Difference between revisions of "Montaigne 2011 Mitochondrion"
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|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|organism=Human | |organism=Human | ||
|tissues= | |tissues=Heart | ||
|preparations=Isolated Mitochondria | |preparations=Isolated Mitochondria | ||
}} | }} | ||
TPP: WPI electrode | TPP: WPI electrode | ||
Revision as of 12:03, 27 February 2013
| Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Doxorubicin induces mitochondrial permeability transition and contractile dysfunction in the human myocardium. Mitochondrion 11: 22-26. |
Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Mitochondrion
Abstract: In human atrial trabeculae, we examined the effects of doxorubicin on the isometric force of contraction, mitochondrial respiration, membrane potential and calcium retention capacity. Compared with untreated controls, doxorubicin induced contractile dysfunction and depression of mitochondrial respiration. Mitochondria isolated from doxorubicin-treated human atrial trabeculae displayed reduced transmembrane potential and calcium retention capacity. Cyclosporine A, a mitochondrial membrane transition pore opening blocker, prevented mitochondrial dysfunction and impaired contractile performance induced by doxorubicin. The study suggests that a mitochondrial membrane transition pore opening is involved in the development of doxorubicin cardiotoxicity in human hearts.
• O2k-Network Lab: FR Lille Neviere R
Labels:
Organism: Human
Tissue;cell: Heart
Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
TPP: WPI electrode
