Antioxidants: promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early calpain activation.
Toxicon
; 51(6): 964-73, 2008 May.
Article
em En
| MEDLINE
| ID: mdl-18377942
ABSTRACT
Cardiotoxin-4b (CTX-4b), isolated from Naja naja sputatrix venom, shows lethality in several cell types. Employing murine primary cortical neurons, this study was undertaken to investigate the molecular mechanisms of CTX-4b in the induction of neuronal death. CTX-4b induced a dose- and time-dependent neuronal death. Strong induction of calpains as early as 4h post-CTX-4b 75 nM treatment was detected in neurons with negligible caspase 3 activation. For the first time in cultured murine primary cortical neurons, it was noted that CTX-4b-mediated cell death triggered oxidative stress with an increase in reactive oxygen species (ROS) levels, and that application of antioxidants showed effective attenuation of cell death. Taken together, these results indicate that CTX-4b-mediated neuronal death is associated with (i) early calpain activation and (ii) oxidative stress. Most importantly, antioxidants have proved to be a promising therapeutic avenue against CTX-4b-induced neuronal death.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Calpaína
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Morte Celular
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Estresse Oxidativo
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Fármacos Neuroprotetores
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Proteínas Cardiotóxicas de Elapídeos
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Neurônios
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Antioxidantes
Limite:
Animals
Idioma:
En
Revista:
Toxicon
Ano de publicação:
2008
Tipo de documento:
Article
País de afiliação:
Singapura