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Mitoquinone (MitoQ)

Catalog No.GC30416

Mitoquinone (MitoQ) Chemical Structure

Mitoquinone (MitoQ) is a ubiquinone-derived antioxidant

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5mg
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10mg
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25mg
$386.00
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Sample solution is provided at 25 µL, 10mM.

Quality Control

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Protocol

Cell experiment [1]:

Cell lines

Mouse Embryonic Fibroblasts (MEF)

Preparation Method

Cells were treated with MitoQ for 16 h. Superoxide anion was determined by incubating the cells with 50 nM MitoSox for 30 min. To analyze the effect of MitoQ 0.05 and 0.1 µM on acute oxidative stress, MEFwt cells were incubated with MitoSox in the absence or presence of 5 µM antimycin A.

Reaction Conditions

0.05 and 0.1 µM, 16h

Applications

MitoQ at 2.5 and 5 μM produced a significant decrease in ROS production generated by antimycin A or collagen on platelets.

Animal experiment [2]:

Male Sprague-Dawley rats

C57BL/10ScSn DMD mdx mice

Preparation Method

Mitoquinone (10 mg•kg−1•day−1; MitoQ, New Zealand; n = 10) or vehicle (dimethyl sulfoxide 0.7%; n = 10) administration by gavage was started 3 days after CBDL and continued for 4 wk. Three hours after the last administration, rats were euthanized.

Dosage form

10 mg•kg−1•day−1, p.o.

Applications

The weight of livers from rats treated with mitoquinone was significantly lower than that of livers from untreated cirrhotic animals and similar to that of controls, likely due to the reduction of hepatic inflammation.

References:

[1]. Méndez D, et al. Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. Int J Mol Sci. 2020 Aug 27;21(17):6192

[2]. Turkseven S, et al. Mitochondria-targeted antioxidant mitoquinone attenuates liver inflammation and fibrosis in cirrhotic rats. Am J Physiol Gastrointest Liver Physiol. 2020 Feb 1;318(2):G298-G304.

Background

Mitoquinone (MitoQ) is a ubiquinone-derived antioxidant that can covalently attach to a lipophilic triphenylphosphonium (TPP) cation, specifically targets mitochondria.[1] MitoQ is usually stored within mitochondria in vivo in order to prevent and protect the cellular damage induced by mitochondrial ROS overproduction and oxidative stress.[2]

In vitro experiment it shown that washed platelets incubated with MitoQ 10 µM (4.8% ± 0.8%) markedly increased calcein-negative population (cytotoxic effect) compared to a non-treated control group; MitoQ 10 μM (8.5% ± 2.2%) induced a significant increase in PS exposure on the platelet membrane when compared to the basal control.[3] In addition, MitoQ (5 μM) inhibited collagen and ADP-induced platelet aggregation in PRP samples. In the meanwhile, MitoQ at 2.5 and 5 μM produced a obvious decrease in ROS production generated by antimycin A or collagen on platelet.[3]

In vivo, treatment with 2.5 mg/kg and 5 mg/kg MitoQ can alleviate mouse lung histologic changes induced by CS (Cigarette smoke).[1] In vivo experiment it shown that mitoquinone treatment with 10 mg/kg/day by gavage after 4 weeks, liver structure obiviously improved in association with a significant decrease in collagen deposition. In the meanwhile, mitoquinone treatment determined a significant reduction in hepatic inflammation and fibrosis. Moreover, TIMP-1, MMP-2, and MMP-13 gene expressions were decreased by Mitoquinone treatment.[4]

References:
[1]. Yang D, et al. Mitoquinone ameliorates cigarette smoke-induced airway inflammation and mucus hypersecretion in mice. Int Immunopharmacol. 2021 Jan;90:107149.
[2]. Chen W, et al. Inhibition of Mitochondrial ROS by MitoQ Alleviates White Matter Injury and Improves Outcomes after Intracerebral Haemorrhage in Mice. Oxid Med Cell Longev. 2020 Jan 4;2020:8285065.
[3]. Méndez D, et al. Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. Int J Mol Sci. 2020 Aug 27;21(17):6192.
[4]. Turkseven S, et al. Mitochondria-targeted antioxidant mitoquinone attenuates liver inflammation and fibrosis in cirrhotic rats. Am J Physiol Gastrointest Liver Physiol. 2020 Feb 1;318(2):G298-G304.

