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We investigated the effects of nimesulide, a recently developed non‐steroidal anti‐inflammatory drug, and of a metabolite resulting from reduction of the nitro group to an amine derivative, on succinate‐energized isolated rat liver mitochondria incubated in the absence or presence of 20 μM Ca²⁺, 1 μM cyclosporin A (CsA) or 5 μM ruthenium red.

Nimesulide uncoupled mitochondria through a protonophoretic mechanism and oxidized mitochondrial NAD(P)H, both effects presenting an EC₅₀ of approximately 5 μM.

Within the same concentration range nimesulide induced mitochondrial Ca²⁺ efflux in a partly ruthenium red‐sensitive manner, and induced mitochondrial permeability transition (MPT) when ruthenium red was added after Ca²⁺ uptake by mitochondria. Nimesulide induced MPT even in de‐energized mitochondria incubated with 0.5 mM Ca²⁺.

Both Ca²⁺ efflux and MPT were prevented to a …