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. 2015 Feb 19;4(2):183–191. doi: 10.1002/open.201402091

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© 2014 The Authors. Published by Wiley-VCH Verlag GmbH & Co. KGaA.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Compound 1 is able to induce reactive oxygen species (ROS) and sensitize the permeability transition pore (PTP). a) Dose-response and ROS kinetics measured on mitochondria of MEF-NF1^−/− treated up to 120 min with 20 μm and 40 μm of 1; values represent the mean ± S.D. of at least n=5. b) Left: changes on pore permeability transition induced by compound 1 on purified mitochondria from mouse liver and measured by calcium retention capacity (CRC). Right: same experiments carried out in the presence of the inhibitor cyclosporine A (CSA), added 1 h before treatment. Values represent the mean ± S.D. of at least n=4. c) Left: example of a single experiment of PTP sensibility measured by a CRC assay on whole MEF-NF1^−/−cells treated with different doses of 1. Mitochondrial calcium uptake is plotted in terms of Calcium Green-5N fluorescence. Right: average histogram of the total Ca²⁺ uptake before PTP opening (error bars represent the S.D. for n=3).