Chemical Properties

Cas No. 444890-41-9 SDF
Synonyms N/A
Chemical Name N/A
Canonical SMILES O=C(C(CCCCCCCCCC[P+](C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=CC=C3)=C4C)C(OC)=C(OC)C4=O
Formula C37H44O4P M.Wt 583.72
Solubility DMSO : 50 mg/mL (73.66 mM) Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

Mitoquinone mesylate (MitoQ) prevents sepsis-induced diaphragm dysfunction

J Appl Physiol (1985)2021 Aug 1;131(2):778-787.PMID: 34197233DOI: 10.1152/japplphysiol.01053.2020

Sepsis-induced diaphragm dysfunction is a major contributor to respiratory failure in mechanically ventilated patients. There are no pharmacological treatments for this syndrome, but studies suggest that diaphragm weakness is linked to mitochondrial free radical generation. We hypothesized that administration of mitoquinone mesylate (MitoQ), a mitochondrially targeted free radical scavenger, would prevent sepsis-induced diaphragm dysfunction. We compared diaphragm function in 4 groups of male mice: 1) sham-operated controls treated with saline (0.3 mL ip), 2) sham-operated treated with MitoQ (3.5 mg/kg/day given intraperitoneally in saline), 3) cecal ligation puncture (CLP) mice treated with saline, and 4) CLP mice treated with MitoQ. Forty-eight hours after surgery, we assessed diaphragm force generation, myosin heavy chain content, state 3 mitochondrial oxygen consumption (OCR), and aconitase activity. We also determined effects of MitoQ in female mice with CLP sepsis and in mice with endotoxin-induced sepsis. CLP decreased diaphragm specific force generation and MitoQ prevented these decrements (e.g. maximal force averaged 30.2 ± 1.3, 28.0 ± 1.3, 12.8 ± 1.9, and 30.0 ± 1.0 N/cm2 for sham, sham + MitoQ, CLP, and CLP + MitoQ groups, respectively, P < 0.001). CLP also reduced diaphragm mitochondrial OCR and aconitase activity; MitoQ blocked both effects. Similar responses were observed in female mice and in endotoxin-induced sepsis. Moreover, delayed MitoQ treatment (by 6 h) was as effective as immediate treatment. These data indicate that MitoQ prevents sepsis-induced diaphragm dysfunction, preserving force generation. MitoQ may be a useful therapeutic agent to preserve diaphragm function in critically ill patients with sepsis.NEW & NOTEWORTHY This is the first study to show that mitoquinone mesylate (MitoQ), a mitochondrially targeted antioxidant, treats sepsis-induced skeletal muscle dysfunction. This biopharmaceutical agent is without known side effects and is currently being used by healthy individuals and in clinical trials in patients with various diseases. When taken together, our results suggest that MitoQ has the potential to be immediately translated into treatment for sepsis-induced skeletal muscle dysfunction.

Protective role of mitoquinone against impaired mitochondrial homeostasis in metabolic syndrome

Crit Rev Food Sci Nutr2021;61(22):3857-3875.PMID: 32815398DOI: 10.1080/10408398.2020.1809344

Mitochondria control various processes in cellular metabolic homeostasis, such as adenosine triphosphate production, generation and clearance of reactive oxygen species, control of intracellular Ca2+ and apoptosis, and are thus a critical therapeutic target for metabolic syndrome (MetS). The mitochondrial targeted antioxidant mitoquinone (MitoQ) reduces mitochondrial oxidative stress, prevents impaired mitochondrial dynamics, and increases mitochondrial turnover by promoting autophagy (mitophagy) and mitochondrial biogenesis, which ultimately contribute to the attenuation of MetS conditions, including obesity, insulin resistance, hypertension and cardiovascular disease. The regulatory effect of MitoQ on mitochondrial homeostasis is mediated through AMPK and its downstream signaling pathways, including MTOR, SIRT1, Nrf2 and NF-κB. However, there are few reviews focusing on the critical role of MitoQ as a therapeutic agent in the treatment of MetS. The purpose of this review is to summarize the mitochondrial role in the pathogenesis of MetS, especially in obesity and type 2 diabetes, and discuss the effect and underlying mechanism of MitoQ on mitochondrial homeostasis in MetS.

