Marine toxins and the cytoskeleton: okadaic acid and dinophysistoxins
Okadaic acid (OA) and its analogs, the dinophysistoxins, are potent inhibitors of protein phosphatases 1 and 2A. This action is well known to cause diarrhea and gastrointestinal symptons when the toxins reach the digestive tract by ingestion of mollusks. A less well-known effect of these group of to...
| Autores: | , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2008 |
| País: | España |
| Institución: | Universidad de Santiago de Compostela (USC) |
| Repositorio: | Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela |
| Idioma: | inglés |
| OAI Identifier: | oai:dnet:minerva_____::6fb2dd914f0dd5bf6c84384f85126dce |
| Acceso en línea: | https://hdl.handle.net/10347/46868 |
| Access Level: | acceso abierto |
| Palabra clave: | Actin Cytoskeleton Diarrheic shellfish poisoning Dinophysistoxins DSP Methyl okadaate Microtubules OA Okadaic acid Phycotoxin Investigación |
| Sumario: | Okadaic acid (OA) and its analogs, the dinophysistoxins, are potent inhibitors of protein phosphatases 1 and 2A. This action is well known to cause diarrhea and gastrointestinal symptons when the toxins reach the digestive tract by ingestion of mollusks. A less well-known effect of these group of toxins is their effect in the cytoskeleton. OA has been shown to stimulate cell motility, loss of stabilization of focal adhesions and a consequent loss of cytoskeletal organization due to an alteration in the tyrosine-phosphorylated state of the focal adhesion kinases and paxillin. OA causes cell rounding and loss of barrier properties through mechanisms that probably involve disruption of filamentous actin (F-actin) and/or hyperphosphorylation and activation of kinases that stimulate tight junction disassembly. Neither methyl okadaate (a weak phosphatase inhibitor) nor OA modify the total amount of F-actin, but both toxins cause similar changes in the F-actin cytoskeleton, with strong retraction and rounding, and in many cases cell detachment. OA and dinophysistoxin-1 (35S-methylokadaic acid) cause rapid changes in the structural organization of intermediate filaments, followed by a loss of microtubules, solubilization of intermediate filament proteins, and disruption of desmosomes. The detailed pathways that coordinate all these effects are not yet known. |
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