitoneal implantation techniques were developed for transmitter attachment on pike. Experments using dummy transmitters on pike and rainbow trout showed no effect on growth, survival or reproduction, but tissue reactions differed. Male and female pike, location-tracked with implanted transmitters before, during and after spawning time exhibited increased overall activity during the apparent spawning period, as well as changes in diet activity. Males were significantly more active than females in three out of seven weeks. Spawning appears to be a period of high energy expenditure for pike.

The Scottish brown trout (Salmo trutta L.) is identified as an important resource which requires responsible and continual management. This study was divided into two parts; an electrophoretic survey of wild trout populations in Scotland, and a quantitative assessment of the genetic component to growth rate in various stocks, grown under hatchery and farm conditions. Sixty wild populations were sampled by various methods. All fish were typed using brain, eye, heart, liver and muscle tissue and starch gel electrophoresis for thirty four enzyme loci, thirteen of which were found to be polymorphic. Gene diversity analysis was conducted on the data collected, 33% of the diversity being attributed to differences between populations, much of the variation was thought to be due to founder effects. Evidence is presented to support a hypothesis that the trout in Scotland are derived from two main post glacial invasion stocks. Future management strategies for wild stocks of Scottish brown trout are discussed. Growth trials were conducted at Howietoun fish farm in order to calculate heritability estimates for growth rate. Hierarchical and factoral crossing schemes were employed, using broodstock from three stocks. Heritability estimates for growth rate were found to be high and it was concluded, significant genetic gains could be achieved if growth rate was the only trait of commercial interest and truncated mass selection was adopted. Attempts were made to investigate the relationship between heterozygosity and growth rate in the hatchery populations. It was concluded that more data were required to make a meaningful assessment, but from this study little evidence exists for a positive correlation between heterozygosity and growth rate. Correlations between early life cycle stages and subsequent growth are discussed.