Selective and reversible disruption of mitochondrial inner membrane protein complexes by lipophilic cations
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
MC_UU_00015/7
Medical Research Council - United Kingdom
MC_ UU_00015/7
Medical Research Council - United Kingdom
PubMed
36402364
DOI
10.1016/j.mito.2022.11.006
PII: S1567-7249(22)00103-9
Knihovny.cz E-resources
- Keywords
- Inner mitochondrial membrane, Lipophilic cations, MitoQ, Mitochondria, Mitochondrial dynamics, Respiratory chain,
- MeSH
- Antioxidants * pharmacology MeSH
- Cations metabolism pharmacology MeSH
- Membrane Proteins metabolism MeSH
- Membrane Potential, Mitochondrial MeSH
- Mitochondrial Membranes metabolism MeSH
- Mitochondria * metabolism MeSH
- Organophosphorus Compounds pharmacology MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants * MeSH
- Cations MeSH
- Membrane Proteins MeSH
- Organophosphorus Compounds MeSH
Triphenylphosphonium (TPP) derivatives are commonly used to target chemical into mitochondria. We show that alkyl-TPP cause reversible, dose- and hydrophobicity-dependent alterations of mitochondrial morphology and function and a selective decrease of mitochondrial inner membrane proteins including subunits of the respiratory chain complexes, as well as components of the mitochondrial calcium uniporter complex. The treatment with alkyl-TPP resulted in the cleavage of the pro-fusion and cristae organisation regulator Optic atrophy-1. The structural and functional effects of alkyl-TPP were found to be reversible and not merely due to loss of membrane potential. A similar effect was observed with the mitochondria-targeted antioxidant MitoQ.
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