RESEARCH STUDIES & CLINICAL TRIALS

Founded in science, studied around the world, clinically tested.

MitoQ encourages the scientific community to explore and discover the benefits of our ingredient Mitoquinol Mesylate.

INDEPENDENT RESEARCH

19 clinical trials, 750+ peer-reviewed scientific papers, and over $60 million invested in a broad range of independent studies.

TOP UNIVERSITIES

Harvard University, UCLA, University of Cambridge and more leading institutions around the world have studied MitoQ’s cellular health optimization.

CONTINUED INNOVATION

Our product development team continues to explore the leading edge of cellular health science, resulting in over 60 global patents for our molecular technology.

Meet our MitoQ science experts

a headshot of Professor Mike Murphy in cell shape

PROFESSOR MIKE MURPHY

Ph.D., MitoQ co-founder and Professor of Mitochondrial Redox Biology at the University of Cambridge

a headshot of Dr Richard Siow in cell shape

DR RICHARD SIOW

Ph.D., Director of Ageing Research at King’s College London, Honorary Secretary General of European Society of Preventive Medicine

a headshot of Professor Marcia Haigis in cell shape

PROFESSOR MARCIA HAIGIS

Ph.D., Professor of Cell Biology at Harvard Medical School, National Academy of Medicine's Emerging Leader in Health and Medicine

a headshot of Professor Doug Seals in cell shape

PROFESSOR DOUG SEALS

Ph.D., Professor in Integrative Physiology at the University of Colorado Boulder

a headshot of Dr Molly Maloof in cell shape

DR MOLLY MALOOF

M.D., author, entrepreneur, lecturer, medical advisor

Dr Mark Menolascino

DR MARK MENOLASCINO

M.D., quadruple Board-Certified in internal and integrative medicine

750+ independent high-impact, peer-reviewed journals, and 19 clinical trials. Here are some highlights.

HEART

Chronic supplementation with a mitochondrial antioxidant (MitoQ) improves vascular function in healthy older adults

Rossman MJ et al. Hypertension. 71:1056-1063 (2018)

DOI: DOI: 10.1161/HYPERTENSIONAHA.117.10787 source

MitoQ decreases free radical production by mitochondria, and significantly supports arterial function in older adults and therefore the health of the arteries. In this clinical trial it was confirmed that: MitoQ greatly improved the ability of arteries to dilate (by 42%). MitoQ significantly supports the health of aorta and factors related to heart lipid metabolism.

Read the summary

EXERCISE/CELL HEALTH

The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage

Williamson et al. REDOX Biology

DOI: DOI: 10.1016/j.redox.2020.101673 Source

High-intensity exercise increases our respiration rate and can lead to oxidative stress. The free radicals that are produced during exercise are known to damage our DNA. This study showed that after 3 weeks of chronic supplementation, 20 mg/day of MitoQ was able to protect against exercise-induced DNA damage in young healthy men (20-30 years old). MitoQ significantly reduced both nuclear and mitochondrial DNA damage in the blood and in muscle tissue after intense exercise.

Read the study

EXERCISE

Mitochondria-targeted antioxidant supplementation improves 8km time trial performance in middle-aged trained male cyclist

Broome SC et al. J. Int. Soc. Sports Nutr. 18, 58 (2021).

DOI: DOI: 10.1186/s12970-021-00454-0 source

The study showed that after 4 weeks of MitoQ supplementation, the mean completion time for a time trial was 10.8 seconds faster and an increase of 10 watts of power. MitoQ supplementation may be an effective nutritional strategy to attenuate exercise-induced increases in oxidative damage to lipids and improve cycling performance.

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SAFETY

The influence of acute high dose MitoQ on urinary kidney injury markers in healthy adults

Linder BA et al. The FASEB Journal. 36, S1 (2022).

DOI: DOI: 10.1096/fasebj.2022.36.S1.L7715 source

Results found that acute, high-dose MitoQ supplementation did not result in high concentrations of kidney injury biomarkers compared to placebo samples. Preliminary evidence is that ongoing MitoQ use in the normal range (10mg-20mg) supports kidney health.

