scholarly journals Relationships of diverse apoptotic death process patterns to mitochondrial membrane potential (Δψm) evaluated by three-parameter flow cytometric analysis

2012 ◽  
Vol 65 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Yuhgi Suzuki ◽  
Hiroo Hasegawa ◽  
Tomohiro Tsuji ◽  
Kazuto Tsuruda ◽  
Daisuke Sasaki ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Flow Cytometric Analysis ◽  
Death Process ◽  
Flow Cytometric ◽  
Apoptotic Death

scholarly journals Evaluation of DNA integrity and mitochondrial membrane potential in catfish Pseudoplatystoma magdaleniatum, induced by exposure to different concentrations of ibuprofen

2021 ◽  
Author(s):  
Sara E. Gallego Ríos ◽  
Gustavo A. Peñuela
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Flow Cytometric Analysis ◽  
Dna Integrity ◽  
Neotropical Fish ◽  
Reliable Technique ◽  
Flow Cytometric ◽  
Striped Catfish ◽  
Integrity Of Dna

Abstract There are few studies to date that determine the effects of ibuprofen on mitochondrial membrane potential (ΔΨM) and DNA integrity in neotropical fish. The objective of this study is to determine if four months’ exposure to ibuprofen in different concentrations (25 and 50 µg/L) produces effects on ΔΨM and alters the integrity of DNA in striped catfish Pseudoplatystoma magdaleniatum. For this study, the fish were placed in tanks with water at constant concentrations of 0 (control), 25, and 50 µg/L of ibuprofen for four months. Subsequently, blood samples were taken for analysis of ΔΨM and DNA integrity, using a flow cytometer LSRFortessa BD Biosciences. After four months of exposure to ibuprofen at different concentrations, the results showed no increase in Low ΔΨM, indicating that there are no alterations in the mitochondrial membrane potential. On the other hand, the percentages of DNA damage were below 0.39, which indicates that there were no alterations in DNA integrity. It is possible that under the conditions in which this study was conducted (ibuprofen levels, exposure time), they are not sufficient to demonstrate the effects caused by this drug. Higher ibuprofen levels and/or longer exposures may be required to determine alteration in ΔΨM and DNA integrity. Flow cytometric analysis for these types of samples is a fast, specific, and reliable technique, compared to traditional methods.

scholarly journals Evaluation of mitochondrial membrane potential and DNA integrity in Catfish Pseudoplatystoma magdaleniatum, when exposed for prolonged times to different concentrations of ibuprofen.

2021 ◽  
Author(s):  
Sara E. Gallego Ríos ◽  
Gustavo A. Peñuela
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Flow Cytometric Analysis ◽  
Dna Integrity ◽  
Neotropical Fish ◽  
Reliable Technique ◽  
Flow Cytometric ◽  
Striped Catfish ◽  
Integrity Of Dna

Abstract There are few studies to date that determine the effects of ibuprofen on mitochondrial membrane potential (ΔΨM) and DNA integrity in neotropical fish. The objective of this study is to determine if four months’ exposure to ibuprofen in different concentrations (25 and 50 µg/L) produces effects on ΔΨM and alters the integrity of DNA in striped catfish Pseudoplatystoma magdaleniatum. For this study, the fish were placed in tanks with water at constant concentrations of 0 (control), 25, and 50 µg/L of ibuprofen for four months. Subsequently, blood samples were taken for analysis of ΔΨM and DNA integrity, using a flow cytometer LSRFortessa BD Biosciences. After four months of exposure to ibuprofen at different concentrations, the results showed no increase in Low ΔΨM, indicating that there are no alterations in the mitochondrial membrane potential. On the other hand, the percentages of DNA damage were below 0.39, which indicates that there were no alterations in DNA integrity. It is possible that under the conditions in which this study was conducted (ibuprofen levels, exposure time), they are not sufficient to demonstrate the effects caused by this drug. Higher ibuprofen levels and/or longer exposures may be required to determine alteration in ΔΨM and DNA integrity. Flow cytometric analysis for these types of samples is a fast, specific, and reliable technique, compared to traditional methods.

Flow Cytometric Detection of Mitochondrial Membrane Potential

BIO-PROTOCOL ◽  
2013 ◽  
Vol 3 (8) ◽  
Author(s):  
Hsin-Yi Chang ◽  
Hsuan-Cheng Huang ◽  
Tsui-Chin Huang ◽  
Pan-Chyr Yang ◽  
Yi-Ching Wang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Flow Cytometric

scholarly journals In vitro activity of 1H-phenalen-1-one derivatives against Leishmania spp. and evidence of programmed cell death

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Atteneri López-Arencibia ◽  
María Reyes-Batlle ◽  
Mónica B. Freijo ◽  
Ines Sifaoui ◽  
Carlos J. Bethencourt-Estrella ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Programmed Cell Death ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Chromatin Condensation ◽  
Death Process ◽  
Leishmania Spp ◽  
Characteristic Features

