## 1 Introduction  
Reactive oxygen species (ROS) play pivotal roles in health and disease. This super-ordinate term describes an array of molecular oxygen derivatives that can cause lethal oxidative distress when applied at supraphysiological levels while mediating pleiotropic physiological signaling pathways per se [1]. Two main types of ROS produced by body cells are hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) and hypochlorous acid (HOCI). The former either spontaneously or enzymatically dismutates from superoxide that leaks the electron transport chain of mitochondria. Alternatively, superoxide is intentionally produced during inflammation and infection via NADPH and dual oxidases (NOX, DUOX) [2]. Persistently high H\({}_{2}\)O\({}_{2}\) levels are associated with several pathologies, such as chronic kidney and liver disease, cancer, and lung and neurodegenerative disease [3; 4; 5; 6; 7; 8]. Besides the induced oxidative stress in cells exposed to H\({}_{2}\)O\({}_{2}\), the molecule is also used for antimicrobial defense, as evident in wound healing [9]. The enzyme myeloperoxidase (MPO) catalyzes a reaction with H\({}_{2}\)O\({}_{2}\) to form HOCI, a dismutase's potent antimicrobial type of ROS [10]. MPO is expressed mainly by professional phagocytes and activated upon inflammatory stimuli. Chlorinated proteins testify aberrant MPO-activity in chronically inflamed tissues [11]. Despite endogenous ROS generation in cellular respiration, metabolism, or by cells in antimicrobial defense [12], ROS can come from exogenous sources such as radiation, photodynamic therapy, various chemotherapeutics, and also medical gas plasmas. Thisinnovative technology exploits the feature of partially ionized gases to generate vast amounts of ROS/RNS and has emerged as a promising tool for treating cancers in recent years [13; 14]. Emphasizing results have been reported from preclinical studies in various tumor models, including leukemia in vitro [15; 16], in vivo [17; 18], and the palliation of head and neck cancer patients in clinical dermato-oncology [19; 20]. Intriguingly, species chemistries can be influenced, e.g., by operating devices with different feed gases or feed gas admixtures [21]. Due to the high reactivity of short-lived species in the gas phase, biological effects in vitro, where cells are surrounded by liquids, are mainly mediated by secondary, long-lived species. Hereof, H\({}_{2}\)O\({}_{2}\) plays a major role in argon feed gas conditions [22; 23], while helium-oxygen (HeO\({}_{2}\)) plasmas generate vast amounts of HOCI during treatment [24; 25]. Oxidative stress implies a somewhat collective action of oxidants, leading to impaired redox signaling and molecular damage [26]. Irreversible damage to biomolecules such as nucleic acids, lipids, or proteins can cause ROS-induced cell death, often linked to characteristics of apoptotic signaling [27; 28]. To protect themselves from such potential damage, the cells set up a series of defense mechanisms including detoxification of the ROS by enzymes such as superoxide dismutases (SODs), glutathione peroxididases (GPOXs), and catalases (CATs) [29]. Albeit several activities can be attributed to different types of ROS and the enzymes controlling subsequent biological programs [30], an often subliminal assumption is that overall oxidative stress sensitivity or resistance is similar among different cell lines for different types of ROS, although only H\({}_{2}\)O\({}_{2}\) induced stress is mainly investigated [31; 32; 33; 34]. Little is known about differential effects, especially between H\({}_{2}\)O\({}_{2}\) and HOCI, which are both likely to act in concert during inflammation and play a crucial role in the therapeutic efficacy of ROS/RNS-based therapy approaches, such as gas plasmas.