ArticleMarine drugs2013
Exposure to the neurotoxic dinoflagellate, Alexandrium catenella, induces apoptosis of the hemocytes of the oyster, Crassostrea gigas.
Article in Marine drugs, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
- Evolutionary trajectories, early diversification, and species-specific amplification of the metazoan inhibitor of apoptosis (IAP) repertoire.Molecular biology and evolution · 2026Article
- Sublethal exposure of eastern oyster Crassostrea virginica to the goniodomin-producing dinoflagellate Alexandrium monilatum: Fate of toxins, histopathology, and gene expression.Journal of aquatic animal health · 2024Article
- Toxicogenomic Effects of Dissolved Saxitoxin on the Early Life Stages of the Longfin Yellowtail (Marine drugs · 2023Article
- The Caspase Homologues in ScallopToxins · 2022Article
- Harmful algal blooms and shellfish in the marine environment: an overview of the main molluscan responses, toxin dynamics, and risks for human health.Environmental science and pollution research international · 2021Review
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- Article
- From the raw bar to the bench: Bivalves as models for human health.Developmental and comparative immunology · 2019Review
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- Environmental microbiology as a mosaic of explored ecosystems and issues.Environmental science and pollution research international · 2015Review
- RNA sequencing and de novo assembly of the digestive gland transcriptome in Mytilus galloprovincialis fed with toxinogenic and non-toxic strains of Alexandrium minutum.BMC research notes · 2014Article
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Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study assessed the apoptotic process occurring in the hemocytes of the Pacific oyster, Crassostrea gigas, exposed to Alexandrium catenella, a paralytic shellfish toxins (PSTs) producer. Oysters were experimentally exposed during 48 h to the toxic algae. PSTs accumulation, the expression of 12 key apoptotic-related genes, as well as the variation of the number of hemocytes in apoptosis was measured at time intervals during the experiment. Results show a significant increase of the number of hemocytes in apoptosis after 29 h of exposure. Two pro-apoptotic genes (Bax and Bax-like) implicated in the mitochondrial pathway were significantly upregulated at 21 h followed by the overexpression of two caspase executor genes (caspase-3 and caspase-7) at 29 h, suggesting that the intrinsic pathway was activated. No modulation of the expression of genes implicated in the cell signaling Fas-Associated protein with Death Domain (FADD) and initiation-phase (caspase-2) was observed, suggesting that only the extrinsic pathway was not activated. Moreover, the clear time-dependent upregulation of five (Bcl2, BI-1, IAP1, IAP7B and Hsp70) inhibitors of apoptosis-related genes associated with the return to the initial number of hemocytes in apoptosis at 48 h of exposure suggests the involvement of strong regulatory mechanisms of apoptosis occurring in the hemocytes of the Pacific oyster.
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