2011
DOI: 10.1016/j.neuint.2011.03.025
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Role of oxidative stress in epileptic seizures

Abstract: Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. Therefore, antioxidant therapies aimed at reducing oxidative stress have received considerable attention in epilepsy treatment. However, much evidence suggests that oxidative stress does not always have the same pattern in all seizures models. Thus, this review provides an overview aimed at achieving a better understanding of this issue. We summarize work regarding seizure models (… Show more

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Cited by 360 publications
(253 citation statements)
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References 231 publications
(266 reference statements)
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“…Many studies have demonstrated that repeated seizure activity results in increased oxidation of cellular macromolecules such as proteins, lipids and nucleotides, which in turn can lead to neuronal death. It has been hypothesised that a cascade of events including excessive neuronal firing, increased glutamate release, Nmethyl-D-aspartate receptor activation, influx of calcium into the cytosol and mitochondria and increased ATP consumption leads to abundant production of reactive oxygen species (ROS) (Shin et al 2011). The brain is rich in mitochondria due to its high metabolic demand and it is plausible that this ROS production may overwhelm the normal mitochondrial antioxidant defences leading to mitochondrial dysfunction and greater superoxide production through a damaged respiratory chain, thus producing a self-perpetuating vicious cycle of oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…Many studies have demonstrated that repeated seizure activity results in increased oxidation of cellular macromolecules such as proteins, lipids and nucleotides, which in turn can lead to neuronal death. It has been hypothesised that a cascade of events including excessive neuronal firing, increased glutamate release, Nmethyl-D-aspartate receptor activation, influx of calcium into the cytosol and mitochondria and increased ATP consumption leads to abundant production of reactive oxygen species (ROS) (Shin et al 2011). The brain is rich in mitochondria due to its high metabolic demand and it is plausible that this ROS production may overwhelm the normal mitochondrial antioxidant defences leading to mitochondrial dysfunction and greater superoxide production through a damaged respiratory chain, thus producing a self-perpetuating vicious cycle of oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…For all these reasons, the nervous system is very sensitive to the destructive effects of ROS [28,29]. Additionally, oxidative stress has been shown to induce neuronal degeneration in experimental models of epilepsy and many other neurodegenerative disorders including Alzheimer's disease and Parkinson's disease [7,[30][31][32][33]. In contrast, ROS is scavenged by defense mechanisms such as enzymatic antioxidants such as SOD and GPx, and thus reducing the deleterious effects of oxidative stress [8].…”
Section: Discussionmentioning
confidence: 99%
“…[18] The cytotoxic mechanism by which reactive oxygene species (ROS) induce neuronal damage may involve direct oxidative attack on cellular macromolecules and initiation or propagation of free radical chain reaction, ultimately leading to macromolecular damage. [19] Proteins, lipids and DNA are sensitive targets of ROS. As seizure induced inflammation is associated with free radical production and oxidative stress, there is also an increase in lipid peroxidation level.…”
Section: Discussionmentioning
confidence: 99%