Effects of the mitochondrial respiration inhibitor, rotenone, on apoptosis, clonogenic survival and delayed luminescence of human leukemia jurkat T-cells

We investigated apoptosis and delayed luminescence (DL) of human leukemia Jurkat cells treated with the mitochondrial respiration inhibitor, rotenone (ROT). ROT decreased clonogenic survival and induced apoptosis in a dose-dependent manner. Apoptosis evolved slowly, with a maximum effect observed at 48 h, when the apoptotic cell fraction was strongly correlated with clonogenic survival. Our data indicate that DL detected at 686 nm in the rime range 100 us – 1 ms can be a good measure of the electron transfer at the level of the N2 center, the closest to the ubiquinone site in Complex I of the mitochondrial respiratory chain, which was characterized by a dominant decay time constant of 132 us. In addition, our measurements suggest that DL is quantitatively correlated with the level of reduced nicotinamide adenine dinucleotide (NADH), the substrate of mitochondrial respiration at the level of Complex I