Detection and effects of harmful algal toxins in Scottish harbour seals and potential links to population decline

Over the past 15 years or so, several Scottish harbour seal (Phoca vitulina) populations have declined in abundance and several factors have been considered as possible causes, including toxins from harmful algae. Here we explore whether a link could be established between two groups of toxins, domo...

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Bibliographic Details
Published in:Toxicon
Main Authors: Jensen, S-K, Lacaze, J-P, Hermann, G, Kershaw, J, Brownlow, A, Turner, A
Format: Article in Journal/Newspaper
Language:English
Published: 2015
Subjects:
Online Access:https://pure.sruc.ac.uk/en/publications/1b2f2f19-fc19-42e6-a884-6574a2d8b0d1
https://doi.org/10.1016/j.toxicon.2015.02.002
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Summary:Over the past 15 years or so, several Scottish harbour seal (Phoca vitulina) populations have declined in abundance and several factors have been considered as possible causes, including toxins from harmful algae. Here we explore whether a link could be established between two groups of toxins, domoic acid (DA) and saxitoxins (STXs), and the decline in the harbour seal populations in Scotland. We document the first evidence that harbour seals are exposed to both DA and STXs from consuming contaminated fish. Both groups of toxins were found in urine and faeces sampled from live captured (n ¼ 162) and stranded animals (n ¼ 23) and in faecal samples collected from seal haul-out sites (n ¼ 214) between 2008 and 2013. The proportion of positive samples and the toxins levels measured in the excreta were significantly higher in areas where harbour seal abundance is in decline. There is also evidence that DA has immunomodulatory effects in harbour seals, including lymphocytopenia and monocytosis. Scottish harbour seals are exposed to DA and STXs through contaminated prey at potentially lethal levels and with this evidence we suggest that exposure to these toxins are likely to be important factors driving the harbour seal decline in some regions of Scotland. © 2015 Elsevier Ltd. All rights reserved.