Difference between revisions of "Kuznetsov 2011 Biochim Biophys Acta"
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{{Publication | {{Publication | ||
|title=Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M | |title=Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M (2011) Changes in mitochondrial redox state, membrane potential and calcium precede mitochondrial dysfunction in doxorubicin-induced cell death. Biochim Biophys Acta 1813:1144-52. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21406203 PMID:21406203] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/21406203 PMID:21406203] | ||
|authors=Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M | |authors=Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M | ||
|year=2011 | |year=2011 | ||
|journal=Biochim | |journal=Biochim Biophys Acta | ||
|abstract=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 (<30 min) effects include i) rapid changes in mitochondrial redox potentials towards a more oxidized state (flavoproteins and NADH), ii) mitochondrial depolarization, iii) elevated matrix calcium levels, and iv) mitochondrial ROS production, demonstrating a complex pattern of mitochondrial alterations. Significant inhibition of mitochondrial endogenous and uncoupled respiration, ATP depletion and changes in the activities of marker enzymes were observed after 48 h of DOX treatment (long-term effects) associated with cell cycle arrest and death. | |abstract=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 (<30 min) effects include i) rapid changes in mitochondrial redox potentials towards a more oxidized state (flavoproteins and NADH), ii) mitochondrial depolarization, iii) elevated matrix calcium levels, and iv) mitochondrial ROS production, demonstrating a complex pattern of mitochondrial alterations. Significant inhibition of mitochondrial endogenous and uncoupled respiration, ATP depletion and changes in the activities of marker enzymes were observed after 48 h of DOX treatment (long-term effects) associated with cell cycle arrest and death. | ||
|keywords=confocal imaging, doxorubicin, mitochondria, mitochondrial function, redox state, reactive oxygen species (ROS) | |keywords=confocal imaging, doxorubicin, mitochondria, mitochondrial function, redox state, reactive oxygen species (ROS) | ||
|mipnetlab=FR_Grenoble_Saks | |mipnetlab=FR_Grenoble_Saks VA | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Human | |||
|tissues=Endothelial;epithelial;mesothelial cell | |||
|preparations=Intact cells | |||
|injuries=Cell death, Oxidative stress;RONS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |additional=colon cancer, breast cancer | ||
}} | }} | ||
Latest revision as of 15:53, 16 February 2015
| Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M (2011) Changes in mitochondrial redox state, membrane potential and calcium precede mitochondrial dysfunction in doxorubicin-induced cell death. Biochim Biophys Acta 1813:1144-52. |
Kuznetsov AV, Margreiter R, Amberger A, Saks V, Grimm M (2011) Biochim Biophys Acta
Abstract: 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 (<30 min) effects include i) rapid changes in mitochondrial redox potentials towards a more oxidized state (flavoproteins and NADH), ii) mitochondrial depolarization, iii) elevated matrix calcium levels, and iv) mitochondrial ROS production, demonstrating a complex pattern of mitochondrial alterations. Significant inhibition of mitochondrial endogenous and uncoupled respiration, ATP depletion and changes in the activities of marker enzymes were observed after 48 h of DOX treatment (long-term effects) associated with cell cycle arrest and death. • Keywords: confocal imaging, doxorubicin, mitochondria, mitochondrial function, redox state, reactive oxygen species (ROS)
• O2k-Network Lab: FR_Grenoble_Saks VA
Labels:
Stress:Cell death, Oxidative stress;RONS Organism: Human Tissue;cell: Endothelial;epithelial;mesothelial cell Preparation: Intact cells
HRR: Oxygraph-2k
colon cancer, breast cancer
