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The effect of mitochondrially targeted anticancer agents on mitochondrial (super)complexes
M. Vondrusova, A. Bezawork-Geleta, K. Sachaphibulkij, J. Truksa, J. Neuzil,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- elektronový transportní řetězec antagonisté a inhibitory MeSH
- frakcionace buněk MeSH
- lidé MeSH
- mitochondriální proteiny metabolismus MeSH
- mitochondrie účinky léků metabolismus MeSH
- protinádorové látky farmakologie MeSH
- transport elektronů účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The mitochondrial respiratory chain is organized into dynamic high molecular weight complexes that associate to form supercomplexes. The function of these SCs is to minimize the production of reactive oxygen species (ROS) generated during electron transfer within them and to efficiently transfer electrons to complex IV. These supra-molecular structures as well as whole mitochondria are stress-responsive and respond to mitochondrially targeted anti-cancer agent by destabilization and induction of massive production of ROS leading to apoptosis. We have recently developed mitochondrially targeted anti-cancer agents epitomized by the mitochondrially targeted analogue of the redox-silent compound vitamin E succinate, which belongs to the group of agents that kill cancer cells via their mitochondria-destabilizing activity, referred to as mitocans. To understand the molecular mechanism of the effect of such agents, the use of native blue gel electrophoresis and clear native electrophoresis coupled with in-gel activity assays, are methods of choice. The relevant methodology is described in this chapter.
Citace poskytuje Crossref.org
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- $a The mitochondrial respiratory chain is organized into dynamic high molecular weight complexes that associate to form supercomplexes. The function of these SCs is to minimize the production of reactive oxygen species (ROS) generated during electron transfer within them and to efficiently transfer electrons to complex IV. These supra-molecular structures as well as whole mitochondria are stress-responsive and respond to mitochondrially targeted anti-cancer agent by destabilization and induction of massive production of ROS leading to apoptosis. We have recently developed mitochondrially targeted anti-cancer agents epitomized by the mitochondrially targeted analogue of the redox-silent compound vitamin E succinate, which belongs to the group of agents that kill cancer cells via their mitochondria-destabilizing activity, referred to as mitocans. To understand the molecular mechanism of the effect of such agents, the use of native blue gel electrophoresis and clear native electrophoresis coupled with in-gel activity assays, are methods of choice. The relevant methodology is described in this chapter.
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