Veratridine induces apoptotic death in bovine chromaÅn cellsthrough superoxide production
The molecular mechanisms involved in veratridine-induced chromaffin cell death have been explored.We have found that exposure to veratridine (30 µm, 1 h) produces a delayed cellular death that reaches 55% of the cells 24 h after veratridine exposure. This death has the features of apoptosis as DNA f...
| Autores: | , , , , |
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| Tipo de documento: | artigo |
| Data de publicação: | 2000 |
| País: | España |
| Recursos: | Universidad de Castilla-La Mancha |
| Repositório: | RUIdeRA. Repositorio Institucional de la UCLM |
| OAI Identifier: | oai:ruidera.uclm.es:10578/33370 |
| Acesso em linha: | https://hdl.handle.net/10578/33370 |
| Access Level: | Acceso aberto |
| Palavra-chave: | Apoptosis Caspases Chromaffin cells Free radicals Mitochondria Veratridine |
| Resumo: | The molecular mechanisms involved in veratridine-induced chromaffin cell death have been explored.We have found that exposure to veratridine (30 µm, 1 h) produces a delayed cellular death that reaches 55% of the cells 24 h after veratridine exposure. This death has the features of apoptosis as DNA fragmentation can be observed.Calcium ions play an important role in veratridine-induced chromaffin cell death because the cell permeant Ca2+ chelator BAPTA-AM and extracellular Ca2+ removal completely prevented veratridine-induced toxicity.Following veratridine treatment, there is a decrease in mitochondrial function and an increase in superoxide anion production. Veratridine-induced increase in superoxide production was blocked by tetrodotoxin (TTX; 10 µm), extracellular Ca2+ removal and the mitochondrial permeability transition pore blocker cyclosporine A (10 µm).Veratridine-induced death was prevented by different antioxidant treatments including catalase (100 IU ml-1), N-acetyl cysteine (100 µm), allopurinol (100 µm) or vitamin E (50 µm).Veratridine-induced DNA fragmentation was prevented by TTX (10 µm).Veratridine produced a time-dependent increase in caspase activity that was prevented by Ca2+ removal and TTX (10 µm). In addition, calpain and caspases inhibitors partially prevented veratridine-induced death.These results indicate that chromaffin cells share with neurons the molecular machinery involved in apoptotic death and might be considered a good model to study neuronal death during neurodegeneration. |
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