Thesis (Ph. D.)--University of Washington, 1990. / Vita. Includes bibliographical references (leaves [109]-120).

Thesis (Ph.D.) -- McMaster University, 2001. / Includes bibliographical references. Also available via World Wide Web.

Aflatoxin B₁ (AFB₁) is a mold-produced toxin which has been shown to be a potent hepatocarcinogen in many animal species. Of the species studied thus far, rainbow trout have proven to be the most sensitive. Experiments were conducted to investigate various aspects of AFB₁ metabolism in this species, including in vitro mutagenesis, and effects of dietary modifiers of AFB, carcinogenesis on in vitro metabolism and mutagenesis. A comparative study of AFB₁ metabolism in two salmonid species was also conducted. In the first study, the relative mutagenic potencies of several alfatoxin metabolites were evaluated using a trout liver fraction system. Preliminary studies characterizing trout liver fractions for use as an activation system were described. The results from comparative mutagenicity experiments demonstrated that in vitro mutagenic potencies qualitatively correlated with the in vivo carcinogenic activities of various aflatoxins in rainbow trout. The importance of these findings is discussed. In the second study fish hepatocytes were characterized to examine possible differences in activation of AFB₁ to bacterial mutagens by hepatocytes from rainbow trout and coho salmon, two species which are known to differ markedly in sensitivity to the carcinogenic effects of AFB₁. Activation efficiency was approximately three times greater in hepatocytes from trout compared to salmon. A more marked difference was seen when S20 liver fractions from the two species were used. Analysis of unbound [³H]AFB₁ metabolites revealed that trout hepatocytes metabolized [³H]AFB₁ to a greater extent than salmon. The results accurately reflected in vivo carcinogenesis trends in salmonid fish. Additional experiments were conducted to evaluate the effects of dietary modifiers of AFB₁ carcinogenesis on in vitro mutagenesis and metabolism of AFB₁. Dietary β-naphthoflavone (β-NF) was shown to induce the production of a novel trout metabolite of AFB₁, aflatoxicol M₁ (AFL-M₁). AFL-M₁ exhibited a mutagenic potency less than AFB₁ or aflatoxicol (AFL), but greater than that of aflatoxin-M₁ (AFM₁). Dietary β-NF, however, appeared to have no effect on in vitro mutagenic activation of AFB₁ using hepatocytes or liver S20 fraction from trout. Dietary PCBs (Aroclor 1254) was shown to significantly decrease in vitro mutagenesis of AFB₁, which reflected a similar PCB-mediated inhibitory effect on AFB₁ carcinogenesis in trout in vivo. Cyclopropenoid fatty acids (CPFAs) present in the diet (0-600 ppm) were shown to have no effect on in vitro mutagenesis of AFB₁, indicating CPFAs may not significantly alter in vivo initiation of AFB₁ carcinogenesis. / Graduation date: 1983

Triplicate groups of rainbow trout (Salmo gairdneri) fed six diets; five based on fish protein concentrate (FPC) ranging in caloric density from 4.36 to 6.19 kcal/g, and one based on vitamin free casein with a caloric density of 5.26 kcal/g were evaluated with respect to diet ingredient utilization. The parameters used to evaluate efficiency of diet utilization were: feed conversion, energy and protein conversion, and growth. The desirability of the edible portion of the fish produced on the different treatments from a flavor and texture standpoint was determined. The protein level was maintained at 38% of the dry diet, with 7.8% supplied by gelatin and the remainder by either FPC or casein. The herring oil levels of the diets ranged from 25% to 45% of the dry diet, and was the primary source of calories. Alpha-cellulose was included as a filler and ranged from 12.2% to 31.2% of the dry diet. The FPC based diets produced statistically superior weight gains when compared to the casein based diet. The efficiency of feed conversion was improved as the level of herring oil was increased. The energy and protein conversions were relatively constant for the FPC based diets, with the casein based diet being lower (P < 0.05). / Graduation date: 1975

