Trophic transfer of paralytic shellfish toxin (PST): Physiological and reproductive effects in the carnivorous gastropod Acanthina monodon (Pallas, 1774)

摘要

Harmful algal blooms can adversely affect different levels of the trophic chain, from primary consumers, such as bivalve molluscs, to higher links such as large fish, birds and mammals, including humans. Among secondary consumers, it has been described that carnivorous gastropods can accumulate these toxins when they prey on bivalves that have been exposed to toxic microalgae; these could also harm human health. In Chile, frequent events of harmful algal blooms caused by the dinoflagellate Alexandriurn catenella have been described. This organism produces paralytic shellfish toxin (PST) which has been identified in some carnivorous gastropods. The objective of this research was to identify the physiological and reproductive response of the carnivorous gastropod Acanthina monodon fed on the Mytilid Perumytilus purpuratus, which had previously been maintained on a diet containing PST. Specimens of A. monodon showed a decrease in ingestion and absorption rate when they consumed PST indirectly through their diet. The oxygen consumption rate was also affected by the diet-time interaction. The variations of these parameters were reflected in the scope for growth, since the available energy was lower in gastropods exposed to toxic diet. Consumption of PST had a negative effect on the reproduction of A. monodon, since intoxicated adults presented lower egg-masses and delayed start of oviposition. We observed a delay in the development of the embryos inside the capsules, and a lower number of hatched juveniles, although these few juveniles from intoxicated parents accomplished higher growth rates during the next 6 months. We may therefore suggest that toxin transfer, from harmful microalgae through the trophic chain, can generate deleterious effects on the physiological energetics of the organisms that consume them, affecting their reproductive capacity and early ontogenetic development.