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|Title:||Mechanisms of copper toxicity and acclimation to copper in rainbow trout (Salmo gairdneri R.)|
|Authors:||Lauren, Jon Darrel|
|Department:||Physiology and Pharmacology|
|Abstract:||<p>Experiments were conducted on rainbow trout to analyse 1) the physiological mechanisms of short-term copper toxicity, 2) the effects of water hardness, pH, and alkalinity on copper toxicity, and 3) the physiological and biochemical mechanisms of acclimation to copper toxicity. Unidirectional and net sodium fluxes were the basic parameters measured. Disruption of the ionoregulatory functions of the gill accounted for short-term (24 h) and long-term (28 day) copper toxicity. Copper inhibited sodium uptake at concentrations as low as 12.5 μg/L, and stimulated sodium efflux at copper concentrations greater than 100 μg/L. High alkalinity water (i.e., 1000 μM Ca(CO)₃) significantly reduced copper effects on both sodium uptake and sodium efflux. Although water hardness (i.e., 25 vs. 1000 μM Ca(NO₃)₂) had no effect on sodium uptake (at either pH 7.8 or pH 5.0), hardwater fish were better able to reduce sodium efflux than softwater fish. At pH 5.0 (in both hard and softwater), a significant additional inhibition of sodium uptake was found at low levels of copper but not at higher levels. Juvenile trout were about twice as sensitive to copper as adult trout. Juvenile trout were able to acclimate to 55 μg/L copper. Acclimation was defined as the return of sodium uptake and whole body sodium to control levels during continuous exposure to copper. Sodium uptake kinetics and whole body sodium concentration were analysed weekly during 4 weeks of exposure. The recovery of sodium uptake took about 3 weeks to complete, but whole body sodium recovered within 1 week. The time necessary for the recovery of influx was provided by a reduction in efflux. The inhibition and recovery of sodium influx was correlated with the inhibition and recovery of the Na⁺-K⁺-ATPase transport pool of the gill. Metal binding proteins played no apparent protective role in the recovery of Na⁺-K⁺-ATPase. Metal binding proteins were induced in the liver, but a significant portions of the whole body copper burden was accumulated by other tissues.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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