Neuroprotective effects of mitoquinone and oleandrin on Parkinson's disease model in zebrafish

Int J Neurosci2020 Jun;130(6):574-582.PMID: 31771386DOI: 10.1080/00207454.2019.1698567

Aim: The aim of this study is to investigate the possible protective effects of mitoquinone and oleandrin on rotenone induced Parkinson's disease in zebrafish. Materials and methods: Adult zebrafish were exposed to rotenone and mitoquinone for 30 days. Biochemical parameters were determined by spectrophotometric method and Parkinson's disease-related gene expressions were determined by reverse transcription polymerase chain reaction method. Measurement of neurotransmitters was performed by liquid chromatography tandem-mass spectrometry instrument. The accumulation of synuclein was demonstrated by immunohistochemical staining. In vitro thiazolyl blue tetrazolium bromide method was applied to determine the mitochondrial function of synaptosomal brain fractions using rotenone as a neurotoxic agent and mitoquinone and oleandrin as neuroprotective agents. Results: Mitoquinone improved the oxidant-antioxidant balance and neurotransmitter levels that were disrupted by rotenone. Mitoquinone also ameliorated the expressions of Parkinson's disease-related gene expressions that were disrupted by rotenone. According to thiazolyl blue tetrazolium bromide assay results, mitoquinone and oleandrin increased mitochondrial function which was decreased due to rotenone exposure. Conclusion: Based on the results of our study, positive effects of mitoquinone were observed in Parkinson's disease model induced by rotenone in zebrafish.

Mitoquinone Inactivates Mitochondrial Chaperone TRAP1 by Blocking the Client Binding Site

J Am Chem Soc2021 Dec 1;143(47):19684-19696.PMID: 34758612DOI: 10.1021/jacs.1c07099

Heat shock protein 90 (Hsp90) family proteins are molecular chaperones that modulate the functions of various substrate proteins (clients) implicated in pro-tumorigenic pathways. In this study, the mitochondria-targeted antioxidant mitoquinone (MitoQ) was identified as a potent inhibitor of mitochondrial Hsp90, known as a tumor necrosis factor receptor-associated protein 1 (TRAP1). Structural analyses revealed an asymmetric bipartite interaction between MitoQ and the previously unrecognized drug binding sites located in the middle domain of TRAP1, believed to be a client binding region. MitoQ effectively competed with TRAP1 clients, and MitoQ treatment facilitated the identification of 103 TRAP1-interacting mitochondrial proteins in cancer cells. MitoQ and its redox-crippled SB-U014/SB-U015 exhibited more potent anticancer activity in vitro and in vivo than previously reported mitochondria-targeted TRAP1 inhibitors. The findings indicate that targeting the client binding site of Hsp90 family proteins offers a novel strategy for the development of potent anticancer drugs.

Mitochondria-targeted antioxidant mitoquinone attenuates liver inflammation and fibrosis in cirrhotic rats

Am J Physiol Gastrointest Liver Physiol2020 Feb 1;318(2):G298-G304.PMID: 31813234DOI: 10.1152/ajpgi.00135.2019

In liver cirrhosis, oxidative stress plays a major role in promoting liver inflammation and fibrosis. Mitochondria dysregulation is responsible for excessive reactive oxygen species production. Therefore, in an experimental model of cirrhosis, we investigated the effect of mitochondria-targeted antioxidant mitoquinone. Liver cirrhosis was induced in Spraque-Dawley rats by common bile duct ligation (CBDL). Mitoquinone (10 mg·kg-1·day-1, oral gavage) or vehicle was administered from 3rd to 28th day after CBDL, when animals were euthanized; liver oxidative stress, inflammation, fibrosis, mitophagy were evaluated; and in vivo and ex vivo hemodynamic studies were performed. In cirrhotic rats, mitoquinone prevented liver inflammation, hepatocyte necrosis, and fibrosis at histological examination; decreased circulating TNF-α, gene expression of transforming growth factor-β1, collagen type 1a1, TNF-α, IL-6, IL-1β, tissue inhibitor of metalloproteinase-1, matrix metalloproteinase (MMP)-2, and MMP-13; and reduced hepatic oxidative stress, as shown by reduced oxidative carbonylation of the proteins, by modulating antioxidants catalase, Mn superoxide dismutase, and Cu/Zn superoxide dismutase. Furthermore, mitoquinone attenuated apoptosis by reducing hepatic protein expression of cleaved caspase-3. A selective removal of dysfunctional mitochondria was improved by mitoquinone, as shown by the increase in Parkin translocation to mitochondria. Treatment with mitoquinone normalized the weight of the spleen; however, it increased portal blood flow and reduced splenic artery intrahepatic resistance, suggesting an effect on resistance index. Mitochondria-targeted antioxidant mitoquinone improves liver inflammation and fibrosis in cirrhotic rats by reducing hepatic oxidative stress, preventing apoptosis, and promoting removal of dysfunctional mitochondria. Therefore, it may represent a promising strategy for the prevention and treatment of liver cirrhosis.

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