Read the summary

CELL HEALTH

MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle‑aged men

Pham et al. European Journal of Applied Physiology

DOI: DOI: 10.1007/s00421-020-04396-4 Source

Mitochondria are the main source of oxidative stress in our bodies. Oxidative stress is caused by an imbalance of free radicals and our levels of antioxidants. Over time, oxidative stress can lead to cell damage and have flow-on effects for our health. This study compared the effects of 20 mg/day MitoQ and 200 mg/day CoQ10 on biomarkers of mitochondrial health and oxidative stress in healthy middle-aged men (40-60 years old). After six weeks of supplementation, MitoQ was found to be 24% more effective than CoQ10 at reducing hydrogen peroxide levels in the mitochondria during states of stress. Unlike CoQ10, MitoQ supplementation also increased levels of the important internal antioxidant, catalase, by 36%.

Read the study

EXERCISE

MitoQ supplementation augments acute exercise-induced increases in muscle PGC1α mRNA and improves training-induced increases in peak power independent of mitochondrial content and function in untrained middle-aged men

Broome et al. REDOX Biology

DOI: DOI: 10.1016/j.redox.2022.102341 Source

Regular high-intensity exercise leads to adaptations in our bodies and mitochondria that help improve performance and recovery. This study showed that in untrained middle-aged men, just 10 days of supplementation of 20mg/day MitoQ improved exercise performance in middle-aged men (35-55 years old). MitoQ significantly increased peak power generation during a 20km cycling trial compared to placebo. This result was accompanied by an increase in skeletal muscle PGC1α mRNA expression, a gene activator associated with the regulation of mitochondrial health and function.

Read the study

More studies

*Intended for a researcher audience, for research purposes only

VASCULAR HEALTH (18)

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Vasodilatory and vascular mitochondrial respiratory function with advancing age: Evidence of a free radically-mediated link in the human vasculature.. Park SH et al. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2020 Feb 5DOI: 10.1152/ajpregu.00268.2019 Source

Pekas L et al. July 2020. Med Sci Sports Exerc 52(7S):902-902DOI: 10.1249/01.mss.0000685352.94627.34

Sheak JR et al. American Journal of Physiology-Heart and Circulatory Physiology. 2020 Jan 20DOI: 10.1152/ajpheart.00629.2019

Effects of treadmill exercise and MitoQ treatment on vascular function in D-galactose-induced aging rat.. Kim D et al. Korean Journal of Sport Science. 2019, Vol. 30. No.4689-699DOI: 10.24985/kjss.201930.4.689

Chronic supplementation with a mitochondrial antioxidant (MitoQ) improves vascular function in healthy older adults. Rossman MJ et al. Hypertension. 2018;71:1056-1063DOI: 10.1161/HYPERTENSIONAHA.117.10787 Source

Suresh K et al. 2018. American Journal of Physiology-Lung Cellular and Molecular PhysiologyDOI: 10.1152/ajplung.00430.2017 Source

Pak O et al. European Respiratory Journal. 2018. pii: 1701024DOI: 10.1183/13993003.01024-2017

Age-related endothelial dysfunction in human skeletal muscle feed arteries: The role of free radicals derived from mitochondria in the vasculature. Park SY et al. Acta Physiologica . 2018; 222(1)DOI: 10.1111/apha.12893 Source

Gioscia-Ryan RA et al. Journal of Applied Physiology. 2017: jap006702017DOI: 10.1152/japplphysiol.00670.2017 Source

Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice. Gioscia-Ryan RA et al. Aging (Albany NY). 2016;8(11):2897-2914DOI: 10.18632/aging.101099 Source

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Redox signalling via oxidative inactivation of PTEN modulates pressure-dependent myogenic tone in rat middle cerebral arteries. Gebremedhin D et al. PLoS One. 2013; 8(7): e68498DOI: 10.1371/journal.pone.0068498 Source

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CARDIAC HEALTH (24)

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Ribeiro Junior RF et al. Free Radical Biology and Medicine. 2018; 117:18-29DOI: 10.1016/j.freeradbiomed.2018.01.012

Ice-free cryopreservation of heart valve tissue: The effect of adding MitoQ to a VS83 formulation and its influence on mitochondrial dynamics. Sui Y et al. Cryobiology. 2018. pii: S0011-2240(17)30599-0DOI: 10.1016/j.cryobiol.2018.01.008 Source

