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TMRE [Tetramethylrhodamine ethyl ester] *CAS#: 115532-52-0*

Positively charged rhodamine dyes (such as rhodamine esters and rosamines) are selectively localized in mitochondria, thus they are widely used for labeling mitochondria of live cells. Like JC-1, TMRM and TMRE are widely used for measuring mitochondrial membrane potential besides their selective mitochondrial staining. These two particular rhodamine esters stain mitochondria orange in fluorescence. Their spectral properties are similar to those of TRITC, making the use of TMRM and TMRE quite convenient. TMRE is slightly more hydrophobic than TMRM.

Calculators

Common stock solution preparation

Table 1. Volume of DMSO needed to reconstitute specific mass of TMRE [Tetramethylrhodamine ethyl ester] *CAS#: 115532-52-0* to given concentration. Note that volume is only for preparing stock solution. Refer to sample experimental protocol for appropriate experimental/physiological buffers.

0.1 mg0.5 mg1 mg5 mg10 mg
1 mM194.194 µL970.968 µL1.942 mL9.71 mL19.419 mL
5 mM38.839 µL194.194 µL388.387 µL1.942 mL3.884 mL
10 mM19.419 µL97.097 µL194.194 µL970.968 µL1.942 mL

Molarity calculator

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Spectrum

Citations

View all 24 citations: Citation Explorer
Targeting mitochondrial metabolism by the mitotoxin bromoxib in leukemia and lymphoma cells
Authors: Schmitt, Laura and Krings, Karina S and Wolsing, Andre and Buque, Xabier and Zimmermann, Marcel and Flores-Romero, Hector and Lenz, Thomas and Lechtenberg, Ilka and Peter, Christoph and Stork, Bj{\"o}rn and others,
Journal: Cell Communication and Signaling: CCS (2024): 541
Palmitic Acid Exerts Anti-Tumorigenic Activities by Modulating Cellular Stress and Lipid Droplet Formation in Endometrial Cancer
Authors: Zhao, Ziyi and Wang, Jiandong and Kong, Weimin and Newton, Meredith A and Burkett, Wesley C and Sun, Wenchuan and Buckingham, Lindsey and O’Donnell, Jillian and Suo, Hongyan and Deng, Boer and others,
Journal: Biomolecules (2024): 601
Targeting mitochondrial metabolism by the mitotoxin bromoxib as a therapeutic approach for the treatment of leukemia and lymphoma
Authors: Schmitt, Laura and Krings, Karina S and Wolsing, Andre and Buque, Xabier and Zimmermann, Marcel and Flores-Romero, Hector and Lenz, Thomas and Lechtenberg, Ilka and Peter, Christoph and Stork, Bj{\"o}rn and others,
Journal: (2024)
Do the same chlorinated organophosphorus flame retardants that cause cytotoxicity and DNA damage share the same pathway?
Authors: Yuan, Shengwu and Zhang, Hong and Wang, Shuhang and Jiang, Xia and Ma, Mei and Xu, Yiping and Han, Yingnan and Wang, Zijian
Journal: Ecotoxicology and Environmental Safety (2024): 116158
Linoleic acid exhibits anti-proliferative and anti-invasive activities in endometrial cancer cells and a transgenic model of endometrial cancer
Authors: Qiu, Jianqing and Zhao, Ziyi and Suo, Hongyan and Paraghamian, Sarah E and Hawkins, Gabrielle M and Sun, Wenchuan and Zhang, Xin and Hao, Tianran and Deng, Beor and Shen, Xiaochang and others,
Journal: Cancer Biology \& Therapy (2024): 2325130

