Oxidative stress associated with neuronal apoptosis in experimental models of epilepsy

Abstract

Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

Figure 1

A proposed model of the relationship between apoptosis cell death in epilepsy models. AIF (apoptosis-inducing factor); Apaf 1 (apoptosis protease activating factor-1); Bcl-2 (antiapoptotic protein); Bax (proapoptotic proteins); CAD (caspase activated DNase); ICAD (inhibitor of caspase activated DNase); NOS (nitric oxide synthase), ON (oxide nitric); OONHO⁻ (peroxide nitrite); LPO (lipid peroxidation); ROS (reactive oxygen species); RNS (reactive nitrogen species); Ca²⁺ (calcium); FADD (Fas-associated protein with death domain); Cyto c (cytochrome c).

Figure 2

Representative photomicrographs of hippocampal fields of rats at several times after injection of KA or PTZ. Sections stained with cresyl violet, showing neuronal cells in the hippocampus CA1 field (a, b, and c). Hippocampus showing immunoreactive pyramidal cells to caspase-9 (d, e, and f). Immunoreactive cells to caspase-3. The caspase-3 staining was observed in the cytoplasm and nucleus (g, h, and i). Some pyramidal cells (j and k) and granular cells (l) of dentate gyrus were stained positively for TUNEL (↑).