Survival and toxin accumulation in Crassostrea virginica larvae following exposure to various Dinophysis species

This study investigates the effects of Dinophysis cells and their toxins on the viability of oyster larvae, a critical stage for the aquaculture industry. Specifically, the effects of toxigenic Dinophysis species ( D. acuminata , D. caudata , D. fortii , and D. ovum ) on 7-day-old Crassostrea virginica larvae were investigated through exposures to living cells, cell lysates (dead cells), dialysates (living cells separated by a membrane), and purified toxins in concentrations equivalent to 10 cells mL −1 . After 48 h, mortality and toxin uptake were assessed. Larvae experienced the highest mortality rates when exposed to living D. caudata (28 ± 4 %) and D. fortii (25 ± 6 %) cells, coinciding with elevated intra- and extracellular levels of pectenotoxin-2 (PTX2) and hydroxyPTX2. In contrast, no significant mortality was observed with lysates or dialysates from these species . In addition, D. acuminata (a low PTX2 producer) and D. ovum (producing only okadaic acid; OA) did not cause mortality under any condition. Exposure to purified OA had no detectable effect on mortality, however, exposure to pure PTX2 at 1.5 nM significantly increased larval mortality (17 ± 2 %), albeit to a lesser extent than exposure to living cells of D. caudata and D. fortii . Furthermore, dissolved PTX2 was adsorbed onto Pavlova pinguis cells, the larval food, potentially increasing toxin bioavailability for larvae. These results indicate that living Dinophysis cells producing high concentrations of PTXs (but not OA), along with other bioactive compounds, are responsible for the higher mortality in oyster larvae. Such exposure, along with other multi-stressor environmental factors such as ocean acidification, temperature and salinity fluctuations, hypoxia, poses risks to oyster recruitment, with potential socio-economic and ecological consequences for aquaculture. • PTX producers, D. caudata and D. fortii , induced significant oyster mortality. • Higher mortality when exposed to live D. caudata and D. fortii cells than pure PTX2. • Oyster larvae accumulated dissolved PTXs, but OA and DTX1 were not detectable in tissue. • Dissolved PTX2 adsorbed onto Pavlova pinguis cells, enhancing its bioavailability.