Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis

Abstract The selective in vitro anti-tumor mechanisms of cold atmospheric plasma (CAP) and plasma-activated media (PAM) follow a sequential multi-step process. The first step involves the formation of primary singlet oxygen (1O2) through the complex interaction between NO2 − and H2O2. 1O2 then inact...

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Autores principales:	Georg Bauer, Dominika Sersenová, David B. Graves, Zdenko Machala
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b65425227d2c482c802c5b9bd01821ef
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spelling	oai:doaj.org-article:b65425227d2c482c802c5b9bd01821ef2021-12-02T15:09:15ZCold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis10.1038/s41598-019-50291-02045-2322https://doaj.org/article/b65425227d2c482c802c5b9bd01821ef2019-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-50291-0https://doaj.org/toc/2045-2322Abstract The selective in vitro anti-tumor mechanisms of cold atmospheric plasma (CAP) and plasma-activated media (PAM) follow a sequential multi-step process. The first step involves the formation of primary singlet oxygen (1O2) through the complex interaction between NO2 − and H2O2. 1O2 then inactivates some membrane-associated catalase molecules on at least a few tumor cells. With some molecules of their protective catalase inactivated, these tumor cells allow locally surviving cell-derived, extracellular H2O2 and ONOO─ to form secondary 1O2. These species continue to inactivate catalase on the originally triggered cells and on adjacent cells. At the site of inactivated catalase, cell-generated H2O2 enters the cell via aquaporins, depletes glutathione and thus abrogates the cell’s protection towards lipid peroxidation. Optimal inactivation of catalase then allows efficient apoptosis induction through the HOCl signaling pathway that is finalized by lipid peroxidation. An identical CAP exposure did not result in apoptosis for nonmalignant cells. A key conclusion from these experiments is that tumor cell-generated RONS play the major role in inactivating protective catalase, depleting glutathione and establishing apoptosis-inducing RONS signaling. CAP or PAM exposure only trigger this response by initially inactivating a small percentage of protective membrane associated catalase molecules on tumor cells.Georg BauerDominika SersenováDavid B. GravesZdenko MachalaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-28 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Georg Bauer Dominika Sersenová David B. Graves Zdenko Machala Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
description	Abstract The selective in vitro anti-tumor mechanisms of cold atmospheric plasma (CAP) and plasma-activated media (PAM) follow a sequential multi-step process. The first step involves the formation of primary singlet oxygen (1O2) through the complex interaction between NO2 − and H2O2. 1O2 then inactivates some membrane-associated catalase molecules on at least a few tumor cells. With some molecules of their protective catalase inactivated, these tumor cells allow locally surviving cell-derived, extracellular H2O2 and ONOO─ to form secondary 1O2. These species continue to inactivate catalase on the originally triggered cells and on adjacent cells. At the site of inactivated catalase, cell-generated H2O2 enters the cell via aquaporins, depletes glutathione and thus abrogates the cell’s protection towards lipid peroxidation. Optimal inactivation of catalase then allows efficient apoptosis induction through the HOCl signaling pathway that is finalized by lipid peroxidation. An identical CAP exposure did not result in apoptosis for nonmalignant cells. A key conclusion from these experiments is that tumor cell-generated RONS play the major role in inactivating protective catalase, depleting glutathione and establishing apoptosis-inducing RONS signaling. CAP or PAM exposure only trigger this response by initially inactivating a small percentage of protective membrane associated catalase molecules on tumor cells.
format	article
author	Georg Bauer Dominika Sersenová David B. Graves Zdenko Machala
author_facet	Georg Bauer Dominika Sersenová David B. Graves Zdenko Machala
author_sort	Georg Bauer
title	Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
title_short	Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
title_full	Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
title_fullStr	Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
title_full_unstemmed	Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis
title_sort	cold atmospheric plasma and plasma-activated medium trigger rons-based tumor cell apoptosis
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/b65425227d2c482c802c5b9bd01821ef
work_keys_str_mv	AT georgbauer coldatmosphericplasmaandplasmaactivatedmediumtriggerronsbasedtumorcellapoptosis AT dominikasersenova coldatmosphericplasmaandplasmaactivatedmediumtriggerronsbasedtumorcellapoptosis AT davidbgraves coldatmosphericplasmaandplasmaactivatedmediumtriggerronsbasedtumorcellapoptosis AT zdenkomachala coldatmosphericplasmaandplasmaactivatedmediumtriggerronsbasedtumorcellapoptosis
_version_	1718387897165414400

Cold Atmospheric Plasma and Plasma-Activated Medium Trigger RONS-Based Tumor Cell Apoptosis

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