Involvement of mitochondrial ATP-sensitive potassium channels in etomidate preconditioning-induced protection in human myeloid HL-60 cells

Abstract Exposure of HL-60 cells, a human myeloid cell line, to 500 μM etomidate for 24 h reduced cell viability and increased nitric oxide production and mitochondrial permeability transition pore (mPTP) opening. Preconditioning (1 h) with 1 μM etomidate 4 h before exposure to the 500 μM dose of etomidate attenuated those detrimental effects. The mitochondrial ATP-sensitive potassium channel (mitoK ATP channel) inhibitor 5-hydroxydecanoic acid reduced the etomidate preconditioning effects. The mitoK ATP channel opener diazoxide attenuated the mPTP opening caused by the large dose of etomidate. Our results suggest that etomidate can induce a preconditioning effect that may involve mitoK ATP channel activation.