Mitoquinone (MitoQ) |
| Catalog No.: GC30416 |
Mitoquinone (MitoQ) is a ubiquinone-derived antioxidant
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Mouse Embryonic Fibroblasts (MEF) |
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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. |
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Reaction Conditions |
0.05 and 0.1 µM, 16h |
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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]: | |
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Male Sprague-Dawley rats |
C57BL/10ScSn DMD mdx mice |
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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. |
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Dosage form |
10 mg•kg−1•day−1, p.o. |
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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. |
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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. |
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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.
| Cas No. | 444890-41-9 | SDF | |
| 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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Mitoquinone mesylate (MitoQ) prevents sepsis-induced diaphragm dysfunction
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.
MitoQ alleviates LPS-mediated acute lung injury through regulating Nrf2/Drp1 pathway
Lipopolysaccharide (LPS) has been known to cause alveolar epithelial cell (AEC) apoptosis and barrier breakdown that characterize acute lung injury (ALI) and acute respiratory distress syndrome. We aimed to investigate whether mitoquinone (MitoQ), a mitochondria-targeted antioxidant, could alleviate LPS-induced AEC damage in ALI and its underlying mechanisms. In vitro studies in AEC A549 cell line, we noted that LPS could induce dynamin-related protein 1 (Drp1)-mediated mitochondrial fission, AEC apoptosis and barrier breakdown, which could be reversed with MitoQ and mitochondrial division inhibitor 1 treatment. Moreover, the protective role of MitoQ was attenuated with Drp1 overexpression. Nuclear factor E2-related factor 2 (Nrf2) downregulation could block the effect of MitoQ by decreasing the expression of Nrf2 target genes in LPS-treated AEC, such as heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). Nrf2 gene knockdown in LPS-treated A549 cells prevented the protective effect of MitoQ from decreasing Drp1-mediated mitochondrial fission, AEC apoptosis and barrier breakdown. The lung protective effect of MitoQ by regulating the Drp1-mediated mitochondrial fission, AEC apoptosis and barrier breakdown was further confirmed in vivo with LPS-induced ALI mouse model. Additionally, the protective effect of MitoQ was inhibited by Nrf2 inhibitor ML385. We therefore conclude that MitoQ exerts ALI-protective effects by preventing Nrf2/Drp1-mediated mitochondrial fission, AEC apoptosis as well as barrier breakdown.
The mitochondria-targeted antioxidant MitoQ ameliorated tubular injury mediated by mitophagy in diabetic kidney disease via Nrf2/PINK1
Mitochondria play a crucial role in tubular injury in diabetic kidney disease (DKD). MitoQ is a mitochondria-targeted antioxidant that exerts protective effects in diabetic mice, but the mechanism underlying these effects is not clear. We demonstrated that mitochondrial abnormalities, such as defective mitophagy, mitochondrial reactive oxygen species (ROS) overexpression and mitochondrial fragmentation, occurred in the tubular cells of db/db mice, accompanied by reduced PINK and Parkin expression and increased apoptosis. These changes were partially reversed following an intraperitoneal injection of mitoQ. High glucose (HG) also induces deficient mitophagy, mitochondrial dysfunction and apoptosis in HK-2 cells, changes that were reversed by mitoQ. Moreover, mitoQ restored the expression, activity and translocation of HG-induced NF-E2-related factor 2 (Nrf2) and inhibited the expression of Kelch-like ECH-associated protein (Keap1), as well as the interaction between Nrf2 and Keap1. The reduced PINK and Parkin expression noted in HK-2 cells subjected to HG exposure was partially restored by mitoQ. This effect was abolished by Nrf2 siRNA and augmented by Keap1 siRNA. Transfection with Nrf2 siRNA or PINK siRNA in HK-2 cells exposed to HG conditions partially blocked the effects of mitoQ on mitophagy and tubular damage. These results suggest that mitoQ exerts beneficial effects on tubular injury in DKD via mitophagy and that mitochondrial quality control is mediated by Nrf2/PINK.
Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
Platelet activation plays a key role in cardiovascular diseases. The generation of mitochondrial reactive oxygen species (ROS) has been described as a critical step required for platelet activation. For this reason, it is necessary to find new molecules with antiplatelet activity and identify their mechanisms of action. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant that reduces mitochondrial overproduction of ROS. In this work, the antiplatelet effect of MitoQ through platelet adhesion and spreading, secretion, and aggregation was evaluated. Thus MitoQ, in a non-toxic effect, decreased platelet adhesion and spreading on collagen surface, and expression of P-selectin and CD63, and inhibited platelet aggregation induced by collagen, convulxin, thrombin receptor activator peptide-6 (TRAP-6), and phorbol 12-myristate 13-acetate (PMA). As an antiplatelet mechanism, we showed that MitoQ produced mitochondrial depolarization and decreased ATP secretion. Additionally, in platelets stimulated with antimycin A and collagen MitoQ significantly decreased ROS production. Our findings showed, for the first time, an antiplatelet effect of MitoQ that is probably associated with its mitochondrial antioxidant effect.
Mitochondria-Targeted Drugs
Background: Targeting of drugs to the subcellular compartments represents one of the modern trends in molecular pharmacology. The approach for targeting mitochondria was developed nearly 50 years ago, but only in the last decade has it started to become widely used for delivering drugs. A number of pathologies are associated with mitochondrial dysfunction, including cardiovascular, neurological, inflammatory and metabolic conditions.
Objective: This mini-review aims to highlight the role of mitochondria in pathophysiological conditions and diseases, to classify and summarize our knowledge about targeting mitochondria and to review the most important preclinical and clinical data relating to the antioxidant lipophilic cations MitoQ and SkQ1.
Methods: This is a review of available information in the PubMed and Clinical Trials databases (US National Library of Medicine) with no limiting period.
Results and conclusion: Mitochondria play an important role in the pathogenesis of many diseases and possibly in aging. Both MitoQ and SkQ1 have shown many beneficial features in animal models and in a few completed clinical trials. More clinical trials and research efforts are needed to understand the signaling pathways influenced by these compounds. The antioxidant lipophilic cations have great potential for the treatment of a wide range of pathologies.
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