Table 3.

Observed anticonvulsive and neuroprotective actions of novel, potent antioxidants.

Substance	Cells/Animals/Humans	Model	References
Potential antioxidant actions
Aspalatone
GPx mimetic [202]
inhibits seizures, oxidative stress, and hippocampal neuronal death enhances antiperoxidative enzyme activity, like GPx and CAT in blood directly scavenges hydroxyl radicals, but not SOD	Animal modelIn vitro ESR study	KA -	[115] [115]
EUK-134 (new, potent SOD mimetic)
Prevents oxidative stress and reduces neuronal damage [117] blocks neuronal death, LPO, nitrite formation and NA oxidation mediates suppression of: AP-1 and NF-jB DNA-binding activity transcription factors susceptible for oxidative stress	In vitro model Animal model	- KA	[203] [127]
does not affect seizure latency and duration	Animal model	KA	[117, 118]
MnTBAP
Inhibits mitochondrial oxidative stress and neuronal loss inhibits rat hippocampal superoxide production, 8-OHdG formation and neuronal loss inhibits neuronal loss in hippocampus CA3 region by 60% prevents KA-induced mitochondrial aconitase inactivation by 75% inhibits KA-induced raise in 8-OHdG/2-dG ratio by 50% inhibits mitochondrial O2- formation and DNA oxidative damage with no effects exerted on behavioural seizures	Animal model (rats)	KA	[118-120]
Tempol
Protects neuronal cells and exerts anticonvulsant effects via: suppression of apoptosis suppression of SOD formation inhibition of nitrite formation	Animal models	KA	[121]
There were no effects exerted on seizure-like activity in hippocampus	Animal models	KA	[121]

8-OHdG – 8-hydroxy-2-deoxyguanosine, AP-1 – activator protein, CAT – catalase, DNA – deoxyribonucleic acid, ESR - electron spin resonance, GPx – glutathione peroxidase, GSH – glutathione, MnTBAP – Mn(III)tetrakis (4-benzoic acid) porphyrin, KA – kainic acid, LPO- lipid peroxidation, NF – nuclear factor, SOD - superoxide dismutase.