Abstract
Mitochondrial dysfunctions have been highlighted as a contributing factor in epileptic seizures and subsequent neuronal cell death. Soman is an irreversible inhibitor of cholinesterase, triggering epileptic seizures leading to massive neuronal cell death in brain areas, such as the hippocampus and cerebral cortex. Mitochondrial respiratory chain enzymatic assays were performed in hippocampus and cerebral cortex homogenates from mouse brains collected 3 hours, 24 hours, 3 days, and 7 days after soman poisoning. Our results suggest that mitochondrial enzymatic alterations stem more likely from secondary effects of the poisoning, rather than from any fallout effect from neuronal cell death.
Acknowledgments
This work was supported by grants from the DGA-DSP-STTC-SH (Délégation Générale pour l’Armement; grant nos. 02-CO-006 and 07-CO-501 to J-MC) of the French Ministry of Defense.
Declaration of interest: The authors report no financial conflicts of interest. The authors alone are responsible for the content and writing of this paper.