IMPACT OF OXIDATIVE STRESS ON NEURONAL SURVIVAL
Version of Record online: 6 JUL 2004
Clinical and Experimental Pharmacology and Physiology
Volume 31, Issue 7, pages 397–406, July 2004
How to Cite
Taylor, J. M. and Crack, P. J. (2004), IMPACT OF OXIDATIVE STRESS ON NEURONAL SURVIVAL. Clinical and Experimental Pharmacology and Physiology, 31: 397–406. doi: 10.1111/j.1440-1681.2004.04017.x
- Issue online: 6 JUL 2004
- Version of Record online: 6 JUL 2004
- Received 13 December 2003; revision 25 March 2004; accepted 11 April 2004.
- nuclear factor-κB;
- oxidative stress;
- phosphatidylinositol 3-kinase;
- akt pathway;
- signal transduction;
1. Reactive oxygen species and oxidative state are slowly gaining acceptance in having a physiological relevance rather than just being the culprits in pathophysiological processes. The control of the redox environment of the cell provides for additional regulation in relation to signal transduction pathways. Conversely, aberrant regulation of oxidative state manifesting as oxidative stress can predispose a cell to adverse outcome.
2. The phosphatidylinositol 3-kinase/akt pathway is one such pathway that is partially regulated via oxidative state and, in an oxidative stress paradigm such as ischaemic–reperfusion injury, may be inactivated, which can lead to exacerbation of cell death.
3. Activation of nuclear factor (NF)-κB has been associated with oxidative stress. The role of NF-κB in neuronal cell death is widely debated, with major studies highlighting both a pro- and anti-apoptotic role for NF-κB, with the outcome being region, stimulus, dose and duration specific.
4. Oxidative state plays a key role in the regulation and control of numerous signal transduction pathways in the cell. Elucidating the mechanisms behind oxidative stress-mediated neuronal cell death is important in identifying potential putative targets for the treatment of diseases such as stroke.