Enhanced hippocampal F2-isoprostane formation following kainate-induced seizures.

Patel M, Liang LP, Roberts LJ
J Neurochem. 2001 79 (5): 1065-9

PMID: 11739620 · DOI:10.1046/j.1471-4159.2001.00659.x

We attempted to obtain evidence for the occurrence of oxidant injury following seizure activity by measuring hippocampal F2-isoprostanes (F2-IsoPs), a reliable marker of free radical-induced lipid peroxidation. Formation of F2-IsoPs esterified in hippocampal phospholipids was correlated with hippocampal neuronal loss and mitochondrial aconitase inactivation, a marker of superoxide production in the kainate model. F2-IsoPs were measured in microdissected hippocampal CA1, CA3 and dentate gyrus (DG) regions at various times following kainate administration. Kainate produced a large increase in F2-IsoP levels in the highly vulnerable CA3 region 16 h post injection. The CA1 region showed small, but statistically insignificant increases in F2-IsoP levels. Interestingly, the DG, a region resistant to kainate-induced neuronal death also showed marked (2.5-5-fold) increases in F2-IsoP levels 8, 16, and 24 h post injection. The increases in F2-Isop levels in CA3 and DG were accompanied by inactivation of mitochondrial aconitase in these regions. This marked subregion-specific increase in F2-Isop following kainate administration suggests that oxidative lipid damage results from seizure activity and may play an important role in seizure-induced death of vulnerable neurons.

MeSH Terms (17)

Aconitate Hydratase Animals Cell Count Cell Death Cell Survival Excitatory Amino Acid Agonists F2-Isoprostanes Fumarate Hydratase Hippocampus Kainic Acid Lipid Peroxidation Male Mitochondria Rats Rats, Sprague-Dawley Seizures Superoxides

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