Epilepsy is thought to be associated with oxidative stress, which play its role in the seizures-induced neuronal death (1, 2). On the other hand, the brain, due to a high content of polyunsaturated fatty acids, is an easy target for the peroxidation. Luckily, it has neuroprotective systems such as superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione (3, 4).
Exogenous antioxidants like vitamin E and C, can inhibit the neuronal damage provoced by lipid peroxidation during seizures and prevent the increase in brain free fatty acid levels, suggesting that the protection may be mediated by, for example, increase of hippocampal catalase activity (5). Vitamin C significantly decreased the lipid peroxidation after seizures induced by cholinergic agonist pilocarpine supporting the idea of interaction of the C and E vitamins with catalase activity to produce neuronal protection amd to decrease the lipid peroxidation level (6).
When oxidative damage accumulates over years, it may account for the increased incidence of neurodegenerative diseases in aged populations. The mechanisms of neuronal degeneration in these cases remain unknown and this is a major obstacle in the development of effective therapies targeting the causes of the diseases.
Sources
- Neurosci Lett 420 (2007), pp. 76–79
- Neurosci Lett 291 (2000), pp. 179–182
- Cell signaling and neurotoxic events. In: L.W. Chang, Editor, Principles of Neurotoxicology, Marcel Dekker, New York (1994), pp. 475–493
- Neurosci Lett 8 (2007), pp. 76–79
- Epilepsy Res 46 (2001), pp. 121–128
- Pharmac Biochem & Behavior, Volume 89, Issue 1, March 2008, Pages 1-5
