Abstract
Hydroethidine is reported to be selectively oxidized to ethidium by superoxide. Using digital imaging and fluorescence microscopy it is possible to evaluate neuronal ethidium accumulation in specific brain regions of rats damaged in the lithium–pilocarpine model of status epilepticus. Intravenous or intraperitoneal administration of hydroethidine prior to 1 h of status epilepticus produced diffuse cytosolic distribution of ethidium fluorescence suggesting an increased neuronal production of superoxide that was not observed in control animals. A significantly increased number of neurons with the enhanced ethidium fluorescence was observed in parietal cortex, piriform cortex, perirhinal cortex, lateral amygdala, mediodorsal thalamus and laterodorsal thalamus, suggesting superoxide as a mechanism of neuronal injury in those regions. Other regions injured by lithium-pilocarpine seizures, such as the basolateral amygdala and hippocampus, did not demonstrate the enhanced neuronal ethidium fluorescence. In such regions it is possible that superoxide is not a mechanism of injury or that 1 h of status epilepticus is not sufficient to produce superoxide or other reactive oxygen species.
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