Scheibe S et al. Free Radical Biology and Medicine. Vol 108, Suppl. 1, July 2017, S74DOI: 10.1016/j.freeradbiomed.2017.04.250 Source

Yong Goh K et al. Federation of American Societies For Experimental Biology Journal. 2017;31:1 supplement, 59.7-59.7DOI: 10.1152/ajpheart.00638.2014

An antioxidant to attenuate aoritc aging. Hine C. Science Translational Medicine. 2017;9(416):eaaq1235DOI: 10.11.1126/scitranslmed.aaq1235

Dare AJ et al. The Journal of Heart and Lung Transplantation. 2015; 34(11): 1471–1480DOI: 10.1016/j.healun.2015.05.007

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BRAIN AND NEUROLOGICAL HEALTH (42)

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Teo E et al. Translational Medicine of Aging. 2020DOI: 10.1016/j.tma.2019.12.002

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Mitochondrial redox and pH signalling occurs in axonal and synaptic organelle clusters. Breckwoldt MO et al. Scientific Reports. 2016;22(6):23251DOI: 10.1038/srep23251 Source

Manus MJ et al. Mol Cell Neurosci. 2014; 63:13-23DOI: 10.1016/j.mcn.2014.09.002 Source

The LRRK2 inhibitor GSK2578215A induces protective autophagy in SH-SY5Y cells: Involvement of Drp-1-mediated mitochondrial fission and mitochondrial-derived ROS signalling. Saez-Atienzar S et al. Cell Death & Disease. 2014; 5(8): e1368DOI: 10.1038/cddis.2014.320 Source

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Manganese potentiates lipopolysaccharide-induced expression of NOS2 in C6 glioma cells through mitochondrial-dependent activation of nuclear factor kappaB. Barhoumi R et al. Molecular Brain Research. 2004;122(2):167-79DOI: 10.1016/j.molbrainres.2003.12.009 Source

LIVER HEALTH (22)

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KIDNEY (18)

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MUSCULOSKELETAL HEALTH AND EXERCISE (14)

MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men. Pham T et al. European Journal of Applied Physiology. 2020 May 26DOI: 10.1007/s00421-020-04396-4 Source

Targeting reactive oxygen species (ROS) to combat the age-related loss of muscle mass and function. Thoma A et al. Biogeronology. 2020 May 23DOI: 10.1007/s10522-020-09838-x

Kang L et al. Cell Proliferation. 2020 Feb 5;e12779DOI: 10.1111/cpr.12779

Myocardial NADPH oxidase-4 regulates the physiological response to acute exercise. Hancock M et al. Elife. 2018;7. pii: e41044DOI: 10.7554/eLife.41044 Source

MitoQ supplementation improves leg-extension power in healthy late middle-aged and older adults. Bispham NZ et al. The Journal of the Federation of American Societies for Experimental Biology. 2017; 31 (1) (suppl) abs. lb852DOI: 10.1096/fasebj.31.1_supplement.lb852 Source

Farnaghi S et al. The Journal of the Federation of American Societies for Experimental Biology. 2017;31(1):356-367DOI: 10.1096/fj.201600600R

Mitochondria‐specific antioxidant supplementation does not influence endurance exercise training‐induced adaptations in circulating angiogenic cells, skeletal muscle oxidative capacity or maximal oxygen uptake. Shill DD et al. J Physiol. 2016; 594(23): 7005–7014DOI: 10.1113/JP272491

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MitoQ supplementation improves motor function and muscle mitochondrial health in old male mice. Justice JN et al. Gerontologist 2015;55(2):163DOI: 10.1093/geront/gnv535.02 Source

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Mechanical stress and ATP synthesis are coupled by mitochondrial oxidants in articular cartilage. Wolff KJ et al. Journal of Orthopaedic Research. 2013; 31(2): 191–196DOI: 10.1002/jor.22223

Mitochondrial electron transport and glycolysis are coupled in articular cartilage. Martin AJ et al. Osteoarthritis and Cartilage. 2012; 20(4): 323–329DOI: 10.1016/j.joca.2012.01.003

