The effect of mitochondrially targeted anticancer agents on mitochondrial (super)complexes
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Electron Transport Chain Complex Proteins antagonists & inhibitors MeSH
- Cell Fractionation MeSH
- Humans MeSH
- Mitochondrial Proteins metabolism MeSH
- Mitochondria drug effects metabolism MeSH
- Antineoplastic Agents pharmacology MeSH
- Electron Transport drug effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Electron Transport Chain Complex Proteins MeSH
- Mitochondrial Proteins MeSH
- Antineoplastic Agents 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.
References provided by Crossref.org
Alternative assembly of respiratory complex II connects energy stress to metabolic checkpoints