The DOI matches its Crossref record; 130 of the 130 references it cites were found in a registry or an index.
Targeting Antioxidants to Mitochondria by Conjugation to Lipophilic Cations
Abstract
Mitochondrial oxidative damage contributes to a range of degenerative diseases. Consequently, the selective inhibition of mitochondrial oxidative damage is a promising therapeutic strategy. One way to do this is to invent antioxidants that are selectively accumulated into mitochondria within patients. Such mitochondria-targeted antioxidants have been developed by conjugating the lipophilic triphenylphosphonium cation to an antioxidant moiety, such as ubiquinol or α-tocopherol. These compounds pass easily through all biological membranes, including the blood-brain barrier, and into muscle cells and thus reach those tissues most affected by mitochondrial oxidative damage. Furthermore, because of their positive charge they are accumulated several-hundredfold within mitochondria driven by the membrane potential, enhancing the protection of mitochondria from oxidative damage. These compounds protect mitochondria from damage following oral delivery and may therefore form the basis for mitochondria-protective therapies. Here we review the background and work to date on this class of mitochondria-targeted antioxidants.
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In the citing paper
“MitoQ rapidly crosses the blood– brain barrier and neuronal membranes and concentrates several hundred-fold in mitochondria driven by the high membrane potential across the inner mitochondrial membrane (IMM; Murphy and Smith, 2007).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Murphy and Smith, 2007
In the citing paper
“The recently developed, mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienlyl) decyl triphenylphosphonium methanesulfonate]) possesses these qualities (James et al., 2005, 2007; Murphy and Smith, 2007).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Murphy and Smith, 2007
In the citing paper
“Although in most cases this semiquinone is rapidly oxidized, its reaction with oxygen leads to superoxide production at this site (567, 678).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [678]
In the citing paper
“Although the majority of electrons entering the ETC ultimately reduce oxygen to water at complex IV, a small proportion (~2–11%) of electrons escape from the chain at complex I or III to generate superoxide (34, 115, 678).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [678]
In the citing paper
“Importantly, specific complex III inhibitors, such as Antimycin A, can stabilize this semiquinone radical, significantly enhancing superoxide production by complex III (678).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [678]
In the citing paper
“Moreover, treatment with MitoQ, a substance known to scavenge matrix mtROS (see Section 6) [314,315], gave contrasting results: only IL-1β cleavage was reduced, whereas TNF and IL-10 levels remained unaltered.”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [314]
In the citing paper
“whereas MitoQ is an analog of ubiquinone and prevents lipid peroxidation in mitochondrial membranes [314,315].”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [314]
In the citing paper
“MitoTEMPO is a combination of the antioxidant TEMPO attached to the TPP group and hence dismutates O2●− to H2O2 in the mitochondrial matrix [314,391]”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [314]
In the citing paper
“MitoTEMPO and MitoQ both are targeted to and accumulated in mitochondria due to their TPP group.”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [314]
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Self-citationChapter 22 The Uptake and Interactions of the Redox Cycler Paraquat with Mitochondria
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Metadata
- Authors
- Murphy, M. P., & Smith, R. A. J.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- University of Otago (NZ)
- ORCID
- Murphy, Michael P.
- Venue
- Annual Review of Pharmacology and Toxicology
- Publisher
- Annual Reviews
- Published
- 2007-02-01
- Volume
- 47
- Issue
- 1
- Pages
- 629-656
- ISSN
- 0362-1642 (ISSN-L)
- 1545-4304
- OpenAlex
- W2140014506
- Cited by
- 1,173
- References
- 130
- Citations by year
- 2026: 64 · 2025: 62 · 2024: 72 · 2023: 42 · 2022: 65 · 2021: 67 · 2020: 61 · 2019: 57 · 2018: 61 · 2017: 62 · 2016: 67 · 2015: 67 · 2014: 62 · 2013: 59 · 2012: 68
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Annual Review of Pharmacology and Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Keywords
- mitochondria-targeted antioxidants, triphenylphosphonium cation, lipophilic cations, mitochondrial oxidative damage, ubiquinol, alpha-tocopherol, mitochondrial membrane potential, blood-brain barrier, oral drug delivery, degenerative diseases, mitochondrial protection
- MeSH terms
- Antioxidants, Cations, Drug Carriers, Humans, Membrane Potentials, Mitochondria, Tissue Distribution, Drug Delivery Systems, Reactive Oxygen Species, Mitochondrial Diseases
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