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      Atmospheric-Pressure Plasma Jet Induces Apoptosis Involving Mitochondria via Generation of Free Radicals

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          Abstract

          The plasma jet has been proposed as a novel therapeutic method for anticancer treatment. However, its biological effects and mechanism of action remain elusive. Here, we investigated its cell death effects and underlying molecular mechanisms, using air and N 2 plasma jets from a micro nozzle array. Treatment with air or N 2 plasma jets caused apoptotic death in human cervical cancer HeLa cells, simultaneously with depolarization of mitochondrial membrane potential. In addition, the plasma jets were able to generate reactive oxygen species (ROS), which function as surrogate apoptotic signals by targeting the mitochondrial membrane potential. Antioxidants or caspase inhibitors ameliorated the apoptotic cell death induced by the air and N 2 plasma jets, suggesting that the plasma jet may generate ROS as a proapoptotic cue, thus initiating mitochondria-mediated apoptosis. Taken together, our data suggest the potential employment of plasma jets as a novel therapy for cancer.

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          Role of the mitochondrial membrane permeability transition in cell death.

          Shigeomi Shimizu, Yoshihide Tsujimoto (2007)
          In recent years, the role of the mitochondria in both apoptotic and necrotic cell death has received considerable attention. An increase of mitochondrial membrane permeability is one of the key events in apoptotic or necrotic death, although the details of the mechanism involved remain to be elucidated. The mitochondrial membrane permeability transition (MPT) is a Ca(2+)-dependent increase of mitochondrial membrane permeability that leads to loss of Deltapsi, mitochondrial swelling, and rupture of the outer mitochondrial membrane. The MPT is thought to occur after the opening of a channel that is known as the permeability transition pore (PTP), which putatively consists of the voltage-dependent anion channel (VDAC), the adenine nucleotide translocator (ANT), cyclophilin D (Cyp D: a mitochondrial peptidyl prolyl-cis, trans-isomerase), and other molecule(s). Recently, significant progress has been made by studies performed with mice lacking Cyp D at several laboratories, which have convincingly demonstrated that Cyp D is essential for the MPT to occur and that the Cyp D-dependent MPT regulates some forms of necrotic, but not apoptotic, cell death. Cyp D-deficient mice have also been used to show that the Cyp D-dependent MPT plays a crucial role in ischemia/reperfusion injury. The anti-apoptotic proteins Bcl-2 and Bcl-x(L) have the ability to block the MPT, and can therefore block MPT-dependent necrosis in addition to their well-established ability to inhibit apoptosis.
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            VDAC-dependent permeabilization of the outer mitochondrial membrane by superoxide induces rapid and massive cytochrome c release

            Muniswamy Madesh, György Hajnóczky (2001)
            Enhanced formation of reactive oxygen species (ROS), superoxide (O2 ·−), and hydrogen peroxide (H2O2) may result in either apoptosis or other forms of cell death. Here, we studied the mechanisms underlying activation of the apoptotic machinery by ROS. Exposure of permeabilized HepG2 cells to O2 ·− elicited rapid and massive cytochrome c release (CCR), whereas H2O2 failed to induce any release. Both O2 ·− and H2O2 promoted activation of the mitochondrial permeability transition pore by Ca2+, but Ca2+-dependent pore opening was not required for O2 ·−-induced CCR. Furthermore, O2 ·− alone evoked CCR without damage of the inner mitochondrial membrane barrier, as mitochondrial membrane potential was sustained in the presence of extramitochondrial ATP. Strikingly, pretreatment of the cells with drugs or an antibody, which block the voltage-dependent anion channel (VDAC), prevented O2 ·−-induced CCR. Furthermore, VDAC-reconstituted liposomes permeated cytochrome c after O2 ·− exposure, and this release was prevented by VDAC blocker. The proapoptotic protein, Bak, was not detected in HepG2 cells and O2 ·−-induced CCR did not depend on Bax translocation to mitochondria. O2 ·−-induced CCR was followed by caspase activation and execution of apoptosis. Thus, O2 ·− triggers apoptosis via VDAC-dependent permeabilization of the mitochondrial outer membrane without apparent contribution of proapoptotic Bcl-2 family proteins.
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              Glutathione depletion is necessary for apoptosis in lymphoid cells independent of reactive oxygen species formation.

              M I Panayiotidis, Rodrigo Franco, J Cidlowski (2007)
              Changes in the intracellular redox environment of cells have been reported to be critical for the activation of apoptotic enzymes and the progression of programmed cell death. Glutathione (GSH) depletion is an early hallmark observed in apoptosis, and we have demonstrated that GSH efflux during death receptor-mediated apoptosis occurs via a GSH transporter. We now evaluate the relationship between GSH depletion, the generation of reactive oxygen species (ROS), and the progression of apoptosis. Simultaneous single cell analysis of changes in GSH content and ROS formation by multiparametric FACS revealed that loss of intracellular GSH was paralleled by the generation of different ROS including hydrogen peroxide, superoxide anion, hydroxyl radical, and lipid peroxides. However, inhibition of ROS formation by a variety of antioxidants showed that GSH loss was independent from the generation of ROS. Furthermore, GSH depletion was observed to be necessary for ROS generation. Interestingly, high extracellular thiol concentration (GSH and N-acetyl-cysteine) inhibited apoptosis, whereas, inhibition of ROS generation by other non-thiol antioxidants was ineffective in preventing cell death. Finally, GSH depletion was shown to be a necessary for the progression of apoptosis activated by both extrinsic and intrinsic signaling pathways. These results document a necessary and critical role for GSH loss in apoptosis and clearly uncouple for the first time GSH depletion from ROS formation.
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2011
                Publication date (Electronic): 29 November 2011
                Volume: 6
                Issue: 11
                Electronic Location Identifier: e28154
                Affiliations
                [1 ]Department of Molecular Science and Technology and Department of Life Science, Ajou University, Suwon, Gyounggi-Do, Korea
                [? ]Department of Electrical and Computer Engineering, Ajou University, Suwon, Gyounggi-Do, Korea
                Karolinska Institutet, Sweden
                Author notes

                Conceived and designed the experiments: JSL SSY. Performed the experiments: HJA KIK. Analyzed the data: HJA KIK GYK EPM SSY JSL. Contributed reagents/materials/analysis tools: HJA KIK SSY JSL. Wrote the paper: HJA KIK SSY JSL.

                Article
                Publisher ID: PONE-D-11-13750
                DOI: 10.1371/journal.pone.0028154
                PMC ID: 3226649
                PubMed ID: 22140530
                SO-VID: ce00fb99-e3a1-4b62-af7d-62a3aaf6ae42
                Copyright © Ahn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Date received : 18 July 2011
                Date accepted : 2 November 2011
                Page count
                Pages: 7
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Biochemistry
                Subject: Biophysics
                Subject: Developmental Biology
                Subject: Morphogenesis
                Subject: Cell Migration
                Subject: Molecular Cell Biology
                Subject: Cell Death
                Subject: Toxicology
                Subject: Engineering
                Subject: Bioengineering
                Subject: Medicine
                Subject: Oncology
                Subject: Cancer Treatment
                Subject: Physics
                Subject: Plasmas

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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