Toxicity of pentachlorophenol to trout alevins Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/wh246x39h

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  • A study was conducted at the Pacific Cooperative Water Pollution and Fisheries Research Laboratories, Oregon State University, to determine the effects of pentachlorophenol (PCP) on the early developmental stages of the steelhead trout (Salmo gairdneri). Experiments were performed from May, 1965, through May, 1968, on the survival, growth, and bioenergetics of embryos, alevins, and juveniles exposed to sodium pentachlorophenate (NaPCP). A technical grade sodium salt of PCP was used in all experiments. Preliminary static bioassays were conducted to determine the concentrations of NaPCP which were lethal to embryos and alevins. In an experiment where embryos were exposed to NaPCP from fertilization to hatching, 100% mortality occurred within 1 week after fertilization at concentrations down to 300 ppb; within 24 hours post-hatch, 100% mortality occurred down to 50 ppb of NaPCP. Alevin dry weight at hatch was decreased by exposure to NaPCP, and hatching was delayed. In 5-day bioassays, alevins usually died within 24 hours at concentrations down to 200 ppb; but little mortality occurred at lower concentrations. Seven experiments were subsequently conducted with alevins (20-41 days duration), one with juveniles (21 days), and one with embryos and alevins (92 days). In all but one experiment, alevins were denied exogenous food and grew to a maximum weight before starvation occurred when the yolk supply was exhausted. Holding alevins in 30 to 100 ppb of NaPCP throughout the alevin stage, retarded growth, increased yolk catabolism, and increased mortality. Little mortality occurred during the first week; but after 3 to 4 weeks, mortality was nearly complete at 70 and 100 ppb. An NaPCP concentration of 45 ppb caused little mortality and no mortality occurred at 30 ppb or in controls (no NaPCP). Maximum dry weight gain of alevins reared in NaPCP was decreased approximately 6% for each 10 ppb increase in NaPCP concentration. Intermittent exposure of alevins to NaPCP indicated that recovery from toxic effects occurred within several days after removal from NaPCP. In the only experiment where alevins were given an exogenous food, the dry weight gain 57 days post-hatch of alevins in 40 ppb NaPCP was reduced about 75% from that of controls (33mg vs 120mg). Controls began feeding after 20 days post-hatch, while in NaPCP, feeding began about 40 days post-hatch. Juvenile steelhead held in 30 and 70 ppb NaPCP for 3 weeks showed retardation of growth but little mortality, indicating a greater tolerance to NaPCP than alevins or embryos. Continuous exposure to NaPCP from fertilization to complete yolk absorption produced 100% mortality at 40 ppb of NaPCP but little mortality at 20 or 10 ppb. However, at 5 mg/liter dissolved oxygen concentration, 20 ppb was 100% lethal and at 3 mg/liter, 10 ppb was 100% lethal. Little mortality occurred at these oxygen levels in the absence of NaPCP. Oxygen consumption rates of alevins in 40 ppb of NaPCP were higher than those of control alevins at 1 0 and 5 mg/liter of dissolved oxygen but not at 3 mg/liter. While determinations of oxygen consumption, growth, and yolk utilization efficiency were too gross to produce definitive information as to the mechanism of action of PCP, the bioenergetic data obtained in this study were consistent with the concept that PCP disrupts energy metabolism. Alevins exposed to NaPCP grew less rapidly than controls due to higher rates of yolk catabolism and resultant lower efficiencies of yolk utilization. Congruently, NaPCP reared alevins also had higher rates of oxygen consumption.
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