We investigate the effects of quercetin on apoptosisinduced by menadione and hydrogen peroxide undertreatments of different time and dosage of the flavonoid in leukemic Jurkat T-cells and provide a series of useful data regarding the optimization of the time and dosage of quercetin administration in a flavonoid-menadionecombined treatment of leukemia. Our results indicate the ability of quercetin to enhance menadione-inducedapoptosis in Jurkat leukemia cells even at physiologicallevels of 5-10 μM. Having in view the growing interest ofusing delayed luminescence (DL) spectroscopy in clinical applications, a second goal of our study was to gain new insights into the biochemical mechanisms responsible for delayed luminescence of living cells. Thus, we haveinvestigated, for the first time to our knowledge, thecorrelation between apoptosis, oxidative stress and delayed luminescence. Our data are consistent with 1) the involvement of Complex I of the mitochondrial respiratory chain as an important source of delayed light emission on the 10 s - 10 ms scale, 2) the ability of superoxide anions to quench DL on the 100 s - 10 ms scale, probably via inhibition of reverse electron transferat the Fe/S centers in Complex I, and 3) the relative insensitivity of DL to intracellular OH°and H2O2 levels
Correlation between delayed luminescence and oxidative stress-induced apoptosis in human leukaemia Jurkat T-cells
SCORDINO, Agata;MUSUMECI, Francesco;BARRESI, VINCENZA;GRASSO, ROSARIA;CONDORELLI, Daniele Filippo;
2010-01-01
Abstract
We investigate the effects of quercetin on apoptosisinduced by menadione and hydrogen peroxide undertreatments of different time and dosage of the flavonoid in leukemic Jurkat T-cells and provide a series of useful data regarding the optimization of the time and dosage of quercetin administration in a flavonoid-menadionecombined treatment of leukemia. Our results indicate the ability of quercetin to enhance menadione-inducedapoptosis in Jurkat leukemia cells even at physiologicallevels of 5-10 μM. Having in view the growing interest ofusing delayed luminescence (DL) spectroscopy in clinical applications, a second goal of our study was to gain new insights into the biochemical mechanisms responsible for delayed luminescence of living cells. Thus, we haveinvestigated, for the first time to our knowledge, thecorrelation between apoptosis, oxidative stress and delayed luminescence. Our data are consistent with 1) the involvement of Complex I of the mitochondrial respiratory chain as an important source of delayed light emission on the 10 s - 10 ms scale, 2) the ability of superoxide anions to quench DL on the 100 s - 10 ms scale, probably via inhibition of reverse electron transferat the Fe/S centers in Complex I, and 3) the relative insensitivity of DL to intracellular OH°and H2O2 levelsFile | Dimensione | Formato | |
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