Exposure to toxic Alexandrium minutum activates the detoxifying and antioxidant systems in gills of the oyster Crassostrea gigas

Type Article
Date 2015-09
Language English
Author(s) Fabioux Caroline1, Sulistiyani Yeni1, Haberkorn Hansy1, Hegaret HeleneORCID1, Amzil Zouher2, Soudant Philippe1
Affiliation(s) 1 : Univ Bretagne Occidentale, Lab Sci Environm Marin LEMAR, Inst Univ European Mer, UMR 6539,CNRS UBO IRD IFREMER, F-29280 Plouzane, France.
2 : IFREMER, Lab Phycotoxines, F-44311 Nantes, France.
Source Harmful Algae (1568-9883) (Elsevier Science Bv), 2015-09 , Vol. 48 , P. 55-62
DOI 10.1016/j.hal.2015.07.003
WOS© Times Cited 22
Keyword(s) Crassostrea gigas, Alexandrium minutum, Paralytic shellfish toxins, Antioxidant enzymes, Detoxification enzymes, mRNA
Abstract Harmful algal blooms of Alexandrium spp. dinoflagellates regularly occur in French coastal waters contaminating shellfish. Studies have demonstrated that toxic Alexandrium spp. disrupt behavioural and physiological processes in marine filter-feeders, but molecular modifications triggered by phycotoxins are less well understood. This study analyzed the mRNA levels of 7 genes encoding antioxidant/detoxifying enzymes in gills of Pacific oysters (Crassostrea gigas) exposed to a cultured, toxic strain of A. minutum, a producer of paralytic shellfish toxins (PST) or fed Tisochrysis lutea (T. lutea, formerly Isochrysis sp., clone Tahitian (T. iso)), a non-toxic control diet, in four repeated experiments. Transcript levels of sigma-class glutathione S-transferase (GST), glutathione reductase (GR) and ferritin (Fer) were significantly higher in oysters exposed to A. minutum compared to oysters fed T. lutea. The detoxification pathway based upon glutathione (GSH)-conjugation of toxic compounds (phase II) is likely activated, and catalyzed by GST. This system appeared to be activated in gills probably for the detoxification of PST and/or extra-cellular compounds, produced by A. minutum. GST, GR and Fer can also contribute to antioxidant functions to prevent cellular damage from increased reactive oxygen species (ROS) originating either from A. minutum cells directly, from oyster hemocytes during immune response, or from other gill cells as by-products of detoxification.
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