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Changes in mitochondrial redox state, membrane potential and calcium precede mitochondrial dysfunction in doxorubicin-induced cell death.

Andrey V AV Kuznetsov, Raimund R Margreiter, Albert A Amberger, Valdur V Saks, and Michael M Grimm

ACTA-BIOENERG 1813(6):1144-52 (2011) PMID 21406203

Mitochondria play central roles in cell life as a source of energy and in cell death by inducing apoptosis. Many important functions of mitochondria change in cancer, and these organelles can be a target of chemotherapy. The widely used anticancer drug doxorubicin (DOX) causes cell death, inhibition of cell cycle/proliferation and mitochondrial impairment. However, the mechanism of such impairment is not completely understood. In our study we used confocal and two-photon fluorescence imaging together with enzymatic and respirometric analysis to study short- and long-term effects of doxorubicin on mitochondria in various human carcinoma cells. We show that short-term (

Copyright © 2011 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.bbamcr.2011.03.002
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