MitoQ10 induces adipogenesis and oxidative metabolism in myotube cultures. Nierobisz LS et al. Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology. 2011;158(2):125-31DOI: 10.1016/j.cbpb.2010.10.003

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Protective effect of mitochondrially targeted antioxidant MitoQ on oxidatively stressed fibroblasts. Valachová K et al. L. Chemical Paper. 2018 72: 1223DOI: 10.1007/s11696-017-0359-5 Source

Anti-aging potentials of methylene blue for human skin longevity. Xiong Z-M et al. Scientific Reports. 2017 May. 7; 24DOI: 10.1038/s41598-017-02419-3

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Collagen fragmentation promotes oxidative stress and elevates matrix metalloproteinase-1 in fibroblasts in aged human skin. Fisher GJ et al. The American Journal of Pathology. 2009; 174(1): 101–114DOI: 10.2353/ajpath.2009.080599 Source

Cellular response to infrared radiation involves retrograde mitochondrial signalling. Schroeder P et al. Free Radical Biology and Medicine. 2007;43(1):128-35DOI: 10.1016/j.freeradbiomed.2007.04.002 Source

7-Dehydrocholesterol enhances ultraviolet A-induced oxidative stress in keratinocytes: Roles of NADPH oxidase, mitochondria and lipid rafts. Valencia A et al. Free Radical Biology and Medicine. 2006; 41(11): 1704–1718DOI: 10.1016/j.freeradbiomed.2006.09.006 Source

MitoQ counteracts telomere shortening and elongates lifespan of fibroblasts under mild oxidative stress. Saretzki G et al. Aging Cell. 2003;2(2):141-3DOI: 10.1046/j.1474-9728.2003.00040.x Source

IMMUNOLOGY (33)

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Budd R et al. Lupus Science & Medicine. 2019;6DOI: 10.1136/lupus-2019-lsm.38

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EYE HEALTH (5)

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Mitochondrial-targeted antioxidants attenuate TGF-β2 signaling in human trabecular meshwork cells. Rao VR et al. Investigative Ophthalmology & Visual Science. 2019;60:3613-3624DOI: 10.1167/iovs.19-27542 Source

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Mitochondria-targeted antioxidant mitoquinone protects post-thaw human sperm against oxidative stress injury. Liu L et al. Zhonghua Nan Ke Xue. 2016;22(3):205-11Source

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Inhibition of ROS production through mitochondria-targeted antioxidant and mitochondrial uncoupling increases post-thaw sperm viability in yellow catfish. Fang L et al. Cryobiology. 2014;69(3):386-93DOI: 10.1016/j.cryobiol.2014.09.005 Source

Aljunaidy MM et al. Pharmacological Research.;134:332-342DOI: 10.1016/j.phrs.2018.05.006

Sukjamnong S et al. Scientific Reports. 2018; 8: 6631DOI: 10.1038/s41598-018-24949-0 Source

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Nuzzo AM et al. The American Journal of Pathology. 2018 Sep 21. pii: S0002-9440(18)30019-1DOI: 10.1016/j.ajpath.2018.07.027 Source

Vaka VR et al. Hypertension. 2018 Jul 16. piiDOI: 10.1161/HYPERTENSIONAHA.118.11290 Source

Ganguly E et al. Frontiers in Physiology. 2019 May 24DOI: 10.3389/fphys.2019.00562 Source

Exposing mouse oocytes to MitoQ during in vitro maturation improves maturation and developmental competence. Hosseinzadeh Shirzeyli M et al. Iranian Journal of Biotechnology. 2019DOI: 10.30498/IJB.2020.154641.2454 Source

Zhang J et al. Toxicology and Applied Pharmacology. 2019 Mar 2. pii: S0041-008X(19)30075-4DOI: 10.1016/j.taap.2019.03.001

Autophagy regulates functional differentiation of mammary epithelial cells. Elswood J et al. Autophagy. 2020DOI: 10.1080/15548627.2020.1720427

Marei W et al. Human Reproduction. 2019DOI: 10.1093/humrep/dez161 Source

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Consequences of long-term oral administration of the mitochondria-targeted antioxidant MitoQ to wild-type mice. Rodriguez-Cuenca S et al. Free Radical Biology and Medicine. 2010;48(1):161-72DOI: 10.1016/j.freeradbiomed.2009.10.039 Source

