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The pathways of cell death in cardiomyocytes induced by vanadate
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Orientador(es)
Resumo(s)
After 24 hours, cardiac myocytes exposure to 10 μM (LD50) vanadate (meta or decavanadate) an increased (30%) of caspase 3-activation was observed, although not significant. On contrary, a significant decrease (40%) of
ATP content, characteristic of necrotic cell death was detected. Furthermore,
vanadate treatment increased intracellular Ca2+ level from 60 nM to 240 nM,
whereas it decreases mitochondria superoxide anion generation and induces
mitochondria membrane depolarization (IC50=6.5 μM). In conclusion, micromolar
vanadate exposure induces large chances in two major bioenergetic markers in cardiac myocytes: intracellular calcium concentration and superoxide anion
mitochondrial production, suggesting a necrotic cell death through a mitochondrial
toxic pathway.
Descrição
Palavras-chave
Cell death Vanadate