Mitoq

Manufactured by MedKoo Biosciences

Sourced in Japan, United States

MitoQ is a mitoprotective antioxidant that targets the mitochondria within cells. It is designed to support mitochondrial function and protect against oxidative stress.

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Lab products found in correlation

Fetal bovine serum (fbs), by Thermo Fisher Scientific (4 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (2 mentions) Gentamicin, by Thermo Fisher Scientific (1 mentions) Opti mem 1 medium, by Thermo Fisher Scientific (1 mentions) Bafilomycin a1, by Merck Group (1 mentions) Chondroitin sulfate, by Merck Group (1 mentions) Ifn γ, by R&D Systems (1 mentions) Bcl 2, by Merck Group (1 mentions) Zvad fmk, by Avantor (1 mentions) Abt 737, by Abbvie (1 mentions) Fluoro carbonyl cyanide phenylhydrazone (fccp), by Merck Group (1 mentions) Hoechst 33342, by AnaSpec (1 mentions) Cellrox, by Thermo Fisher Scientific (1 mentions) Cell culture reagents, by Thermo Fisher Scientific (1 mentions) Nutlin 3a, by Merck Group (1 mentions) Antimycin a, by Merck Group (1 mentions) Mitosox, by Thermo Fisher Scientific (1 mentions) Etoposide, by Merck Group (1 mentions) Staurosporine, by Merck Group (1 mentions) Ss 31, by ChinaPeptides (1 mentions)

6 protocols using mitoq

Platelet Isolation and Preparation

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Platelets were obtained by phlebotomy from healthy donors (two weeks without drugs) that had previously accepted informed consent, as previously reported [23 (link)]. Briefly, whole blood was obtained with acid-citrate-dextrose (ACD) solution (proportion 4:1 v/v) and centrifuged at room temperature (RT) for 10 min × 200 g in order to collect platelet-rich plasma (PRP). Then PRP was centrifuged for 8 min × 900 g. Platelets pellet was suspended in calcium-free Tyrode’s buffer: ACD (proportion 5:1 v/v) and this was centrifuged again for 8 min × 900 g and platelets were resuspended in calcium-free Tyrode’s buffer and adjusted to the assays by a hematological counter (Mindray BC-3000 Plus, Japan) and used within 3 h for MitoQ (MedKoo Biosciences, Morrisville, NC, USA) assays.

Méndez D., Arauna D., Fuentes F., Araya-Maturana R., Palomo I., Alarcón M., Sebastián D., Zorzano A, & Fuentes E. (2020). Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. International Journal of Molecular Sciences, 21(17), 6192.

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Conditionally Immortalized Mouse Corneal Endothelial Cells

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The generation of conditionally immortalized mouse corneal endothelial cells (MCEC) Slc4a11^+/+ and Slc4a11^−/− is described previously.¹⁸ (link) Cells were cultured in Complete Media, which contains OptiMEM-I medium (#51985; Thermo Fisher Scientific, Canoga Park, CA, USA), 14 mM glucose and 4 mM L-alanyl glutamine supplemented with 8% heat-inactivated fetal bovine serum (FBS; #10082139; Thermo Fisher Scientific), epidermal growth factor (EGF) 5 ng/mL (#01-107; Millipore, Darmstadt, Germany), pituitary extract 100 µg/mL (Hyclone 15 Laboratories, Logan, UT, USA), calcium chloride 200 mg/L, 0.08% chondroitin sulfate (#G6737; SigmaAldrich Corp., St. Louis, MO, USA), gentamicin 50 µg/mL (#15710072; Thermo Fisher Scientific), antibiotic/antimycotic solution diluted 1:100 (#15240062; Thermo Fisher Scientific) and 44 units/mL IFN-γ (#485-MI; R&D Systems, Minneapolis, MN, USA).
For the experiments, cells were incubated in Assay Media, which contained Earle's Balanced Salt Solution supplemented with 5.5 mM glucose (#141553; Thermo Fisher Scientific), 0.5 mM glutamine (#250030-081; Thermo Fisher Scientific), and 0.5% dialyzed FBS (#26400-036; Thermo Fisher Scientific) at 33°C for 16 hours. Drug treatments, 50 nM BafilomycinA1 (#SML1661; SigmaAldrich Corp.), 2 µM MitoQ (#317102; Medkoo Biosciences, Morrisville, NC, USA) were added into the assay media for 16 hours.

