Please use this identifier to cite or link to this item:
|Title:||Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early calpain activation||Authors:||Toh, T.B.
|Issue Date:||2008||Citation:||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/10635/28804||ISSN:||00410101||DOI:||10.1016/j.toxicon.2007.11.019|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on May 29, 2020
WEB OF SCIENCETM
checked on May 21, 2020
checked on May 13, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.