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Rapid uptake of lipophilic triphenylphosphonium cations by mitochondria in vivo following intravenous injection: Implications for mitochondria-specific therapies and probes
Abstract
Background Mitochondrial dysfunction contributes to a range of pathologies, consequently there is a need to monitor mitochondrial function and to intervene pharmacologically to prevent mitochondrial damage. One approach to this is to deliver antioxidants, probes and pharmacophores to mitochondria by conjugation to the lipophilic triphenylphosphonium (TPP) cation that is taken up selectively by mitochondria driven by the membrane potential.Conclusions Oral administration of TPP-conjugated antioxidants protects against mitochondrial damage in vivo. However, there is also a need to deliver molecules rapidly to mitochondria to respond quickly to pathologies and for the real-time assessment of mitochondrial function.Methods To see if this was possible we investigated how rapidly TPP cations were taken up by mitochondria in vivo following intravenous (iv) administration.Results AlkylTPP cations were accumulated selectively by mitochondria within mice within 5 min of iv injection. The extent of uptake was enhanced 10-30-fold relative to simple alkylTPP cations by attaching functional groups to the TPP cation via long, hydrophobic alkyl chains. Conclusions: Mitochondria-targeted antioxidants, probes and pharmacophores can be delivered into mitochondria within minutes of iv administration.General significance These findings greatly extend the utility of mitochondria-targeted lipophilic cations as therapies and probes.
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“As triphenylphosphonium cations drive accumulation within cardiac mitochondria within minutes of intravenous administration14”
From Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I (2013) · cites this paper as [14]
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Self-citation
Metadata
- Authors
- Porteous, C. M., Logan, A., Evans, C., Ledgerwood, E. C., Menon, D. K., Aigbirhio, F., Smith, R. A. J., & Murphy, M. P.
- Affiliations
- University of Otago (NZ)
- MRC Mitochondrial Biology Unit (GB)
- University of Cambridge (GB)
- Corresponding author
- Murphy, Michael P.
- Venue
- Biochimica et Biophysica Acta (BBA) - General Subjects
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 1800
- Issue
- 9
- Pages
- 1009-1017
- ISSN
- 0304-4165 (ISSN-L)
- OpenAlex
- W1971782930
- Cited by
- 121
- References
- 55
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 1 · 2023: 4 · 2022: 9 · 2021: 8 · 2020: 7 · 2019: 10 · 2018: 6 · 2017: 12 · 2016: 7 · 2015: 7 · 2014: 12 · 2013: 11 · 2012: 9
- FWCI
- 3.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - General Subjects (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute for Health Research
- Asia New Zealand Foundation
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Physical Sciences › Materials Science › Biomaterials › Nanoparticle-Based Drug Delivery
- Keywords
- triphenylphosphonium cation, mitochondrial membrane potential, mitochondrial uptake, mitochondria-targeted antioxidants, hydrophobic alkyl chains, mitochondrial dysfunction, mitochondrial damage, intravenous administration
- MeSH terms
- Animals, Antioxidants, Cations, Female, Injections, Intravenous, Mitochondria, Organophosphorus Compounds, Drug Delivery Systems, Mitochondrial Diseases, Mice, Membrane Potential, Mitochondrial
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