Rhodamine B as a mitochondrial probe for measurement and monitoring of mitochondrial membrane potential in drug-sensitive and -resistant cells

Reungpatthanaphong, Paiboon; Dechsupa, Nathupakorn; Meesungnoen, Jintana; Loetchutinat, Chatchanok; Mankhetkorn, Samlee

doi:10.1016/s0165-022x(03)00032-0

Cited by 107 publications

(69 citation statements)

References 20 publications

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“…Rhodamine B was used as a probe to estimate DY m in drug-sensitive and, particularly, in drug-resistant cells because its rate of uptake by cell is four times higher than the rate of P-glycoproteinmediated efflux and it is not a substrate of MRP1 protein. 28) The accumulation of rhodamine B in cells follows Nernstain distribution, but the plasma membrane potential does not contribute to rhodamine B uptake by cells. The estimation of DY m was done by using Nernst equation:…”

Section: Determination Of Mitochondrial Membrane Potential (D Dy Y M )mentioning

confidence: 98%

Modulation of Multidrug Resistance by Artemisinin, Artesunate and Dihydroartemisinin in K562/adr and GLC4/adr Resistant Cell Lines.

Reungpatthanaphong

Mankhetkorn

2002

Biological & Pharmaceutical Bulletin

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Multidrug resistance (MDR) is a principle cause of failure in human drug treatment. MDR phenomena are intensively studied in anti-cancer, anti-bacterial, anti-paludism, and human immunodeficiency virus-1. [1][2][3][4][5] The MDR phenotype is characterized by a low free intracellular cytotoxic drug concentration in comparison with their corresponding drugsensitive cells. This is frequently associated with protein membrane transporters, such as P-glycoprotein and MRP1-protein, which ATP-dependently extrude cytotoxic agents out of cells, thus reducing their efficacy. To overcome MDR phenomena, the direct interaction between inhibitors and proteins has been researched by many groups. A variety of small molecules, such as verapamil, dihydropyridines, forskolin and cyclosporin were found to bind to P-glycoprotein and inhibit its ability to pump out antitumor drugs. 6-9) All compounds cited are difficult to use in vivo due to their toxicity. As a consequence, the clinical utility of non-toxic derivatives of these and other molecules as chemosensitizing agents has been extensively studied. 10,11) It was reported that in MDR plasmodium falciparum strains, the pfmdr-1 gene and pgh-1 were characterized, which has about 54% homology to mdr-1 gene of MDR cancer cells. [12][13][14][15] However, its function is still not clear. Recently, it was reported that qinghaosu is an effective compound against MDR plasmodium falciparum strains, 16,17) but studies regarding its effect on protein transporters have not been performed, neither in erythrocytes infected by MDR plasmodium falciparum strains nor in cancer MDR cells. Qinghaosu drugs such as artemisinin and artesunate are now in widespread use, particularly in Southast Asia, and are used as a prophylaxis in China. 18,19) In this study we have demonstrated that artemisinin, artesunate and dihydroartemisinin poorly inhibited P-glycoprotein and did not inhibit MRP1 protein function in multidrug resistant K562/adr cells, overexpression P-glycoprotein, or in GLC4/adr cells overexpression of MRP1-protein, respectively. However, they increased in cytotoxic effect induced by pirarubicin or doxorubicin only in MDR cell lines. We also demonstrated that these qinghaosu modulate mitochondrial function, leading to a decrease in intracellular ATP content in all cell lines tested. MATERIALS AND METHODS Cell Culture and Cytotoxicity AssayThe erythromyelogenous leukemic, K562, and its P-glycoprotein-overexpressing K562/adr, 20,21) and the human small cell lung cancer, GLC4 and its MRP1-overexpressing GLC4/adr, [22][23][24] were kindly provided by Professor Arlette Garnier-Suillerot, Laboratoire de Chimie Physique, Biomoleculaire et Cellulaire, UFR Sante Medecine Biologie Humaine, Universite de Paris Nord, France. These cells were routinely cultured in RPMI 1640 medium supplemented with 10% fetal calf serum (Gibco Biocult, Ltd.). The resistant K562/adr and GLC4/adr cells were cultured with 100 nM doxorubicin two weeks before the experiments. For the assays, a culture was initiated at 5ϫ10 5 cells ...

