Cold Physical Plasma Treatment Alters Redox Balance in Human Immune Cells

Abstract

Cold atmospheric pressure plasma is a promising tool for various biomedical applications. Particularly, treatment of cells and tissues in diseases such as chronic wounds possesses high potential. However, detailed knowledge of how plasma mediates its actions on cells is necessary to explore its potentially beneficial effects in clinical settings. Previous studies have shown that plasma induces oxidative stress. We confirmed this hypothesis by showing that plasma significantly oxidized glutathione (GSH), a major cellular reductant. In plasma-treated cells we found elevated levels of GSH, pointing to a change in cellular redox balance. Oxidative stress can induce apoptosis and plasma-mediated apoptosis has been shown before measuring phosphatidylserine exposure. Using primary human immune cells, we investigated what events precede this reaction. Apoptosis is an active cellular process and accordingly it was dependent on incubation temperature after treatment. Damage of mitochondria was linked to apoptosis previously and plasma treatment resulted in mitochondrial oxidation and reduced mitochondrial membrane potential. Further, we measured a treatment time dependent activation of executioner caspase 3 which is known to be crucially involved in apoptosis. Together, our results suggested that plasma-mediated oxidative stress reactions in eukaryotic cells are in line with the foregoing research in redox biology. Establishing this link will help anticipate results in future research and clinical studies involving cold atmospheric pressure plasmas.