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Int J Mol Med. 2016 Jan;37(1):29-38. doi: 10.3892/ijmm.2015.2405. Epub 2015 Nov 9.

Non-thermal dielectric-barrier discharge plasma damages human keratinocytes by inducing oxidative stress.

Author information

1
School of Medicine and Institute for Nuclear Science and Technology, Jeju National University, Jeju 63243, Republic of Korea.
2
Department of Chemical and Biological Engineering, Jeju National University, Jeju 63243, Republic of Korea.
3
Department of Mechanical Engineering and Graduate School of Medical Science and Engineering, KAIST, Daejeon 34141, Republic of Korea.
4
National Fusion Research Institute, Plasma Technology Research Center, Gunsan 54004, Republic of Korea.

Abstract

The aim of this study was to identify the mechanisms through which dielectric-barrier discharge plasma damages human keratinocytes (HaCaT cells) through the induction of oxidative stress. For this purpose, the cells were exposed to surface dielectric-barrier discharge plasma in 70% oxygen and 30% argon. We noted that cell viability was decreased following exposure of the cells to plasma in a time-dependent manner, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The levels of intracellular reactive oxygen species (ROS) were determined using 2',7'-dichlorodihydrofluorescein diacetate and dihydroethidium was used to monitor superoxide anion production. Plasma induced the generation of ROS, including superoxide anions, hydrogen peroxide and hydroxyl radicals. N-acetyl cysteine, which is an antioxidant, prevented the decrease in cell viability caused by exposure to plasma. ROS generated by exposure to plasma resulted in damage to various cellular components, including lipid membrane peroxidation, DNA breaks and protein carbonylation, which was detected by measuring the levels of 8-isoprostane and diphenyl-1-pyrenylphosphine assay, comet assay and protein carbonyl formation. These results suggest that plasma exerts cytotoxic effects by causing oxidative stress-induced damage to cellular components.

PMID:
26573561
PMCID:
PMC4687437
DOI:
10.3892/ijmm.2015.2405
[Indexed for MEDLINE]
Free PMC Article

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