1. Oxidative stress is involved in seizure-induced neurodegeneration in the kindling model of epilepsy.
- Author
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Frantseva MV, Perez Velazquez JL, Tsoraklidis G, Mendonca AJ, Adamchik Y, Mills LR, Carlen PL, and Burnham MW
- Subjects
- Animals, Antioxidants pharmacology, Disease Models, Animal, Epilepsy drug therapy, Epilepsy pathology, Hippocampus drug effects, Hippocampus pathology, Hippocampus physiopathology, Kindling, Neurologic pathology, Lipid Peroxidation drug effects, Lipid Peroxidation physiology, Male, Nerve Degeneration drug therapy, Nerve Degeneration pathology, Rats, Rats, Long-Evans, Epilepsy physiopathology, Kindling, Neurologic metabolism, Nerve Degeneration physiopathology, Oxidative Stress physiology
- Abstract
Reactive oxygen species have been implicated in the development of seizures under pathological conditions and linked to seizure-induced neurodegeneration. There has been little direct evidence, however, of free radical production resulting from seizures. Using amygdala-kindled rats, we have examined the generation of reactive oxygen species following seizures, and their possible contribution to seizure development and seizure-induced neuronal loss. The concentrations of two products of free radical-induced lipid peroxidation, malonaldehyde and 4-hydroxy-2(E)-nonenal, were measured using colorimetric assays. Lipid peroxidation was increased in both hemispheres of kindled rats as compared to sham-operated controls. Cell death was also significantly increased in all hippocampal areas. Antioxidants (vitamin E and glutathione) prevented the rise in lipid peroxides and hippocampal neuronal death during kindling, but did not arrest the development of seizures.Thus, epileptiform activity can result in free radical production which may be one of the factors leading to cell death.
- Published
- 2000
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