The pathways of cell death in cardiomyocytes induced by vanadate

Aureliano, M.; S. Soares, Sandra; Henao, Fernando; Gutiérrez-Merino, Carlos

http://hdl.handle.net/10400.1/1309

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Authors

Aureliano, M.

S. Soares, Sandra

Henao, Fernando

Gutiérrez-Merino, Carlos

Abstract(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.