Persistent mitoKATP Activation Is Involved in the Isoflurane-induced Cytotoxicity

摘要: Isoflurane exposure induces apoptosis in cultured cells and the developing brain, while underlying mechanism remains largely unclarified. This study was designed to determine whether disruption of mitoKATP-mediated ATP balance involved cytotoxicity isoflurane. Human neuroglioma U251 7-day-old mice were treated with A specific mitoKATP antagonist 5-HD used, cellular levels, NAD+/NADH ratios, mitochondrial transmembrane potential (ΔΨm) measured. Our data showed that blockage by mitigated isoflurane-induced ΔΨm disruption, reactive oxygen species (ROS) accumulation, cells. Moreover, we found toxic effect isoflurane not observed first 2-h exposure; instead, levels ratios markedly increased. The reduction only detected after this initial phase. dynamical blocked 5-HD. In contrast, a ROS scavenger NAC sustained elevation. Similar results animal studies. And again, attenuated cognitive disorders Intellicage test, system assesses place learning behavior social environment. uncovered isoflurane's toxicity therapeutic future.