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REDOX BIOLOGY (31)

Superoxide activates mitochondrial uncoupling protein 2 from the matrix side. Studies using targeted antioxidants. Echtay KS et al. Journal of Biological Chemistry. 2002;277(49):47129-35DOI: 10.1074/jbc.M208262200 Source

Mitochondrial redox state regulates transcription of the nuclear-encoded mitochondrial protein manganese superoxide dismutase: A proposed adaptive response to mitochondrial  redox imbalance. Kim A et al. Free Radical Biology and Medicine. 2005;38(5):644-54DOI: 10.1016/j.freeradbiomed.2004.10.030

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Redox regulation of cAMP-responsive element-binding protein and induction of manganous superoxide dismutase in nerve growth factor-dependent cell survival. Bedogni B et al. Journal of Biological Chemistry. 2003;278(19):16510-9DOI: 10.1074/jbc.M301089200 Source

Interactions of mitochondria-targeted and untargeted ubiquinones with the mitochondrial respiratory chain and reactive oxygen species. Implications for the use of exogenous ubiquinones as therapies and experimental tools. James AM et al. Journal of Biological Chemistry. 2005;280(22):21295-312DOI: 10.1074/jbc.M501527200 Source

A targeted antioxidant reveals the importance of mitochondrial reactive oxygen species in the hypoxic signalling of HIF-1alpha. Sanjuán-Pla A et al. FEBS Letters. 2005;579(12):2669-74DOI: 10.1016/j.febslet.2005.03.088

Protective role of MnSOD and redox regulation of neuronal cell survival. Galeotti T et al. Biomedicine & Pharmacotherapy. 2005;59(4):197-203DOI: 10.1016/j.biopha.2005.03.002 Source

OxLDL enhances L-type Ca2+ currents via lysophosphatidylcholine-induced mitochondrial reactive oxygen species (ROS) production. Fearon IM. Cardiovascular Research. 2006;69(4):855-64DOI: 10.1016/j.cardiores.2005.11.019 Source

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Long-distance apoptotic killing of cells is mediated by hydrogen peroxide in a mitochondrial ROS-dependent fashion. Pletjushkina OY et al. Cell Death & Differentiation. 2005;12:1442–1444DOI: 10.1038/sj.cdd.4401685 Source

Koopman WJ et al. Cellular Metabolism. 2005;288(6):C1440-50DOI: 10.1152/ajpcell.00607.2004 Source

Respiratory chain deficiency slows down cell-cycle progression via reduced ROS generation and is associated with a reduction of p21CIP1/WAF1. Schauen M et al. Journal of Cellular Physiology. 2006;209(1):103-12DOI: 10.1002/jcp.20711 Source

Production of reactive oxygen species in mitochondria of HeLa cells under oxidative stress. Chernyak BV et al. Biochimica et Biophysica Acta (BBA) – Bioenergetics . 2006;1757(5-6):525-34DOI: 10.1016/j.bbabio.2006.02.019 Source

Flow dilation in rat small mesenteric arteries is mediated by hydrogen peroxide generated from CYP epoxygenases and xanthine oxidase. Ngai CY. The Open Circulation and Vascular Journal. 2009 Apr. 2(1):15-22DOI: 10.2174/1877382600902010015 Source

Doughan AK et al. Antioxidants & Redox Signaling. 2007; 9(11):1825-36DOI: 10.1089/ars.2007.1693

Reactive oxygen and targeted antioxidant administration in endothelial cell mitochondria. O'Malley Y et al. Journal of Biological Chemsitry. 2006;281(52):39766-75DOI: 10.1074/jbc.M608268200

TNFα-induced lysosomal membrane permeability is downstream of MOMP and triggered by caspase-mediated NDUFS1 cleavage and ROS formation. Huai J et al. Journal of Cell Science. 2013;126(Pt 17):4015-25DOI: 10.1242/jcs.129999 Source

Mitochondrial H2O2 generated from electron transport chain complex I stimulates muscle differentiation. Lee S et al. Cell Research. 2011;21(5):817-34DOI: 10.1038/cr.2011.55

