Stress pathways induced by volatile anesthetics and failure of preconditioning in a mitochondrial Complex I mutant.

Mutation of an mETC Complex I subunit generates differential effects of isoflurane and sevoflurane on gene expression that may underlie their differential effects on neurotoxicity. Additionally, the mutation produces resistance to preconditioning by stresses that protect the brain in other contexts. Therefore, Complex I activity modifies molecular and physiological effects of anesthetics in an anesthetic-specific manner.