These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Profiles and levels of fatty acid esters of okadaic acid group toxins and pectenotoxins during toxin depuration. Part I: brown crab (Cancer pagurus).
    Author: Torgersen T, Lindegarth S, Ungfors A, Sandvik M.
    Journal: Toxicon; 2008 Sep 01; 52(3):407-17. PubMed ID: 18619994.
    Abstract:
    In 2002, two outbreaks of diarrhetic shellfish poisoning (DSP) occurred in Norway, which was later confirmed to be caused by the consumption of brown crab (Cancer pagurus) contaminated predominantly by esters of okadaic acid (OA) after feeding on toxic blue mussels (Mytilus edulis). In addition to OA-group toxins, pectenotoxins (PTXs) are commonly detected in the toxin-producing algae (i.e. Dinophysis). In this paper, an experiment was set up to study the fatty acid ester profiles and depuration rates of OA-group toxins and PTXs from C. pagurus after feeding on M. edulis containing these toxin groups. OA, DTX1, DTX2 and PTX2 SA were all detected primarily in the form of fatty acid esters in the crab hepatopancreas (HP). Crabs preferentially assimilated toxins of the OA group after feeding on the mussels for 1 week. Detailed analysis of the fatty acid ester profile in crabs and mussels showed that the ester profiles in the crabs differed slightly from profiles of the fatty acid esters in M. edulis, but neither ester profile nor ester to free toxin ratio appeared to change in the crabs during the first 2 weeks of depuration. Calculations of depuration rates of the free forms of toxins resulted in similar reduction rates for OA and DTX2, whereas the depuration rate of DTX1, PTX2 and PTX2 SA was considerably faster. From the industrial perspective, the PTX-compounds are of minor importance compared to the OA group toxins in crabs, considering (1) the uncertainty regarding the oral toxicity of the PTXs, (2) the preferential ingestion of OA-group toxins compared to PTXs and (3) the faster depuration of PTXs.
    [Abstract] [Full Text] [Related] [New Search]