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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 4271065, 13 pages
Research Article

Cold Atmospheric Plasma Induces Apoptosis and Oxidative Stress Pathway Regulation in T-Lymphoblastoid Leukemia Cells

1Department for Life Quality Studies, Alma Mater Studiorum-Università di Bologna, D’Augusto 237, 47921 Rimini, Italy
2Department of Industrial Engineering, Alma Mater Studiorum-Università di Bologna, Via Saragozza 8, 40123 Bologna, Italy

Correspondence should be addressed to Eleonora Turrini; ti.obinu@inirrut.aronoele

Received 2 March 2017; Revised 18 May 2017; Accepted 19 June 2017; Published 29 August 2017

Academic Editor: Eva-Maria Hanschmann

Copyright © 2017 Eleonora Turrini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cold atmospheric plasma (CAP) has shown its antitumor activity in both in vitro and in vivo systems. However, the mechanisms at the basis of CAP-cell interaction are not yet completely understood. The aim of this study is to investigate CAP proapoptotic effect and identify some of the molecular mechanisms triggered by CAP in human T-lymphoblastoid leukemia cells. CAP treatment was performed by means of a wand electrode DBD source driven by nanosecond high-voltage pulses under different operating conditions. The biological endpoints were assessed through flow cytometry and real-time PCR. CAP caused apoptosis in Jurkat cells mediated by p53 upregulation. To test the involvement of intrinsic and/or extrinsic pathway, the expression of Bax/Bcl-2 and caspase-8 was analyzed. The activation of caspase-8 and the upregulation of Bax and Bcl-2 were observed. Moreover, CAP treatment increased ROS intracellular level. The situation reverts after a longer time of treatment. This is probably due to compensatory cellular mechanisms such as the posttranscriptional upregulation of SOD1, CAT, and GSR2. According to ROS increase, CAP induced a significant increase in DNA damage at all treatment conditions. In conclusion, our results provide a deeper understanding of CAP potential in the oncological field and pose the basis for the evaluation of its toxicological profile.