Uptake, metabolism and loss of clay-flocculated brevetoxins in a surface deposit-feeding clam

Abstract

Blooms of the brevetoxin-producing Karenia brevis in the Gulf of Mexico cause fish kills, food poisoning and respiratory irritation in humans. Sedimentation of toxic cells following clay application could reduce toxin incorporation by commercially important suspension-feeding bivalves and direct public health impacts, but may potentially lead to brevetoxin (PbTx)accumulation by benthic depositfeeders. The goal of this study was to determine whether deposit-feeding could provide a pathway of toxin transfer from deposited clay-K.brevis aggregates. We investigated PbTx uptake, metabolism and detoxification kinetics in a depositfeeding, tellinid clam exposed to clay-deposited brevetoxins. We demonstrate that brevetoxins can be rapidly accumulated by depositfeeding from sedimented K. brevis cells (exceeding the regulatory level of 0.8 mg PbTx g-1 within ~12h as determined by ELISA). LC-MS analysis showed that PbTx-2, the dominant toxin in the clay/cell layer, was rapidly transformed into PbTx-3 and its cysteine derivatives in clam tissues. Detoxification of tissues following deposit-feeding occurred but toxicities remained around the regulatory level for 15 days. This toxicity was due largely to the persistence of the more potent PbTx-3-cys metabolites in tissues. Deposit-feeding clams do not pose a direct threat to humans but may provide a pathway for brevetoxin food web transferPeer reviewed: NoNRC publication: Ye