Role of mitochondrial reactive oxygen species in osteoclast differentiation. Srinivasan S et al. Annals of the New York Academy of Sciences. 2010; 1192(1): 245–252DOI: 10.1111/j.1749-6632.2009.05377.x Source

Hämäläinen RH et al. Cell Reports. 2015; 11(10): 1614–1624DOI: 10.1016/j.celrep.2015.05.009

Huang W-Y et al. PLoS One. 2013;8(11):e81546DOI: 10.1371/journal.pone.0081546 Source

Differential modulation of ROS signals and other mitochondrial parameters by the antioxidants MitoQ, resveratrol and curcumin in human adipocytes. Hirzel E et al. Journal of Receptors and Signal Transduction. 2013; 33(5):304-12DOI: 10.3109/10799893.2013.822887 Source

Mitochondrial ROS-derived PTEN oxidation activates PI3K pathway for mTOR-induced myogenic autophagy. Kim JH et al. Cell Death and Differentiation. 2018 Jul 24DOI: 10.1038/s41418-018-0165-9

Mitochondria-targeted molecules determine the redness of the zebra finch bill. Cantarero A et al. Biology Letters. 2017;13(10). pii: 20170455DOI: 10.1098/rsbl.2017.0455 Source

Reactive oxygen species derived from NADPH oxidase 1 and mitochondria mediate angiotensin II-induced smooth muscle cell senescence. Tsai IC et al. Journal of Molecular and Cellular Cardiology. 2016;98:18-27DOI: 10.1016/j.yjmcc.2016.07.001 Source

Ammonia sensitive SLC4A11 mitochondrial uncoupling reduces glutamine induced oxidative stress. Ogando DG et al. Redox Biology. 2019;26:101260DOI: 10.1016/j.redox.2019.101260 Source

Redox-regulation and life-history trade offs: Scavenging mitochondrial ROS improves growth in a wild bird. Velando A et al. Scientific Reports. 2019;9(1)DOI: 10.1038/s41598-019-3853335-5

Detection of 8-oxoguanine and apurinic/apyrimidinic sites using a fluorophore-labeled probe with cell-penetrating ability. Kang DM et al. BMC Molecular and Cell Biology. 2019 Nov 27;20(1):54DOI: 10.1186/s12860-019-236

A mitochondria-targeted antioxidant affects the carotenoid-based plumage of red crossbills. Cantarero A et al. bioRxiv. 2019DOI: 10.1101/839670

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Delivery of bioactive molecules to mitochondria in vivo. Smith RA et al. Proceedings of the National Academy of Sciences of the United States of America. 2003;100(9):5407-12DOI: 10.1073/pnas.0931245100

Effect of oxidative stress on dynamics of mitochondrial reticulum. Pletjushkina OY et al. Biochimica et Biophysica Acta (BBA) - Bioenergetics. 2006;1757(5-6):518-24DOI: 10.1016/j.bbabio.2006.03.018

Fine-tuning the hydrophobicity of a mitochondria-targeted antioxidant. Asin-Cayuela J et al. FEBS Letters. 2004;571(1-3):9-16DOI: 10.1016/j.febslet.2004.06.045

Interaction of the mitochondrial-targeted antioxidant MitoQ with phospholipid bilayers and ubiquinone oxidoreductases. James AM et al. The Journal of Biological Chemistry. 2007; 282(20):14708-14718DOI: 10.1074/jbc.M611463200

Quantitation and metabolism of mitoquinone, a mitochondria-targeted antioxidant, in rat by liquid chromatography/tandem mass spectrometry. Li Y et al. Rapid Communications in Mass Spectrometry. 2007; 21(13):1958-64DOI: 10.1002/rcm.3048

The effects of exogenous antioxidants on lifespan and oxidative stress resistance in Drosophila melanogaster. Magwere T et al. Mechanisms of Ageing and Development. 2006;127(4):356-70DOI: 10.1016/j.mad.2005.12.009

Thioredoxin 1 and thioredoxin 2 have opposed regulatory functions on hypoxia-inducible factor-1alpha. Zhou J et al. Journal of Biological Chemistry. 2007;282(10):7482-90DOI: 10.1074/jbc.M608289200