Shyam R., Ogando D.G., Choi M., Liton P.B, & Bonanno J.A. (2021). Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy. Investigative Ophthalmology & Visual Science, 62(12), 15.

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Comprehensive Cell Culture Reagents and Antibodies

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All cell culture reagents were from Invitrogen; and standard laboratory reagents were from Sigma-Aldrich or Fisher Scientific. Drugs were from: ABT737 (Abbvie); Antimycin A, Etoposide, FCCP, Nutlin-3a, Staurosporine (Sigma-Aldrich); zVAD-fmk (VWR Scientific); MitoQ (MedKoo Biosciences). Antibodies (clone or source): β-Actin (C4), BCL-2 (100), CH11 (Millipore), BAK (G-23), BAX (N20), BCL-xS/BCL-xL (S-18), MDM2 (SMP14), p53 (DO-1), BCL-2 (100), BIM (22-40), p21 (C-19), pH2A.X (JBW301), SOD-1 (FL-154), Cyclin D1, Chk1 (FL476), Chk1Ser317, Chk1Ser345 (133D3), GST (Z-5), ND1 (C-18), NDUFS1 (E-8), VDAC (FL-283), Cytochrome c (7H8). CellROX® and MitoSOX^™ were from Thermo Fisher Scientific, and Hoechst 33342 was from Anaspec.

Elkholi R., Abraham-Enachescu I., Trotta A.P., Rubio-Patiño C., Mohammed J.N., Luna-Vargas M.P., Gelles J.D., Kaminetsky J.R., Serasinghe M.N., Zou C., Ali S., McStay G.P., Pfleger C.M, & Chipuk J.E. (2019). MDM2 integrates cellular respiration and apoptotic signaling through NDUFS1 and the mitochondrial network.. Molecular cell, 74(3), 452-465.e7.

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Mitochondrial Modulation Protocols

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Unless stated otherwise, all reagents were purchased from Sigma Aldrich. MitoQ was acquired from MedKoo Biosciences and SS‐31 from China Peptides.

Gottwald E.M., Duss M., Bugarski M., Haenni D., Schuh C.D., Landau E.M, & Hall A.M. (2018). The targeted anti‐oxidant MitoQ causes mitochondrial swelling and depolarization in kidney tissue. Physiological Reports, 6(7), e13667.

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Pancreatic Cancer Cell Lines: Erlotinib and Mitochondrial Dynamics

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The PANC-1 (ATCC^® CRL-1469™) and MIA PaCa-2 (ATCC^® CRL-1420™) pancreatic cell lines were used in the present study. These cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Thermo Fisher Scientific, Waltham, MA) supplemented with 10% fetal bovine serum (FBS) (Thermo Fisher Scientific, Waltham, MA) at 37 °C in a 5% CO₂ atmosphere. Different doses of erlotinib (ERL, Sigma. Cat. No. SML2156) were incubated with the cancer cells for 24 h, and these concentrations of ERL were chosen according to a previous study [26 (link)]. FCCP (5 μm, Selleck Chemicals, Houston, TX, USA) and mitochondrial division inhibitor 1 (Mdivi1; 10 mM; Sigma-Aldrich; Merck KGaA) were used to activate and inhibit mitochondrial fragmentation, respectively, according to a previous study. To repress mROS overproduction, mitochondrial-targeted antioxidant MitoQ (2 μM, MedKoo Biosciences, Inc.; CAT#: 317102) was used.

Wan J., Cui J., Wang L., Wu K., Hong X., Zou Y., Zhao S, & Ke H. (2018). Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways. Cancer Cell International, 18, 165.

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Mitochondrial Targeting for SAH Neuroprotection

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MitoQ (MedKoo Biosciences, Morrisville, NC) was administered i.p. after SAH. ML385 (AOBIOUS, Gloucester, MA) diluted in DMSO i.c.v. injected before SAH. Both 500 pmol of PHB2 siRNA and Scr RNA (Origene Technologies, Inc., Rockville, MD) in 5μl was injected i.c.v. 48 hours pre-surgery as previously reported.^{12 (link)}

Zhang T., Wu P., Budbazar E., Zhu Q., Sun C., Mo J., Peng J., Gospodarev V., Tang J., Shi H, & Zhang J.H. (2019). Mitophagy reduces oxidative stress via Keap1/Nrf2/PHB2 pathway after SAH in rats. Stroke, 50(4), 978-988.

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