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Section: Determination Of Mitochondrial Membrane Potential (D Dy Y M )mentioning

confidence: 98%

Modulation of Multidrug Resistance by Artemisinin, Artesunate and Dihydroartemisinin in K562/adr and GLC4/adr Resistant Cell Lines.

Reungpatthanaphong

Mankhetkorn

2002

Biological & Pharmaceutical Bulletin

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“…The membrane potential was evaluated using Rhodamine B hexyl ester probe (Rhodamine B) by confocal microscopy ( Fig. 7B) (Reungpatthanaphong et al, 2003). To obtain a more quantitative data, a time course of Rhodamine B fluorescence was also carried out through flow cytometry analysis with 25 and 100 M (data not shown).…”

Section: Af Does Not Affect Mitochondrial Membrane Potential and Morpmentioning

confidence: 99%

Evidence that the antiproliferative effects of auranofin in Saccharomyces cerevisiae arise from inhibition of mitochondrial respiration

Gamberi

Fiaschi

Modesti

et al. 2015

The International Journal of Biochemistry & Cell Biology

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“…Very recently, it has been reported that the curcumin has a lot of potential to act as an adjuvant remedy in liver cancer through the loss of mitochondrial membrane potential and also protect against the side effects of the currently available chemotherapeutic agents [18]. The efficient role of the Cur/PMMA-AA/ZnO NPs in reducing the mitochondrial membrane potential (∆Ψm) was measured using a cationic fluorescence dye rhodamine1 [19] which diffuses into the mitochondrial matrix, thus bringing about drastic changes on it. The AGS cancer cell lines were treated with these studied nanomaterials which in turn induced a significant loss of mitochondrial membrane potential (∆Ψm) in a time dependent manner.…”

Section: Methodsmentioning

confidence: 99%

pH Triggered Curcumin Release from PMMA-AA Coated ZnO Nanoparticles for Excellent Anti-Gastric Cancer Therapy

Dhivya¹,

Ranjani²,

Rajendhran³

et al. 2018

J Material Sci Eng

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The curcumin loaded PMMA-AA/ZnO nanocomposite potentially inhibited the growth of AGS cancer tumour in male Swiss albino mouse, which showed a promising targeted cancer therapy. Interestingly the given bio-nanocomposite was rapidly cleared from the organs with negligible exhibition of toxicity. From the obtained results it is understood that the apoptosis has been occurred through mitochondrial disruption-mediated pathway. Also these nanomaterials could efficiently hinder the Go/G1 transition along with cycle progression at S-phase transition due to the radiation-induced DNA damage. These findings declared that the auspicious candidate, curcumin could be successfully delivered into the target by the polymer encapsulated ZnO NPs and exhibited a potent activity against gastric cancer cells at molecular and cellular levels as well as cell proliferation in a panel of tumour cells.

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Rhodamine B as a mitochondrial probe for measurement and monitoring of mitochondrial membrane potential in drug-sensitive and -resistant cells

Cited by 107 publications

References 20 publications

Modulation of Multidrug Resistance by Artemisinin, Artesunate and Dihydroartemisinin in K562/adr and GLC4/adr Resistant Cell Lines.

Modulation of Multidrug Resistance by Artemisinin, Artesunate and Dihydroartemisinin in K562/adr and GLC4/adr Resistant Cell Lines.

Evidence that the antiproliferative effects of auranofin in Saccharomyces cerevisiae arise from inhibition of mitochondrial respiration

pH Triggered Curcumin Release from PMMA-AA Coated ZnO Nanoparticles for Excellent Anti-Gastric Cancer Therapy

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