ArticleAnnals of the New York Academy of Sciences2008
The mitochondrial antioxidants MitoE(2) and MitoQ(10) increase mitochondrial Ca(2+) load upon cell stimulation by inhibiting Ca(2+) efflux from the organelle.
Article in Annals of the New York Academy of Sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Article
- The Application and Molecular Mechanisms of Mitochondria-Targeted Antioxidants in Chemotherapy-Induced Cardiac Injury.Current issues in molecular biology · 2025Review
- Mitochondria-Targeted Antioxidant MitoQ Improves In Vitro Maturation and Subsequent Embryonic Development from Culled Cows.Animals : an open access journal from MDPI · 2024Article
- Risks of using mitoquinone during in vitro maturation and its potential protective effects against lipotoxicity-induced oocyte mitochondrial stress.Journal of assisted reproduction and genetics · 2024Article
- Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction.Cellular and molecular life sciences : CMLS · 2024Review
- Mitoquinone mesylate attenuates pathological features of lean and obese allergic asthma in mice.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Mitochondria-Targeted Antioxidants MitoQ and MitoTEMPO Do Not Influence BRAF-Driven Malignant Melanoma and KRAS-Driven Lung Cancer Progression in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Mitochondrial Targeting of Antioxidants Alters Pancreatic Acinar Cell Bioenergetics and Determines Cell Fate.International journal of molecular sciences · 2019Article
- Nanopreparations for mitochondria targeting drug delivery system: Current strategies and future prospective.Asian journal of pharmaceutical sciences · 2017Review
- Mitochondrial thiol modification by a targeted electrophile inhibits metabolism in breast adenocarcinoma cells by inhibiting enzyme activity and protein levels.Redox biology · 2016Article
- Selective Inhibition of the Mitochondrial Permeability Transition Pore Protects against Neurodegeneration in Experimental Multiple Sclerosis.The Journal of biological chemistry · 2016Article
- Mitochondrial Probe Methyltriphenylphosphonium (TPMP) Inhibits the Krebs Cycle Enzyme 2-Oxoglutarate Dehydrogenase.PloS one · 2016Article
- Oxidative stress-induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease.The Journal of allergy and clinical immunology · 2015Article
- Molecular strategies for targeting antioxidants to mitochondria: therapeutic implications.Antioxidants & redox signaling · 2015Review
- Mitochondrial hormesis and diabetic complications.Diabetes · 2015Review
- Lipophilic triphenylphosphonium cations inhibit mitochondrial electron transport chain and induce mitochondrial proton leak.PloS one · 2015Article
- Infrared laser pulse triggers increased singlet oxygen production in tumour cells.Scientific reports · 2013Article
- Mitochondria in lung diseases.Expert review of respiratory medicine · 2013Review
- Mitochondrially targeted compounds and their impact on cellular bioenergetics.Redox biology · 2013Article
- Synaptic mitochondrial pathology in Alzheimer's disease.Antioxidants & redox signaling · 2012Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Mitochondrial reactive oxygen species (ROS) production is recognized as a major pathogenic event in a number of human diseases, and mitochondrial scavenging of ROS appears a promising therapeutic approach. Recently, two mitochondrial antioxidants have been developed; conjugating alpha-tocopherol and the ubiquinol moiety of coenzyme Q to the lipophilic triphenylphosphonium cation (TPP+), denominated MitoE(2) and MitoQ(10), respectively. We have investigated the effect of these compounds on mitochondrial Ca(2+) homeostasis, which controls processes as diverse as activation of mitochondrial dehydrogenases and pro-apoptotic morphological changes of the organelle. We demonstrate that treatment of HeLa cells with both MitoE(2) and MitoQ(10) induces (albeit with different efficacy) a major enhancement of the increase in matrix Ca(2+) concentration triggered by cell stimulation with the inositol 1,4,5-trisphosphate-generating agonist histamine. The effect is a result of the inhibition of Ca(2+) efflux from the organelle and depends on the TPP+ moiety of these compounds. Overall, the data identify an effect independent of their antioxidant activity, that on the one hand may be useful in addressing disorders in which mitochondrial Ca(2+) handling is impaired (e.g., mitochondrial diseases) and on the other may favor mitochondrial Ca(2+) overload and thus increase cell sensitivity to apoptosis (thus possibly counteracting the benefits of the antioxidant activity).
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