Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.toxicon.2007.11.019
Title: Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early calpain activation
Authors: Toh, T.B.
Chen, M.J.
Armugam, A. 
Li, Q.-T. 
Jeyaseelan, K. 
Cheung, N.S. 
Peng, Z.F. 
Keywords: Cardiotoxins
CTX-4b
Neuronal death
Oxidative stress
ROS
Issue Date: 2008
Source: Toh, T.B., Chen, M.J., Armugam, A., Li, Q.-T., Jeyaseelan, K., Cheung, N.S., Peng, Z.F. (2008). Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early calpain activation. Toxicon 51 (6) : 964-973. ScholarBank@NUS Repository. https://doi.org/10.1016/j.toxicon.2007.11.019
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 4 h 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. © 2007 Elsevier Ltd. All rights reserved.
Source Title: Toxicon
URI: http://scholarbank.nus.edu.sg/handle/10635/27372
ISSN: 00410101
DOI: 10.1016/j.toxicon.2007.11.019
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