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The Correlation Between the Cytotoxicity of Cold Atmospheric Plasma and the Extracellular H2O2-Scavenging Rate | IEEE Journals & Magazine | IEEE Xplore

The Correlation Between the Cytotoxicity of Cold Atmospheric Plasma and the Extracellular H2O2-Scavenging Rate


Abstract:

Cold atmospheric plasma (CAP) has shown its promising capability in cancer treatment both in vitro and in vivo. However, the anti-cancer mechanism is still largely unknow...Show More

Abstract:

Cold atmospheric plasma (CAP) has shown its promising capability in cancer treatment both in vitro and in vivo. However, the anti-cancer mechanism is still largely unknown. CAP may kill cancer cells via triggering the rise of intracellular reactive oxygen species, DNA damage, mitochondrial damage, or cellular membrane damage. While the specific vulnerability of cancer cells to CAP has been observed, the underlying mechanism of such cell-based specific vulnerability to CAP is completely unknown. Here, through the comparison of CAP treatment and H2O2 treatment on ten different cancer cell lines in vitro, we observed that the H2O2 consumption rate by cancer cells was strongly correlated to the cytotoxicity of CAP treatment on cancer cells. Cancer cells that clear extracellular H2O2 more quickly are more resistant to the cytotoxicity of CAP treatment. This finding strongly indicates that the anti-oxidant system in cancer cells play a key role in the specific vulnerability of cancer cells to CAP treatment in vitro.
Published in: IEEE Transactions on Radiation and Plasma Medical Sciences ( Volume: 2, Issue: 6, November 2018)
Page(s): 618 - 623
Date of Publication: 24 September 2018

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I. Introduction

As a near-room temperature ionized gas, cold atmospheric plasma (CAP) has demonstrated its promising capability in cancer treatment by causing the selective death of cancer cells in vitro [1]–[3]. The CAP treatment on several subcutaneous xenograft tumors and melanoma in mice has also demonstrated its potential clinical application [4]–[7]. The rise of intracellular reactive oxygen species (ROS), DNA damage, mitochondrial damage, as well as apoptosis have been extensively observed in the CAP-treated cancer cell lines [8]–[10]. The increase of intracellular ROS may be due to the complicated intracellular pathways or the diffusion of extracellular ROS through the cellular membrane [11]. However, the exact underlying mechanism is still far from clear.

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