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

The effects of chloramine-T and its degradation products, sodium hypochlori te (NaOCl) and para-toluene-sulphonamide (pTSA), on whole body acid-base an d branchial and renal ion (Na+ and Cl-) fluxes were examined in rainbow tro ut (Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l(-1)) res ulted in increases in plasma total CO2 but no coincident rise in PaCO2 or r eduction 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 breakdow n product pTSA (dissolved in DMSO) resulted in increased net acid uptake (d ecreased acid excretion) suggesting a metabolic acidosis. Whole body ion fl uxes demonstrated increases in the losses of both Na+ and Cl- with chlorami ne-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolat ed. Confirmatory studies using fish in which the urinary bladder (lo allow collection of urine) and dorsal aorta (to allow injection of [C-14]polyethy lene glycol 4000 ([C-14]PEG), an extracellular fluid marker) were catheteri sed, revealed that changes in whole body ion fluxes during chloramine-T exp osure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [C-14]PEG w ere not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather tha n paracellular processes. (C) 1998 Elsevier Science B.V. All rights reserve d.