The effects of elevated winter temperature and sub-lethal pollutants (low pH, elevated ammonia) on protein turnover in the gill and liver of rainbow trout (Oncorhynchus mykiss)

Appetite, growth, and protein turnover (synthesis, growth and degradation) of liver and gills were measured in juvenile rainbow trout (Oncorhynchus mykiss) fed to satiation, and exposed for 90 days to elevated winter temperatures (+2 °C above ambient) and either low pH (5.2) in softwater or 70 M total ammonia (TAmm) in hardwater. All fish increased in weight during the experiments, but those exposed to +2°C grew significantly more than those at ambient temperature due to a stimulation of appetite. During the relatively constant temperature of the first 75 days, +2 °C caused a significant increase in the rates of protein synthesis and degradation in the liver of hardwater-acclimated fish, as a result of an increase in RNA translational efficiency (KRNA). The elevated temperature also induced an increase in gill protein synthesis in softwater-acclimated fish but in this case the underlying mechanism was an increase in Cs, the capacity for protein synthesis (RNA:protein) rather than in KRNA. The addition of 70 M TAmm had no effect on protein turnover in either liver or gills of hardwater-acclimated fish. Low pH inhibited protein growth in the liver of softwater-acclimated fish at day 90 under both temperature regimes. This inhibition was effected via a decrease in protein synthesis at control temperature but via an increase in protein degradation when the fish were exposed to both low pH and +2 °C. From these results we conclude that a simulated global warming scenario has potentially beneficial rather than detrimental effects on protein turnover and growth of freshwater fish during winter.     

The conversion of plasma HCO 3 − to CO2 by rainbow trout red blood cells in vitro: adrenergic inhibition and the influence of oxygenation status

This study employed a recently developed radioisotopic assay (Wood and Perry 1991) to examine the inhibition, induced by catecholamines, of the conversion of plasma HCO ₃ ^– to CO₂ in acidotic trout blood, and the influence of oxygenation status on the response. Blood was incubated in vitro at P_{CO 2}= 2 torr, and 10^–6 M noradrenaline was employed as the adrenergic stimulus. In particular we investigated whether the inhibition of plasma HCO ₃ ^– conversion could be explained by a limited supply of H⁺s for the intracellular HCO ₃ ^– dehydration reaction because of competition by the adrenergically activated Na /H⁺ exchanger. Hypoxia (P_{O 2}= 15 torr) was employed as a tool to intensify this competition. Hypoxia raised RBC pHi, pHe, and plasma total CO₂ concentration (C_{CO 2}) by the Haldane effect, and increased the magnitude of Na⁺/H⁺ activation, expressed as the change in the transmembrane pH gradient (pHe-pHi). However hypoxia did not alter the inhibition of the conversion of plasma HCO ₃ ^– to CO₂ caused by noradrenaline. Hypoxia itself stimulated the RBC-mediated conversion of plasma HCO ₃ ^– to CO₂ by about 20% in the presence or absence of noradrenaline. The conversion rate was strongly correlated with pHe, pHe-pHi, and plasma C_{CO 2} in these experiments, but not with pHi. We conclude that adrenergically mediated inhibition in the conversion of plasma HCO ₃ ^– to CO₂ by trout RBCs is not due to competitive limitation on intracellular H⁺s, but rather to changes in the electrochemical gradient for HCO ₃ ^– entry and/or to CO₂ recycling from plasma to RBC. The deoxygenated condition helps to promote CO₂ excretion at the level of the RBC.