Jarvis RM et al. Free Radical Research. 2007;41(9):1041-6DOI: 10.1080/10715760701557153

Transport and metabolism of MitoQ10, a mitochondria-targeted antioxidant, in Caco-2 cell monolayers. Li Y et al. Journal of Pharmacy and Pharmacology. 2007;59(4):503-11DOI: 10.1211/jpp.59.4.0004

Jou MJ et al. Journal of Pineal Research. 2007;43(4):389-403DOI: 10.1111/j.1600-079X.2007.00490.x

Role of calcium and cyclophilin D in the regulation of mitochondrial permeabilization induced by glutathione depletion. Lu C et al. Biochemical and Biophysical Research Communications. 2007 Nov;363(3):572-7DOI: 10.1016/j.bbrc.2007.08.196

Is antioxidant potential of the mitochondrial targeted ubiquinone derivative MitoQ conserved in cells lacking mtDNA?. Lu C et al. Antioxidants & Redox Signaling. 2008;10(3):651-60DOI: 10.1089/ars.2007.1865

Quijano C et al. American Journal of Physiology – Heart and Circulatory Physiology. 2007;293(6):H3404-14DOI: 10.1152/ajpheart.00761.2007

Rapid and extensive uptake and activation of hydrophobic triphenylphosphonium cations within cells. Ross MF et al. Biochemical Journal. 2008;411(3):633-45DOI: 10.1042/BJ20080063

Protective effects of mitochondria-targeted antioxidant SkQ in aqueous and lipid membrane environments. Antonenko YN et al. Journal of Membrane Biology. 2008;222(3):141-9DOI: 10.1007/s00232-008-9108-6

Interaction of positively charged ubiquinone analog (MitoQ10) with DT-diaphorase from liver mitochondria. Kargin VI et al. Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology (2008) 2: 33DOI: 10.1007/s11827-008-1006-7

Transport and metabolism of some cationic ubiquinone antioxidants (MitoQn) in Caco-2 cell monolayers. Li Y et al. European Journal of Drug Metabolism and Pharmacokinetics. 2008;33(4):199-204DOI: 10.1007/BF03190873

Cations SkQ1 and MitoQ accumulated in mitochondria delay opening of ascorbate/FeSO4-induced nonspecific pore in the inner mitochondrial membrane. Khailova LS et al. Biochemistry (Moscow). 2008;73(10):1121-4DOI: 10.1134/S0006297908100088

Kinetic analysis of permeation of mitochondria-targeted antioxidants across bilayer lipid membranes. Rokitskaya TI et al. Journal of Membrane Biology. 2008;224(1-3):9-19DOI: 10.1007/s00232-008-9124-6

Electrical relaxation experiments with bilayer lipid membranes in the presence of cationic quinones. Rokitskaya T et al. Biophysical Journal 2009 Feb. 96(3) 663ADOI:  10.1016/j.bpj.2008.12.3505

Mitochondrial targeted coenzyme Q, superoxide, and fuel selectivity in endothelial cells. Fink BD et al. PLoS One. 2009 Jan. 4(1):e4250DOI: 10.1371/journal.pone.0004250

The mitochondrial antioxidants MitoE2 and MitoQ10 increase mitochondrial Ca2+ load upon cell stimulation by inhibiting Ca2+ efflux from the organelle. Leo S et al. Annals of the New York Academy of Sciences. 2008; 1147: 264–274DOI: 10.1196/annals.1427.019

Pro-oxidant mitochondrial matrix-targeted ubiquinone MitoQ10 acts as anti-oxidant at retarded electron transport or proton pumping within Complex I. Plecitá-Hlavatá L et al. The International Journal of Biochemistry & Cell Biology. 2009;41(8-9):1697-707DOI: 10.1016/j.biocel.2009.02.015

Chain-breaking antioxidant activity of reduced forms of mitochondria-targeted quinones, a novel type of geroprotectors. Roginsky VA et al. Aging (Albany NY). 2009; 1(5): 481–489DOI: 10.18632/aging.100049

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Interaction of yeast mitochondria with fatty acids and mitochondria-targeted lipophilic cations. Sukhanova EI et al. Biochemistry (Moscow). 2010;75(2):139-44DOI: 10.1134/S000297910020033

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