Journal article
Non-thermal Plasma Induces Apoptosis in Melanoma Cells via Production of Intracellular Reactive Oxygen Species
Annals of biomedical engineering, v 39(2), pp 674-687
Feb 2011
PMID: 21046465
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Non-thermal atmospheric pressure dielectric barrier discharge (DBD) plasma may provide a novel approach to treat malignancies via induction of apoptosis. The purpose of this study was to evaluate the potential of DBD plasma to induce apoptosis in melanoma cells. Melanoma cells were exposed to plasma at doses that did not induce necrosis, and cell viability and apoptotic activity were evaluated by Trypan blue exclusion test, Annexin-V/PI staining, caspase-3 cleavage, and TUNEL
®
analysis. Trypan blue staining revealed that non-thermal plasma treatment significantly decreased the viability of cells in a dose-dependent manner 3 and 24 h after plasma treatment. Annexin-V/PI staining revealed a significant increase in apoptosis in plasma-treated cells at 24, 48, and 72 h post-treatment (
p<
0.001). Caspase-3 cleavage was observed 48 h post-plasma treatment at a dose of 15 J/cm
2
. TUNEL
®
analysis of plasma-treated cells demonstrated an increase in apoptosis at 48 and 72 h post-treatment (
p<
0.001) at a dose of 15 J/cm
2
. Pre-treatment with
N
-acetyl-L-cysteine (NAC), an intracellular reactive oxygen species (ROS) scavenger, significantly decreased apoptosis in plasma-treated cells at 5 and 15 J/cm
2
. Plasma treatment induces apoptosis in melanoma cells through a pathway that appears to be dependent on production of intracellular ROS. DBD plasma production of intracellular ROS leads to dose-dependent DNA damage in melanoma cells, detected by
γ
-H2AX, which was completely abrogated by pre-treating cells with ROS scavenger, NAC. Plasma-induced DNA damage in turn may lead to the observed plasma-induced apoptosis. Since plasma is non-thermal, it may be used to selectively treat malignancies.
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Details
- Title
- Non-thermal Plasma Induces Apoptosis in Melanoma Cells via Production of Intracellular Reactive Oxygen Species
- Creators
- Rachel Sensenig - Department of Surgery, College of Medicine, Drexel University, Philadelphia, PA 19102, USASameer Kalghatgi - Electrical and Computer Engineering, Drexel University, Philadelphia, PA 19104, USAEkaterina Cerchar - Department of Surgery, College of Medicine, Drexel University, Philadelphia, PA 19102, USAGregory Fridman - School of Biomedical Engineering, Drexel University, Philadelphia, PA 19104, USAAlexey Shereshevsky - Department of Surgery, College of Medicine, Drexel University, Philadelphia, PA 19102, USABehzad Torabi - Molecular Biology and Biochem, College of Medicine, Drexel University, Philadelphia, PA 19102, USAKrishna Priya Arjunan - School of Biomedical Engineering, Drexel University, Philadelphia, PA 19104, USAErica Podolsky - Department of Surgery, College of Medicine, Drexel University, Philadelphia, PA 19102, USAAlexander Fridman - Department of Mechanical Engineering and Mechanics, Drexel University, Philadelphia, PA 19104, USAGary Friedman - Electrical and Computer Engineering, Drexel University, Philadelphia, PA 19104, USAJane Azizkhan-Clifford - Molecular Biology and Biochem, College of Medicine, Drexel University, Philadelphia, PA 19102, USAAri D Brooks - Department of Surgery, College of Medicine, Drexel University, Philadelphia, PA 19102, USA
- Publication Details
- Annals of biomedical engineering, v 39(2), pp 674-687
- Publisher
- Springer Nature
- Grant note
- R01 EB013011-01 || EB / National Institute of Biomedical Imaging and Bioengineering : NIBIB
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biochemistry and Molecular Biology; Electrical and Computer Engineering; Mechanical Engineering and Mechanics; Surgery
- Web of Science ID
- WOS:000287213300006
- Scopus ID
- 2-s2.0-79951550640
- Other Identifier
- 991014877934004721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Engineering, Biomedical