Pharmacokinetics conjugated products

Fish rapidly absorb, metabolize, and excrete chlorpyrifos from the diet. The mechanism of action of chlorpyrifos occurs via phosphorylation of the active site of acetylcholinesterase after initial formation of chlorpyrifos oxon by oxidative desulfuration. In studies with chaimel catfish (Ictalurus punctatus), the oral hioavailability of chlorpyrifos was 41%, substantially higher than in mammals. Catfish muscle contained less than 5% of the oral dose with an elimination half-life (Tbl/2) of 3.3 days. Chlorpyrifos residues in whole catfish were more than 95% chlorpyrifos, while bile and urine primarily contained metabolites. The dephosphorylated metabolite trichloropy-ridinol (TCP) was the major metabolite in the blood while the glucuronide conjugate of TCP was the major metabolite in mine and bile. The toxic metabolite, chlorpyrifos oxon, was not detected in blood, tissues, or excreta. Extensive metabolism resulted in a low potential for chlorpyrifos to accumulate in catfish from dietary exposure. In both fish and mammals, TCP is a major biotransformation product. Chaimel catfish rapidly distribute waterborne chlorpyrifos into the blood and more slowly to peripheral tissues, with concentrations highest in fat and lowest in muscle. As was true with dietary chlorpyrifos, TCP was the major metabolite in blood and the glucuronide conjugate of TCP was the major metabolite in urine and bile. Pharmacokinetics and metabolism of waterborne chlorpyrifos in channel catfish were similar to the disposition of chlorpyrifos in other vertebrates. 

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