References

View all 73 references: Citation Explorer
CRYAB and HSPB2 deficiency increases myocyte mitochondrial permeability transition and mitochondrial calcium uptake
Authors: Kadono T, Zhang XQ, Srinivasan S, Ishida H, Barry WH, Benjamin IJ.
Journal: J Mol Cell Cardiol (2006): 783
Mitochondrial Ca2+ uptake during simulated ischemia does not affect permeability transition pore opening upon simulated reperfusion
Authors: Ruiz-Meana M, Garcia-Dorado D, Miro-Casas E, Abellan A, Soler-Soler J.
Journal: Cardiovasc Res (2006): 715
High concordance of drug-induced human hepatotoxicity with in vitro cytotoxicity measured in a novel cell-based model using high content screening
Authors: O'Brien P J, Irwin W, Diaz D, Howard-Cofield E, Krejsa CM, Slaughter MR, Gao B, Kaludercic N, Angeline A, Bernardi P, Brain P, Hougham C.
Journal: Arch Toxicol (2006): 580
Serofendic acid, a neuroprotective substance derived from fetal calf serum, inhibits mitochondrial membrane depolarization and caspase-3 activation
Authors: Kume T, Taguchi R, Katsuki H, Akao M, Sugimoto H, Kaneko S, Akaike A.
Journal: Eur J Pharmacol (2006): 69
NECA at reperfusion limits infarction and inhibits formation of the mitochondrial permeability transition pore by activating p70S6 kinase
Authors: Forster K, Paul I, Solenkova N, Staudt A, Cohen MV, Downey JM, Felix SB, Krieg T.
Journal: Basic Res Cardiol (2006): 319
Page updated on December 11, 2024

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Physical properties

Molecular weight

514.95

Solvent

DMSO

Spectral properties

Correction Factor (260 nm)

0.27

Correction Factor (280 nm)

0.03

Excitation (nm)

552

Emission (nm)

574

Storage, safety and handling

Certificate of OriginDownload PDF
H-phraseH303, H313, H333
Hazard symbolXN
Intended useResearch Use Only (RUO)
R-phraseR20, R21, R22

Storage

Freeze (< -15 °C); Minimize light exposure
UNSPSC12352200

CAS

115532-52-0
<strong>CcO inhibition and PTM induce mitochondrial dysfunction. </strong>(A) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with NaN<sub>3</sub>. (B) Quantification of fluorescence intensity from (A). (C) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with KCN. (D) Quantification of fluorescence intensity from (C,E) Cellular ATP levels following 2&thinsp;h treatment with NaN<sub>3</sub> and PTM. (F) Cellular ATP levels following 2&thinsp;h treatment with KCN and PTM. Scale bar: 100&thinsp;&micro;m Data are mean&thinsp;+&thinsp;SEM from three independent experiments. Source: <strong>Cytochrome C oxidase Inhibition and Cold Plasma-derived Oxidants Synergize in Melanoma Cell Death Induction</strong> by Gandhirajan et al., <em>Scientific Reports</em>, Aug. 2018.
<strong>CcO inhibition and PTM induce mitochondrial dysfunction. </strong>(A) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with NaN<sub>3</sub>. (B) Quantification of fluorescence intensity from (A). (C) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with KCN. (D) Quantification of fluorescence intensity from (C,E) Cellular ATP levels following 2&thinsp;h treatment with NaN<sub>3</sub> and PTM. (F) Cellular ATP levels following 2&thinsp;h treatment with KCN and PTM. Scale bar: 100&thinsp;&micro;m Data are mean&thinsp;+&thinsp;SEM from three independent experiments. Source: <strong>Cytochrome C oxidase Inhibition and Cold Plasma-derived Oxidants Synergize in Melanoma Cell Death Induction</strong> by Gandhirajan et al., <em>Scientific Reports</em>, Aug. 2018.
<strong>CcO inhibition and PTM induce mitochondrial dysfunction. </strong>(A) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with NaN<sub>3</sub>. (B) Quantification of fluorescence intensity from (A). (C) Mitochondrial membrane potential enumerated by TMRE dye uptake and cellular superoxide levels by nuclear DHE staining in B16F10 cells following 3&thinsp;h treatment with KCN. (D) Quantification of fluorescence intensity from (C,E) Cellular ATP levels following 2&thinsp;h treatment with NaN<sub>3</sub> and PTM. (F) Cellular ATP levels following 2&thinsp;h treatment with KCN and PTM. Scale bar: 100&thinsp;&micro;m Data are mean&thinsp;+&thinsp;SEM from three independent experiments. Source: <strong>Cytochrome C oxidase Inhibition and Cold Plasma-derived Oxidants Synergize in Melanoma Cell Death Induction</strong> by Gandhirajan et al., <em>Scientific Reports</em>, Aug. 2018.
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