Data/hora: 07/06/2024 00:36:26

Provedor de dados: | 5
País: | France
Título: | The paralytic shellfish toxin, saxitoxin, enters the cytoplasm and induces apoptosis of oyster immune cells through a caspase-dependent pathway
Autores: | Abikhalil, Celina; Finkelstein, Darren S.; Conejero, Genevieve; Du Bois, Justin; Destoumieux-garzon, Delphine; Rolland, Jean-luc.
Data: | 2017-09
Ano: | 2017
Palavras-chave: | Shellfish; Toxin; Harmful algae; Phytoplankton.
Resumo: | Exposure of the toxin-producing dinoflagellate Alexandrium catenella (A. catenella) was previously demonstrated to cause apoptosis of hemocytes in the oyster species Crassostrea gigas. In this work, a coumarin-labeled saxitoxin appeared to spread throughout the cytoplasm of the hemocytes. PSTs, including saxitoxin, were also shown to be directly responsible for inducing apoptosis in hemocytes, a process dependent on caspase activation and independent of reactive oxygen species (ROS) production. A series of in vitro labeling and microscopy experiments revealed that STX and analogs there of induced nuclear condensation, phosphatidylserine exposure, membrane permeability, and DNA fragmentation of hemocytes. Unlike in vertebrates, gonyautoxin-5 (GTX5), which is present in high concentrations in A. catenella, was found to be more toxic than saxitoxin (STX) to oyster immune cells. Altogether, results show that PSTs produced by toxic dinoflagellates enter the cytoplasm and induce apoptosis of oyster immune cells through a caspase-dependent pathway. Because of the central role of hemocytes in mollusc immune defense, PST-induced death of hemocytes could negatively affect resistance of bivalve molluscs to microbial infection.
Tipo: | Text
Idioma: | Inglês

Identificador:

http://archimer.ifremer.fr/doc/00391/50272/50905.pdf

DOI:10.1016/j.aquatox.2017.07.001

http://archimer.ifremer.fr/doc/00391/50272/

Editor: | Elsevier Science Bv
Formato: | application/pdf
Fonte: | Aquatic Toxicology (0166-445X) (Elsevier Science Bv), 2017-09 , Vol. 190 , P. 133-141

Fonte:

2017 Elsevier B.V. All rights reserved.

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