Meeting Abstract
The dinoflagellate Karenia brevis is a key organism present during harmful algal blooms (HABs, Red tides) which are increasing in frequency and duration worldwide. K. brevis produces a suite of neurotoxins collectively referred to as brevetoxins (PbTx). Brevetoxin binds to sodium channels which trigger a cascade of events, eventually leading to cells death. PbTx exposure affects marine life by interrupting neurological functions, decreasing immune function, and inducing inflammation. Brevetoxicosis is difficult to treat in endangered sea turtles, as the physiological impacts have not been fully investigated and the magnitude and duration of PbTx exposure is generally unknown. Freshwater turtles (Trachemys scripta) are being used as a model system for experimental toxin exposures. Analyzing uptake, tissue distribution, routes of excretion, immune function and neurological responses will give us insight into the fate of PbTx. PbTx-3 was widely distributed in all tissues and fluids of T. scripta and the toxin shows to clear within 24 hours, following both oral and intratracheal exposures. These short term exposures did not result in obvious tissue pathology. Preliminary results suggest turtle neurons are surprisingly resistant to PbTx. Cell viability decreased in a dose dependent manner across PbTx concentrations from 100-17500nM; the LC50 was significantly higher than is seen in mammalian neurons. PbTx-3 exposure resulted in significant Ca2+ influx, which can trigger a cascade of excitotoxic events leading to cell death. We are currently testing treatment strategies that can be implemented to reduce the number of sea turtle deaths from PbTx-3 exposure.