The fundamental objective of this analysis was to isolate and identify the factors governing the demand for domestically produced rainbow trout in a representative west coast market, and assess the impact on that demand, if any, of the introduction of pansize salmon. The approach taken in this market demand study was to identify those variables hypothesized to determine supply and demand for rainbow trout. Several testable hypotheses concerning the anticipated relationships were specified. It was hypothesized that a negative relationship would exist between the price of trout at the brokerage level and the quantity demanded at that level. Conversely, the price of trout at the wholesale level was hypothesized to be positively correlated with the quantity of rainbow trout demanded at the brokerage level. Further, the signs on the coefficients of variables accounting for the wholesale prices of substitute items were expected to be negative, while comparable prices at the brokerage level should be positive, based upon the hypothesis. It was hypothesized that the presence of Japanese trout in the market place would have a negative impact on the quantity of domestically produced trout demanded. Personal disposable income was hypothesized to be positively correlated with the quantity of trout demanded. Expectations were that seasonal factors tend to cause trout demand to fluctuate cyclically. An econometric simultaneous equations model was specified from which estimates of the parameters of the demand equation were obtained using Two Stage Least Squares techniques. A recognition of the limitations associated with the available data set necessitates the emphasizing of the preliminary nature of these results. Data on quantities and prices of rainbow trout and equivalent price series for hypothesized substitutes were obtained through personal interviews with market participants and close observers thereof. The results of the study, while preliminary, tend to support the original set of hypotheses concerning the interrelationships between quantity of domestic trout demanded and own-price, the price of close substitutes and seasonal demand fluctuations. Somewhat unexpectedly, the regression seems to have uncovered a negative income/quantity demanded relationship for rainbow trout. This raises some interesting questions which might best be addressed in terms of hypotheses for future analysis. / Graduation date: 1977

Graduation date: 1973

Thesis (Ph. D., Animal Physiology)--University of Idaho, June 2009. / Major professor: Ronald W. Hardy. Includes bibliographical references. Also available online (PDF file) by subscription or by purchasing the individual file.

Thesis (M.S.)--Tennessee Technological University, 2009. / Title from title page screen (viewed on June 29, 2010). Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 1987. / Vita. Bibliography: leaves [68]-81.

Studies were carried out to determine the influence of the change in the acid-base status of the blood on regulation of pH in relation to control of ventilation in the rainbow trout. By placing trout in ventilation (VG) boxes direct measurement of ventilation volume and rate could be made. Arterial blood was collected via chronically implanted catheters in the dorsal aorta; these catheters also allowing administration of the various acids and bases. The first series of experiments were designed to determine ventilatory responses to high ambient PCO₂ levels (hypercapnia) and the effect on regulation of arterial blood pH. Both short-term (up to 8 hours) and long-term (up to 72 hours) exposures were studied. PaO₂ levels remained saturated, or nearly so, throughout these experiments. The general response to high PCO₂ levels is an increase in the ventilatory stroke volume, this being mainly due to an increase in rather than VG. Compensation of ventilation during the sustained hypercapnia is slow, taking up to 3 days. Arterial H⁺ levels increased during CO₂ exposure, increasing from a control level of 11.8 ± 0.5 to 41.0 ± 3.5 nM/L within 5 minutes. There is a gradual decrease in arterial H⁺ concentration such that at 72 hours it is near normal. The time course of compensation for both VG and pHa coincide. The hypercapnia experiments indicate that in the face of an increase in ambient PCO₂ trout do not adjust the PCO₂, difference (ΔPCO₂ between arterial blood and water. PaCO₂ changes in proportion to the change in PICO₂ such that PaCO₂ is always about 2 mm Hg above ambient, demonstrating that ΔPCO₂ is not affected by changes in ventilation. The change in arterial blood pH is shown to be related to the transfer of CO₂ rather than by a transfer of H⁺ ions from water to blood. Arterial blood pH is regulated via adjustment of blood HCO⁻₃ levels, adjustment being in the order of 2 - 3 days. HCO⁻₃ can be regulated, or adjusted by either the kidney or the gills. The role of the kidney was shown to be minor in the adjustment of a NaHCO₃ induced alkalosis. Uptake of HCO⁻₃ is shown to occur when fish are placed in NaHCO₃ containing water, demonstrating the role of the gills in the amelioration of arterial blood pH. These observations are discussed in relation to a HCO⁻₃/Cl⁻ exchange. The ventilation volume is dependent on an increase in PaCO₂ and/or PICO₂ and not to pHa or pHI. A decrease in pHI, although causing a fall in pHa, has only a delayed effect on VG. The response in VG is transient. It is postulated that receptors are either adapting or are not located in the blood or water but in another compartment whose contents or properties change in proportion to ventilation. It is hypothesized that a chemosens.itive area may exist on the ventrolateral surface of the medulla as in mammals. Perfusion of the cranial cavity of trout with mock CSF, in which CO₂-HGO⁻₃ was altered, did not elicit respiratory responses. These experiments do not preclude the existence of medullary chemoreceptors. These results are consistent with the hypothesis that ventilation in trout is dependent on the CO₂ tension within the body or elsewhere and that blood pH levels are regulated via ionic exchange mechanisms at the gill surface, rather than by ion exchange at the kidney or by diffusive washout of gaseous CO₂ via ventilation. / Science, Faculty of / Zoology, Department of / Graduate