Pharmacokinetics and metabolism of triclopyr butoxyethyl ester in coho salmon

The pharmacokinetics and metabolism of triclopyr butoxyethyl ester (BEE) were studied in yolk-sac fry of the coho salmon ( Oncorhynchus kisutch). Triclopyr BEE was rapidly absorbed from water, then rapidly de-esterified by the fish, which limited triclopyr BEE accumulation. Triclopyr acid was the principal metabolite observed in fish and exposure water, and was the principal residue in the fish. A compartmental model describing the dynamics of triclopyr BEE and acid in fish and water was developed which allowed prediction of ester accumulation under various exposure regimes. The model indicated that a small fraction of ester escaping metabolism was transferred to a peripheral storage compartment. The slower terminal elimination of triclopyr BEE was due to transfer of ester back into the metabolic compartment, rather than slow metabolism. Exposure to triclopyr BEE in the presence of a carboxylesterase inhibitor had no effect on toxicity or total residue levels in the fish, but ester concentrations in the fish increased by seven times. The observed lack of change in triclopyr acid levels during esterase inhibition was predicted by the pharmacokinetic model, and indicated that mortality resulted from lethal tissue concentrations of triclopyr acid or total residues.