Acid–base and ionic fluxes in rainbow trout ( Oncorhynchus mykiss) during exposure to chloramine-T

Abstract

The effects of chloramine-T and its degradation products, sodium hypochlorite (NaOCl) and para-toluenesulphonamide ( pTSA), on whole body acid–base and branchial and renal ion (Na +and Cl −) fluxes were examined in rainbow trout ( Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l −1) resulted in increases in plasma total CO 2 but no coincident rise in P aCO 2 or reduction in blood pH. Exposure of fish to 2, 9 or 18 mg l −1 chloramine-T (3.5 h duration) resulted in a reduction in net acid uptake suggesting the development of a metabolic alkalosis. Exposure to the chloramine-T breakdown product pTSA (dissolved in DMSO) resulted in increased net acid uptake (decreased acid excretion) suggesting a metabolic acidosis. Whole body ion fluxes demonstrated increases in the losses of both Na +and Cl − with chloramine-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolated. Confirmatory studies using fish in which the urinary bladder (to allow collection of urine) and dorsal aorta (to allow injection of [ 14C]polyethylene glycol 4000 ([ 14C]PEG), an extracellular fluid marker) were catheterised, revealed that changes in whole body ion fluxes during chloramine-T exposure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [ 14C]PEG were not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather than paracellular processes.