Cold atmospheric plasma (CAP) is an ionized gas produced at atmospheric pressure in which heavy particles remain near room temperature. CAP generates a complex mixture of reactive oxygen and nitrogen species (RONS) that can interact with biological systems. Prior studies have shown CAP can trigger cell death in various cancer cell lines in vitro and in vivo, and non-tumoral cells often appear less affected — a phenomenon termed CAP selectivity. This work evaluated whether a CAP jet produced by a dielectric barrier discharge (DBD) exhibits selective cytotoxicity against prostate cancer cells compared with non-tumoral prostate cells and whether observed effects associate with changes in cellular redox status.
The study compared two human prostate cell lines: the prostate cancer cell line PC3 and the non-tumoral prostate epithelial cell line RWPE-1. Cells were exposed to DBD-generated CAP for exposure durations between 5 and 60 seconds. Outcome measures were assessed at 4 hours and 24 hours after CAP treatment.
Assays included:
Cells received a single exposure to the DBD CAP jet ranging from 5 to 60 seconds. Post-exposure assessments were performed at two time points, 4 hours and 24 hours, to capture early and later responses. The abstract reports the exposure durations and assessment times but does not provide further technical parameters of the CAP jet (for example, exact RONS composition, power, or distance), which were not reported in the source summary.
CAP treatment produced a time-dependent decrease in viability of PC3 cells. Significant reductions in PC3 viability were observed at exposure durations of 30 seconds and longer. In contrast, RWPE-1 cells exhibited relative resistance to the same CAP exposure conditions.
PI staining supported these viability findings by demonstrating greater plasma membrane damage in PC3 cells compared with RWPE-1. Morphological changes observed by phase-contrast microscopy — including cell rounding and detachment — were more pronounced in PC3 cells than in RWPE-1 cells after CAP exposure.
DHE staining showed a marked increase in intracellular reactive oxygen species in PC3 cells following CAP exposure, with the highest reported proportion of DHE-positive PC3 cells reaching approximately 73% after 60 seconds of treatment. RWPE-1 cells showed a less pronounced ROS increase under the same conditions. These results indicate that CAP induces stronger oxidative stress in the cancer cell line relative to the non-tumoral line.
Following CAP exposure, PC3 cells exhibited alterations in antioxidant enzyme activities consistent with an oxidative imbalance: SOD activity was upregulated, while catalase and GPx activities were reduced. By contrast, RWPE-1 cells maintained antioxidant enzyme activities to a greater extent, consistent with their relative resistance to CAP-induced cytotoxicity. The abstract reports directional changes in these enzymes but does not include quantitative enzyme activity values or statistical metrics in the summary provided.
Under the tested conditions, DBD-generated CAP produced selective cytotoxic effects in the prostate cancer cell line PC3 relative to non-tumoral RWPE-1 cells. The selective sensitivity correlated with increased intracellular ROS production and perturbation of antioxidant defenses in PC3 cells (SOD upregulation and decreased catalase and GPx activities), suggesting that CAP-induced oxidative stress contributes to cancer cell killing.
The authors conclude that DBD-CAP may represent a promising targeted therapeutic approach for prostate cancer. The abstract does not report in vivo data, detailed CAP device parameters, full quantitative results for enzyme activities, or mechanistic signaling downstream of oxidative stress. Those details would be necessary to evaluate translational potential, reproducibility, and safety. The source also states the authors declared no competing interests.
Keywords: Antioxidant enzymes; Cell viability; Cold atmospheric plasma; Dielectric barrier discharge; Oxidative stress; Prostate cancer; Reactive oxygen and nitrogen species; Selective cytotoxicity.