“…Cocaine also decreased FCCPstimulated respiration and ΔΨ m in complex I-energized brain and liver mitochondria, but not in mitochondria energized with complex II substrates, suggesting an important role of complex I in mediating cocaine effects in both tissues. A decrease in ΔΨ m also occurred in cocaine-exposed liver mitochondria energized through complex II, suggesting that, at least in the liver, cocaine effect on ΔΨ m is independent of mitochondrial respiration impairment (Cunha-Oliveira et al, 2013d), probably due to a dissipation of charge associated with the weak base effect, as described for other intracellular compartments (Sulzer & Rayport, 1990). Cocaine effect on complex I was shown to be independent of disrupted nicotinamide adenine nucleotide reduced form (NADH) supply, because the drug also decreased oxygen consumption in mitochondrial fractions energized with NADH.…”