| pubmed-article:21406203 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0025251 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0030012 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:21406203 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
| pubmed-article:21406203 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:21406203 | pubmed:dateCreated | 2011-5-10 | lld:pubmed |
| pubmed-article:21406203 | pubmed:abstractText | 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. | lld:pubmed |
| pubmed-article:21406203 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21406203 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21406203 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21406203 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:21406203 | pubmed:issn | 0006-3002 | lld:pubmed |
| pubmed-article:21406203 | pubmed:author | pubmed-author:GrimmMichaelM | lld:pubmed |
| pubmed-article:21406203 | pubmed:author | pubmed-author:MargreiterRai... | lld:pubmed |
| pubmed-article:21406203 | pubmed:author | pubmed-author:SaksValdurV | lld:pubmed |
| pubmed-article:21406203 | pubmed:author | pubmed-author:KuznetsovAndr... | lld:pubmed |
| pubmed-article:21406203 | pubmed:author | pubmed-author:AmbergerAlber... | lld:pubmed |
| pubmed-article:21406203 | pubmed:copyrightInfo | Copyright © 2011 Elsevier B.V. All rights reserved. | lld:pubmed |
| pubmed-article:21406203 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:21406203 | pubmed:volume | 1813 | lld:pubmed |
| pubmed-article:21406203 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21406203 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21406203 | pubmed:pagination | 1144-52 | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:meshHeading | pubmed-meshheading:21406203... | lld:pubmed |
| pubmed-article:21406203 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21406203 | pubmed:articleTitle | Changes in mitochondrial redox state, membrane potential and calcium precede mitochondrial dysfunction in doxorubicin-induced cell death. | lld:pubmed |
| pubmed-article:21406203 | pubmed:affiliation | Department of Heart Surgery, Innsbruck Medical University, Innrain 66, Innsbruck A-6020, Austria. andrey.kuznetsov@uki.at | lld:pubmed |
| pubmed-article:21406203 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21406203 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
