Exposure to the Neurotoxic Dinoflagellate, Alexandrium catenella, Induces Apoptosis of the Hemocytes of the Oyster, Crassostrea gigas

• Published in: Marine Drugs
• Main Authors: Medhioub, Walid, Ramondenc, Simon, Vanhove, Audrey Sophie, Vergnes, Agnes, Masseret, Estelle, Savar, Veronique, Amzil, Zouher, Laabir, Mohamed, Rolland, Jean Luc
• Format: Text
• Language: English
• Published: MDPI 2013
• Subjects: Article; Pacific; Crassostrea gigas; Pacific oyster
• Online Access: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877888; http://www.ncbi.nlm.nih.gov/pubmed/24317471; https://doi.org/10.3390/md11124799

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.