Abstract Background The in vitro activity against Leishmania spp. of a novel group of compounds, phenalenone derivatives, is described in this study. Previous studies have shown that some phenalenones present leishmanicidal activity, and induce a decrease in the mitochondrial membrane potential in L. amazonensis parasites, so in order to elucidate the evidence of programmed cell death occurring inside the promastigote stage, different assays were performed in two different species of Leishmania. Methods We focused on the determination of the programmed cell death evidence by detecting the characteristic features of the apoptosis-like process, such as phosphatidylserine exposure, mitochondrial membrane potential, and chromatin condensation among others. Results The results showed that four molecules activated the apoptosis-like process in the parasite. All the signals observed were indicative of the death process that the parasites were undergoing. Conclusions The present results highlight the potential use of phenalenone derivatives against Leishmania species and further studies should be undertaken to establish them as novel leishmanicidal therapeutic agents.

scholarly journals A Highly Selective In Vitro JNK3 Inhibitor, FMU200, Restores Mitochondrial Membrane Potential and Reduces Oxidative Stress and Apoptosis in SH-SY5Y Cells

2021 ◽  
Vol 22 (7) ◽  
pp. 3701
Author(s):  
Stephanie Cristine Hepp Rehfeldt ◽  
Stefan Laufer ◽  
Márcia Inês Goettert
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuroprotective Effect ◽  
Flow Cytometric Analysis ◽  
Unmet Need ◽  
Raw264.7 Cells ◽  
Ros Generation ◽  
Anti Inflammatory

Current treatments for neurodegenerative diseases (ND) are symptomatic and do not affect disease progression. Slowing this progression remains a crucial unmet need for patients and their families. c-Jun N-terminal kinase 3 (JNK3) are related to several ND hallmarks including apoptosis, oxidative stress, excitotoxicity, mitochondrial dysfunction, and neuroinflammation. JNK inhibitors can play an important role in addressing neuroprotection. This research aims to evaluate the neuroprotective, anti-inflammatory, and antioxidant effects of a synthetic compound (FMU200) with known JNK3 inhibitory activity in SH-SY5Y and RAW264.7 cell lines. SH-SY5Y cells were pretreated with FMU200 and cell damage was induced by 6-hydroxydopamine (6-OHDA) or hydrogen peroxide (H2O2). Cell viability and neuroprotective effect were assessed with an MTT assay. Flow cytometric analysis was performed to evaluate cell apoptosis. The H2O2-induced reactive oxygen species (ROS) generation and mitochondrial membrane potential (ΔΨm) were evaluated by DCFDA and JC-1 assays, respectively. The anti-inflammatory effect was determined in LPS-induced RAW264.7 cells by ELISA assay. In undifferentiated SH-SY5Y cells, FMU200 decreased neurotoxicity induced by 6-OHDA in approximately 20%. In RA-differentiated cells, FMU200 diminished cell death in approximately 40% and 90% after 24 and 48 h treatment, respectively. FMU200 reduced both early and late apoptotic cells, decreased ROS levels, restored mitochondrial membrane potential, and downregulated JNK phosphorylation after H2O2 exposure. In LPS-stimulated RAW264.7 cells, FMU200 reduced TNF-α levels after a 3 h treatment. FMU200 protects neuroblastoma SH-SY5Y cells against 6-OHDA- and H2O2-induced apoptosis, which may result from suppressing the JNK pathways. Our findings show that FMU200 can be a useful candidate for the treatment of neurodegenerative disorders.

Role of Mitochondrial Membrane Potential and Lactate Dehydrogenase A in Apoptosis

2021 ◽  
Vol 21 ◽  
Author(s):  
Sumera Zaib ◽  
Aqsa Hayyat ◽  
Naba Ali ◽  
Asma Gul ◽  
Muhammad Naveed ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Lactate Dehydrogenase ◽  
Cytochrome C ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Adenine Nucleotide ◽  
P53 Protein ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Death Process

: Apoptosis is a programmed cell death that occurs due to the production of several catabolic enzymes. During this process, several morphological and biochemical changes occur in mitochondria, the main organelle in the cell that participates in apoptosis and control apoptotic pathways. During apoptosis, cytochrome c is released from mitochondria, and different proteins activate caspase cascades that carry out the cell towards the death process. Apoptosis mainly occurs due to p53 protein that allows the abnormal cells to proliferate. Bcl-2 and Bcl-xl are two anti-apoptotic members of the protein family that prevents apoptosis. The membrane potential of mitochondria decreases by opening of the permeability transition pore (PTP). These PTP are formed by the binding of Bax with adenine nucleotide translocator (ANT) and cause depolarization in the membrane. The depolarization releases apoptogenic factors (cytochrome c) that result in the loss of oxidative phosphorylation. Knockdown in lactate dehydrogenase (LDH) is the cause of the decrease in mitochondrial membrane potential elevating the levels of reactive oxygen species (ROS) and Bax. Consequently, causing an increase in the release of cytochrome c that ultimately leads to apoptosis. In this review, we have summarized the combined effect of mitochondrial membrane potential and LDH enzyme that triggers apoptosis in cells and their role in the mechanism of apoptosis.

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