Abstract
The role of free radical-mediated reactions in human neuropathology continues to attract significant interest. Oxidative injury produced by free radicals may play a role in the initiation and progression of epilepsy and, therapies aimed at reducing oxidative stress may ameliorate tissue damage and favorably alter the clinical course. The prevalence of epilepsy increases with age, and mitochondrial oxidative stress is a leading mechanism of aging and age-related degenerative disease, signifying a further involvement of mitochondrial dysfunction in seizure generation. Oxidative stress occurs when the generation of reactive oxygen species in a system exceeds the body's ability to neutralize and eliminate them, thus creating an imbalance or over abundance of free radicals. Therefore, it is imperative to maintain oxidative balance and control in the brain, and this is tightly regulated by antioxidants. In the last two decades, there has been an explosive interest in the role of antioxidants or neuroprotectants in clinical as well as experimental models of epilepsy. In this regard, the present review is intended to discuss the current state of knowledge pertaining to neuroprotection in epileptic conditions by employing diverse chemical agents including conventional as well as novel anti-epileptic drugs, and to highlight the efficacy of distinct neuroprotective strategies for preventing or treating epilepsy.
Keywords: Antioxidants, free radicals, oxidative stress, neuroprotection
Current Topics in Medicinal Chemistry
Title:Targeting Oxidative Stress Component in the Therapeutics of Epilepsy
Volume: 12 Issue: 9
Author(s): Faizul Azam, M. V.V. Prasad and Neelaveni Thangavel
Affiliation:
Keywords: Antioxidants, free radicals, oxidative stress, neuroprotection
Abstract: The role of free radical-mediated reactions in human neuropathology continues to attract significant interest. Oxidative injury produced by free radicals may play a role in the initiation and progression of epilepsy and, therapies aimed at reducing oxidative stress may ameliorate tissue damage and favorably alter the clinical course. The prevalence of epilepsy increases with age, and mitochondrial oxidative stress is a leading mechanism of aging and age-related degenerative disease, signifying a further involvement of mitochondrial dysfunction in seizure generation. Oxidative stress occurs when the generation of reactive oxygen species in a system exceeds the body's ability to neutralize and eliminate them, thus creating an imbalance or over abundance of free radicals. Therefore, it is imperative to maintain oxidative balance and control in the brain, and this is tightly regulated by antioxidants. In the last two decades, there has been an explosive interest in the role of antioxidants or neuroprotectants in clinical as well as experimental models of epilepsy. In this regard, the present review is intended to discuss the current state of knowledge pertaining to neuroprotection in epileptic conditions by employing diverse chemical agents including conventional as well as novel anti-epileptic drugs, and to highlight the efficacy of distinct neuroprotective strategies for preventing or treating epilepsy.
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Cite this article as:
Azam Faizul, V.V. Prasad M. and Thangavel Neelaveni, Targeting Oxidative Stress Component in the Therapeutics of Epilepsy, Current Topics in Medicinal Chemistry 2012; 12 (9) . https://dx.doi.org/10.2174/156802612800229224
DOI https://dx.doi.org/10.2174/156802612800229224 |
Print ISSN 1568-0266 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4294 |
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