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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
