Responses of Solid Tumor Cells in DMEM to Reactive Oxygen Species Generated by Non-Thermal Plasma and Chemically Induced ROS Systems

Abstract

In this study, we assessed the role of different reactive oxygen species (ROS) generated by soft jet plasma and chemical-induced ROS systems with regard to cell death in T98G, A549, HEK293 and MRC5 cell lines. For a comparison with plasma, we generated superoxide anion (O2−), hydroxyl radical (HO·), and hydrogen peroxide (H2O2) with chemicals inside an in vitro cell culture. Our data revealed that plasma decreased the viability and intracellular ATP values of cells and increased the apoptotic population via a caspase activation mechanism. Plasma altered the mitochondrial membrane potential and eventually up-regulated the mRNA expression levels of BAX, BAK1 and H2AX gene but simultaneously down-regulated the levels of Bcl-2 in solid tumor cells. Moreover, a western blot analysis confirmed that plasma also altered phosphorylated ERK1/2/MAPK protein levels. At the same time, using ROS scavengers with plasma, we observed that scavengers of HO· (mannitol) and H2O2 (catalase and sodium pyruvate) attenuated the activity of plasma on cells to a large extent. In contrast, radicals generated by specific chemical systems enhanced cell death drastically in cancer as well as normal cell lines in a dose-dependent fashion but not specific with regard to the cell type as compared to plasma.

Combination Treatment with Cold Physical Plasma and Pulsed Electric Fields Augments ROS Production and Cytotoxicity in Lymphoma

“…Therefore, we hypothesized that plasma-generated ROS enhance PEF-induced membrane electroporation and cytotoxicity [27,33]. Our second hypothesis was that the combination of plasma and PEF augments ROS production cell death signaling [29,34,35]. While three previous studies investigated the combination of plasma-treated liquids and PEF on cancer cells [36][37][38], our study aimed at elucidating the underlying mechanism of direct plasma treatment and pulsed electric fields (PEFs).…”

High throughput image cytometry micronucleus assay to investigate the presence or absence of mutagenic effects of cold physical plasma

“…This marker was originally associated with DNA damage and DSBs [Whitaker et al, 1991]. An increase of gH2AX in plasma-treated cells was identified in vitro in primary tumor-derived melanoma cells [Sensenig et al, 2011], metastatic melanoma cells [Arndt et al, 2013b], squamous cell carcinoma [Chang et al, 2014], colon cancer cells [Judee et al, 2016], breast epithelial cells , glioblastoma [Kaushik et al, 2015], immortalized fibroblasts [Kim et al, 2011b], and colorectal carcinoma cells [Plewa et al, 2014]. Despite the importance of in vitro experiments, preclinical studies have failed to show an increase of gH2AX in ex vivo plasma-treated human skin [Isbary Fig.…”

The emerging role of xanthine oxidase inhibition for suppression of breast cancer cell migration and metastasis associated with hypercholesterolemia

“…The role of ROS, which are derived from NADPH oxidase, mitochondrial oxidase, and xanthine oxidase (XO), is postulated to be important in tumor biology (e.g., in both ROS-induced damage of DNA and proteins and the activation of the ERK1/2/MAPK pathway) (4). Modification of gene expression by ROS has direct effects on cell proliferation and apoptosis via the activation of transcription factors, including activator protein 1, and via the NF-kB pathways (5).…”