The pathways of cell death in cardiomyocytes induced by vanadate

• Author(s): Aureliano, M. ; Soares, S. S. ; Henao, Fernando ; Gutiérrez-Merino, Carlos
• Date: 2007
• Persistent ID: http://hdl.handle.net/10400.1/1309
• Origin: Sapientia - Universidade do Algarve
• Subject(s): Cell death; Vanadate
• Document Type: Conference Object
• Language: English

Description

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.