scholarly journals Reactive oxygen species regulate Bax translocation and mitochondrial transmembrane potential, a possible mechanism for enhanced TRAIL-induced apoptosis by CCCP

2007 ◽  
Author(s):  
Atul Chaudhari ◽  
Jae-Won Seol ◽  
Shang-Jin Kim ◽  
You-Jin Lee ◽  
Hyung-sub Kang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Transmembrane Potential ◽  
Reactive Oxygen ◽  
Mitochondrial Transmembrane Potential ◽  
Oxygen Species ◽  
Induced Apoptosis

scholarly journals Features of leukocytes’ apoptosis and emoxypine succinate efficacy in case of combined trauma of the chest and both thighs in rats

2019 ◽  
Vol 18 (2) ◽  
pp. 244-251
Author(s):  
Inna Krynytska ◽  
Mariya Marushchak ◽  
Liudmyla Holovatiuk ◽  
Leonid Shkrobot ◽  
Natalia Sokhor ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Medical Treatment ◽  
Transmembrane Potential ◽  
Medical Science ◽  
White Blood Cells ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Mitochondrial Transmembrane Potential ◽  
Oxygen Species ◽  
Laser Cytometry

Objective: This study aims to establish features of blood leukocytes’ apoptosis and substantiate the efficacy of emoxypine succinate applying in case of combined trauma of the chest and both thighs in rats. Materials and Methods: Analysis of cell samples to determine reactive oxygen species was evaluated by the flow laser cytometry method, using 2.7-dichlorodihydrofluorescein diacetate (Sigma Aldrich, Germany). The number of leukocytes with low mitochondrial transmembrane potential was evaluated by the flow laser cytometry method, using a kit of reagents «MitoScreen» («BD Pharmingen», USA). The number of apoptotic leukocytes was evaluated by the flow laser cytometry method, using a kit of reagents “ANNEXIN V FITC” (“Beckman Coulter”, USA). Emoxypine succinate to animals was injected intraperitoneally 1 time per day during 14 days from the first day of experiment in the dosage of 40 mg/kg. Results and Discussion: It was established the progressive, statistically significant increasing of Annexin V- positive cells percentage from the first day of the combined trauma of the chest and both thighs in rats with the highest values within 7-14 days of observation. On 28 day of experiment the reduction of apoptotic white blood cells percentage by 7.7% than the findings on 14 day was observed, but it remained 33.3% higher than control. The analysis of data in case of emoxypine succinate applying indicates that production of reactive oxygen species by leukocytes began to decline after 3 days of experiment and continued to decrease with maximum of action on 7 day. On 28 day of experiment the production of reactive oxygen species by leukocytes has decreased by 39.8 %; the percentage of leukocytes with low transmembrane potential has decreased by 34.6 % vs rats without medical treatment. At the same time the dynamics of FITC Annexin V- positive leukocytes changes in case of combined trauma of the chest and both thighs in rats and emoxypine succinate applying on 28 day of experiment has decreased by 16.7 % vs rats without medical treatment. Conclusion: One of important signaling pathways of apoptosis triggering in case of experimental combined trauma of the chest and both thighs is reactive oxygen species overproduction and disruption of the mitochondrial inner membrane due to the decreasing of transmembrane potential in 3-7 days of observation. Emoxypine succinate applying in post-traumatic period has a positive effect, characterized by decreasing of the production of reactive oxygen species, the percentage of leukocyte with low mitochondrial transmembrane potential and the percentage of FITC Annexin V- positive cells of leukocyte suspension. But the dynamics of FITC Annexin V- positive leukocytes changes leads us to believe that in the initiation and implementation of cell death in case of combined trauma apart mitochondrial, there are other mechanisms. Bangladesh Journal of Medical Science Vol.18(2) 2019 p.244-251

scholarly journals Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death.

1995 ◽  
Vol 182 (2) ◽  
pp. 367-377 ◽  
Author(s):  
N Zamzami ◽  
P Marchetti ◽  
M Castedo ◽  
D Decaudin ◽  
A Macho ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cyclosporin A ◽  
Mitochondrial Function ◽  
Transmembrane Potential ◽  
Reactive Oxygen ◽  
Mitochondrial Transmembrane Potential ◽  
Oxygen Species ◽  
Chromosomal Dna

Programmed cell death (PCD) is a physiological process commonly defined by alterations in nuclear morphology (apoptosis) and/or characteristic stepwise degradation of chromosomal DNA occurring before cytolysis. However, determined characteristics of PCD such as loss in mitochondrial reductase activity or cytolysis can be induced in enucleated cells, indicating cytoplasmic PCD control. Here we report a sequential disregulation of mitochondrial function that precedes cell shrinkage and nuclear fragmentation. A first cyclosporin A-inhibitable step of ongoing PCD is characterized by a reduction of mitochondrial transmembrane potential, as determined by specific fluorochromes (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolcarbocyanine++ + iodide; 3,3'dihexyloxacarbocyanine iodide). Cytofluorometrically purified cells with reduced mitochondrial transmembrane potential are initially incapable of oxidizing hydroethidine (HE) into ethidium. Upon short-term in vitro culture, such cells acquire the capacity of HE oxidation, thus revealing a second step of PCD marked by mitochondrial generation of reactive oxygen species (ROS). This step can be selectively inhibited by rotenone and ruthenium red yet is not affected by cyclosporin A. Finally, cells reduce their volume, a step that is delayed by radical scavengers, indicating the implication of ROS in the apoptotic process. This sequence of alterations accompanying early PCD is found in very different models of apoptosis induction: glucocorticoid-induced death of lymphocytes, activation-induced PCD of T cell hybridomas, and tumor necrosis factor-induced death of U937 cells. Transfection with the antiapoptotic protooncogene Bcl-2 simultaneously inhibits mitochondrial alterations and apoptotic cell death triggered by steroids or ceramide. In vivo injection of fluorochromes such as 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolcarbocyanine iodide; 3,3'dihexyloxacarbocyanine iodide; or HE allows for the detection of cells that are programmed for death but still lack nuclear DNA fragmentation. In particular, assessment of mitochondrial ROS generation provides an accurate picture of PCD-mediated lymphocyte depletion. In conclusion, alterations of mitochondrial function constitute an important feature of early PCD.

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