The phytoalexin resveratrol (RESV) displays antiparasitic activity against Philasterides dicentrarchi, a scuticociliate pathogen of turbot, and causes oxidative stress, inhibition of antioxidant enzyme activity and morphological alterations in the parasite mitochondria. In this study, we analysed the mitochondrial biology of P. dicentrarchi and assessed the effect of RESV on mitochondrial metabolism. We found that RESV caused dose-dependent inhibition of mitochondrial electron transport and O(2) consumption in ciliates permeabilized with digitonin. Although the RESV molecule has a high capacity for antiradical and antioxidant activity, it induced a high level of pro-oxidant activity against the ciliate, thus causing a significant increase in intracellular ROS production. The increased ROS production was accompanied by mitochondrial collapse and dysfunction of mitochondrial membrane potential (ΔΨm) and by a significant increase in intracellular Ca(+2) levels. RESV inhibited parasite growth in a similar way to antimycin A, an inhibitor of mitochondrial electron transport and ROS generator. The findings confirm the mitochondria as a target in the potential development of effective antiparasitic treatments.