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Updated: Jan 25, 2026

Treating Surfaces with a Cold Atmospheric Pressure Plasma using the COST-Jet
Published on: November 2, 2020
Dose-Dependent Tissue-Level Characterization of a Medical Atmospheric Pressure Argon Plasma Jet
Martin Weiss1,2, Jakob Barz2, Michael Ackermann2
1Department of Women's Health , Eberhard Karls Universität Tübingen , Tübingen , Germany.
Cold atmospheric plasma (CAP) offers a promising nonthermal treatment for mucosal conditions. This study quantizes CAP-induced radicals in human tissues, revealing antiproliferative effects on fibroblasts and highlighting cell cycle regulation as a key mechanism.
Area of Science:
- Plasma medicine
- Biophysics
- Cell biology
Background:
- Cold atmospheric plasma (CAP) is a nonthermal treatment with potential for mucosal diseases beyond wound healing.
- Atmospheric pressure plasma jets (APPJs) are versatile but their in vivo tissue effects require better understanding.
- Current characterization often focuses on solutions or plasma effluent, not direct tissue interaction.
Purpose of the Study:
- To investigate the physicochemical effects of APPJ treatment on human primary mucosal tissue and tissue models.
- To assess in vivo tissue-level responses to CAP, focusing on radical generation and cellular effects.
- To establish methods for monitoring CAP effects directly on tissues.
Main Methods:
- Utilized on-tissue infrared (IR) thermography and spatially resolved optical emission spectroscopy (OES) to assess thermal and emission properties.
- Employed electron-spin-resonance (ESR) spectroscopy to quantify CAP-derived radicals in human tissue samples.
- Correlated CAP dosage with radical generation, cell viability, and proliferation of primary human fibroblasts.
Main Results:
- IR thermography and OES showed no evidence of tissue-damaging effects.
- ESR spectroscopy demonstrated dose-dependent generation and distribution of CAP-derived radicals within tissues.
- CAP treatment induced apoptosis-independent antiproliferative effects on fibroblasts, with a dose-dependent G1 cell cycle arrest.
Conclusions:
- CAP treatment at the tissue level is feasible without causing thermal damage.
- Radical generation correlates with antiproliferative effects, suggesting a significant role in CAP's therapeutic mechanisms.
- Cell cycle regulation, particularly G1 arrest, is a key factor in the antiproliferative action of CAP on mucosal tissues.
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