Rotenone Decreases Ischemia-Induced Injury by Inhibiting Mitochondrial Permeability Transition: A Study in Brain

Abstract

Mitochondria participate in many physiological and pathological processes in the cells, including cellular energy supply, regulation of calcium homeostasis, apoptosis, and ROS generation. Alterations of mitochondrial functions, especially the opening of mitochondrial permeability transition pore (mPTP) are the main mechanisms responsible for the ischemic brain damage. Recently, the inhibitors of the Complex I of mitochondrial respiratory chain emerged as promising suppressors of mitochondrial ROS generation and mPTP opening. Here we describe the assay that can be implemented easily to evaluate the protective effects of rotenone or other potential inhibitors of the Complex I of mitochondrial respiratory chain against acute ischemia-induced injuries in brain.

Keywords: Brain ischemia; Calcium retention capacity; Complex I; Complex II; Isolated brain mitochondria; Mitochondrial permeability transition pore; Mitochondrial respiration; ROS generation; Rotenone.