Abstract
Cold atmospheric plasma (CAP), an ionized gas operating at room temperature, has been increasingly studied with respect to its potential use in medicine, where its beneficial effects on tumor reduction in oncology have been demonstrated. This review discusses the cellular changes appearing in cell membranes, cytoplasm, various organelles, and DNA content upon cells’ direct or indirect exposure to CAP or CAP-activated media/solutions (PAM), respectively. In addition, the CAP/PAM impact on the main cellular processes of proliferation, migration, protein degradation and various forms of cell death is addressed, especially in light of CAP use in the oncology field of plasma medicine.
Highlights
Cold atmospheric plasma (CAP) is partially ionized gas, produced at atmospheric pressure and operating at room/body temperature
During cell/tissue treatment with CAP or plasma-activated media (PAM), cellular and organelles membranes represent the natural interphase, which first comes in contact with the above mentioned reactive oxygen and nitrogen species (RONS) produced in PAM or within the cells
None of the long-lived species found in PAM, such as nitrite and H2O2, nor OCl− or nitric oxide (NO) seem to have the potential to interfere with catalase-dependent control of apoptotic cell death-inducing signalling within tumour cells when acting alone
Summary
Cold atmospheric plasma (CAP) is partially ionized gas, produced at atmospheric pressure and operating at room/body temperature. Mammalian cells are equipped to interpret the plasma derived redox signals, their composition, strength, and duration, in either cell endurance/fitness or cell death promoting ways. CAP’s anticancer capacity led to establishing a new field in medicine called “plasma oncology” [6]. In this field, plasma gained attention owing to its ability to induce cancer cell death [4] and significantly reduce tumour size in mice, without damaging normal cells [7]. The mechanisms and processes triggered by CAP-origin reactive species, the rise of intracellular reactive oxygen and nitrogen species (RONS), DNA and mitochondria damage, and deregulated expression of survival inhibiting and death promoting genes will be discussed
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