Diarrhetic shellfish toxicity in relation to the abundance ofDinophysisspp. in the German Bight near Helgoland

Diarrhetic shellfish toxicity is caused by the accumulation of okadaic acid and its derivatives, which are produced by particular species ofDinophysisEhrenberg 1839 andProrocentrumEhrenberg 1833 (Dinoflagellata). In the German Bight (North Sea) around the island of Helgoland, 4 toxicDinophysisspecie...

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Veröffentlicht in:Marine ecology. Progress series (Halstenbek) 2003-09, Vol.259, p.93-102
Hauptverfasser: Klöpper, Sascha, Scharek, Renate, Gerdts, Gunnar
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Sprache:eng
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Zusammenfassung:Diarrhetic shellfish toxicity is caused by the accumulation of okadaic acid and its derivatives, which are produced by particular species ofDinophysisEhrenberg 1839 andProrocentrumEhrenberg 1833 (Dinoflagellata). In the German Bight (North Sea) around the island of Helgoland, 4 toxicDinophysisspecies occur, of which 2 exhibited successive biomass maxima in summer 2000 (D. norvegicaClaparède et Lachmann 1859 with cell concentrations of max. 400 cell l–1andD. acuminataClaparède et Lachmann 1859 with max. cell concentrations of over 4000 cells l–1). In contrast to findings in other marine areas, toxicity ofMytilus edulisLinné 1758 could be clearly attributed to the observed increases in cell abundances of both species. In severalMytilussamples toxin concentrations (max. 460 ng diarrhetic shellfish poisoning [DSP] toxins g–1hepatopancreas) were in a range which is considered dangerous for human consumption. While mussel toxicity coincided with concentration increases of bothDinophysis species, toxicity of the particulate substance in the water (max. 26 ng l–1) could be detected only during cell concentration maxima ofD. acuminata. Mussel toxicity lasted 3 wk after the end of theD. acuminatabloom, and this is attributed to extended toxicity of decayingDinophysiscells and detritus. Elevated summer temperatures and low silicate concentrations evidently supported the development of high concentrations ofD. acuminata.
ISSN:0171-8630
1616-1599