Fig. 2.

Mitochondrial oxidative stress increased in a time-dependent manner following Li-Pilo-induced epileptogenesis. (a) Levels of steady-state mitochondrial H₂O₂ production from the hippocampus expressed as a percentage change compared to controls from 24 h to 3 months post-SE from rats receiving diazepam 90 min following the onset of SE. Bars represent mean ± SEM, n = 5–6 per time point. **p ≤ 0.01, one-way anova. (b) Levels of steady-state mitochondrial H₂O₂ production from the hippocampus up to 48 h post-SE in a subset of rats not receiving diazepam to attenuate motor seizures during SE. Note that mitochondrial H₂O₂ production increased significantly when seizures were allowed to continue unabated during SE. Bars represent mean ± SEM, n = 5 per time point, ***p < 0.001, one-way anova.