» Articles » PMID: 23411150

Mitochondrial Involvement and Oxidative Stress in Temporal Lobe Epilepsy

Overview
Date 2013 Feb 16
PMID 23411150
Citations 104
Authors
Affiliations
Soon will be listed here.
Abstract

A role for mitochondria and oxidative stress is emerging in acquired epilepsies such as temporal lobe epilepsy (TLE). TLE is characterized by chronic unprovoked seizures arising from an inciting insult with a variable seizure-free "latent period." The mechanism by which inciting injury induces chronic epilepsy, known as epileptogenesis, involves multiple cellular, molecular, and physiological changes resulting in altered hyperexcitable circuitry. Whether mitochondrial and redox mechanisms contribute to epileptogenesis remains to be fully clarified. Mitochondrial impairment is revealed in studies from human imaging and tissue analysis from TLE patients. The collective data from animal models suggest that steady-state mitochondrial reactive oxygen species and resultant oxidative damage to cellular macromolecules occur during different phases of epileptogenesis. This review discusses evidence for the role of mitochondria and redox changes occurring in human and experimental TLE. Potential mechanisms by which mitochondrial energetic and redox mechanisms contribute to increased neuronal excitability and therapeutic approaches to target TLE are delineated.

Citing Articles

MTH1 in the disorders of the central nervous system: scope beyond brain tumors and challenges.

Padmakumar L, Menon R, Gopala S, Vilanilam G Acta Neurol Belg. 2025; .

PMID: 39960601 DOI: 10.1007/s13760-025-02747-6.


The Role of Hypothalamic Microglia in the Onset of Insulin Resistance and Type 2 Diabetes: A Neuro-Immune Perspective.

Darwish R, Alcibahy Y, Bucheeri S, Albishtawi A, Tama M, Shetty J Int J Mol Sci. 2024; 25(23).

PMID: 39684879 PMC: 11642714. DOI: 10.3390/ijms252313169.


Abnormal metabolites in the dorsolateral prefrontal cortex of female epilepsy patients with migraine without aura.

Wang L, Pu H, Zhou J, Liu W, Zhang S, Tan Q Neuroreport. 2024; 35(18):1155-1162.

PMID: 39526657 PMC: 11540266. DOI: 10.1097/WNR.0000000000002110.


TBC1D15-regulated mitochondria-lysosome membrane contact exerts neuroprotective effects by alleviating mitochondrial calcium overload in seizure.

Xie Y, Zhang W, Peng T, Wang X, Lian X, He J Sci Rep. 2024; 14(1):23782.

PMID: 39390030 PMC: 11467349. DOI: 10.1038/s41598-024-74388-3.


Metabolic Adaptation in Epilepsy: From Acute Response to Chronic Impairment.

Liotta A, Loroch S, Wallach I, Klewe K, Marcus K, Berndt N Int J Mol Sci. 2024; 25(17).

PMID: 39273587 PMC: 11395010. DOI: 10.3390/ijms25179640.


References
1.
Frantseva M, Perez Velazquez J, Tsoraklidis G, Mendonca A, Adamchik Y, Mills L . Oxidative stress is involved in seizure-induced neurodegeneration in the kindling model of epilepsy. Neuroscience. 2000; 97(3):431-5. DOI: 10.1016/s0306-4522(00)00041-5. View

2.
Floor E, Wetzel M . Increased protein oxidation in human substantia nigra pars compacta in comparison with basal ganglia and prefrontal cortex measured with an improved dinitrophenylhydrazine assay. J Neurochem. 1998; 70(1):268-75. DOI: 10.1046/j.1471-4159.1998.70010268.x. View

3.
Ogunmekan A, Hwang P . A randomized, double-blind, placebo-controlled, clinical trial of D-alpha-tocopheryl acetate (vitamin E), as add-on therapy, for epilepsy in children. Epilepsia. 1989; 30(1):84-9. DOI: 10.1111/j.1528-1157.1989.tb05287.x. View

4.
Chuang Y, Chen S, Liou C, Lin T, Chang W, Chan S . Contribution of nitric oxide, superoxide anion, and peroxynitrite to activation of mitochondrial apoptotic signaling in hippocampal CA3 subfield following experimental temporal lobe status epilepticus. Epilepsia. 2009; 50(4):731-46. DOI: 10.1111/j.1528-1167.2008.01778.x. View

5.
Esposito L, Melov S, Panov A, Cottrell B, Wallace D . Mitochondrial disease in mouse results in increased oxidative stress. Proc Natl Acad Sci U S A. 1999; 96(9):4820-5. PMC: 21775. DOI: 10.1073/pnas.96.9.4820. View