BID and NADH-supported state 3 respiration in normal PBMCs and leukemic blasts treated with α-bisabolol. (A) 24-hour α-bisabolol did not induced the cleavage of BID (full length 22 kDa, cleaved 15 kDa) at any concentration. Etoposide-treated Jurkat cells were used as a positive control for tBID. (B) No BID translocation was detected in mitochondrial fraction at different times and solubilized doses of α-bisabolol. α-tubulin and Hsp60 were used as markers for the cytosol and mitochondria fractions, respectively. A representative case is shown. (C) Permeabilized leukemic cells and healthy lymphocytes were incubated for 10 minutes in respiration buffer at 30°C in the presence or in the absence of 3 μM α-bisabolol. In treated leukemic cells, the G/M oxygen consumption was clearly lower than in untreated leukemic controls (p < 0.05). The S/G3P oxygen consumption was not modified by treatment, and the mitochondrial respiration was not stimulated by FCCP addition. This is in line with a direct effect of α-bisabolol on mitochondrial integrity. Healthy lymphocyte respiration was not affected by treatment. G/M: glutamate plus malate; S/G3P: succinate plus glycerol-3-phosphate; FCCP: carbonylcyanide-4-(trifluoromethoxy)-phenyl-hydrazone. Means ± SD of 6 leukemias and 6 normal donors are depicted.