“…Based on established chemical biology, PAM decomposition by the tumor cells may reflect decomposition of H 2 O 2 and oxidation of NO 2 − to ● NO 2 . Both processes can be catalyzed by catalase 74,98 .Figure 19Consumption of PAM constituents by tumor cells. PAM was generated by CAP treatment of medium for 1 min.…”
Section: Resultsmentioning
confidence: 99%
“…This finding is in good agreement with the results of other investigators 46,57,101 . It is also conceivable that the concentration of NO 2 − is lowered through the oxidation to ● NO 2 by catalase 98 . These catalase-mediated effects are thus establishing conditions where the generation of primary 1 O 2 is rapidly turning to suboptimal conditions.…”
Treatment of tumor cells with cold atmospheric plasma (CAP) or with plasma-activated medium (PAM) leads to a biochemical imprint on these cells. This imprint is mediated by primary singlet oxygen, which is mainly generated through the interaction between CAP-derived H2O2 and NO2−. This imprint is induced with a low efficiency as local inactivation of a few membrane-associated catalase molecules. As sustained generation of secondary singlet oxygen by the tumor cells is activated at the site of the imprint, a rapid bystander effect-like spreading of secondary singlet oxygen generation and catalase inactivation within the cell population is thus induced. This highly dynamic process is essentially driven by NOX1 and NOS of the tumor cells, and finally leads to intercellular RONS-driven apoptosis induction. This dynamic process can be studied by kinetic analysis, combined with the use of specific inhibitors at defined time intervals. Alternatively, it can be demonstrated and quantified by transfer experiments, where pretreated cells are mixed with untreated cells and bystander signaling is determined. These studies allow to conclude that the specific response of tumor cells to generate secondary singlet oxygen is the essential motor for their self-destruction, after a singlet oxygen-mediated triggering process by CAP or PAM.
“…Based on established chemical biology, PAM decomposition by the tumor cells may reflect decomposition of H 2 O 2 and oxidation of NO 2 − to ● NO 2 . Both processes can be catalyzed by catalase 74,98 .Figure 19Consumption of PAM constituents by tumor cells. PAM was generated by CAP treatment of medium for 1 min.…”
Section: Resultsmentioning
confidence: 99%
“…This finding is in good agreement with the results of other investigators 46,57,101 . It is also conceivable that the concentration of NO 2 − is lowered through the oxidation to ● NO 2 by catalase 98 . These catalase-mediated effects are thus establishing conditions where the generation of primary 1 O 2 is rapidly turning to suboptimal conditions.…”
Treatment of tumor cells with cold atmospheric plasma (CAP) or with plasma-activated medium (PAM) leads to a biochemical imprint on these cells. This imprint is mediated by primary singlet oxygen, which is mainly generated through the interaction between CAP-derived H2O2 and NO2−. This imprint is induced with a low efficiency as local inactivation of a few membrane-associated catalase molecules. As sustained generation of secondary singlet oxygen by the tumor cells is activated at the site of the imprint, a rapid bystander effect-like spreading of secondary singlet oxygen generation and catalase inactivation within the cell population is thus induced. This highly dynamic process is essentially driven by NOX1 and NOS of the tumor cells, and finally leads to intercellular RONS-driven apoptosis induction. This dynamic process can be studied by kinetic analysis, combined with the use of specific inhibitors at defined time intervals. Alternatively, it can be demonstrated and quantified by transfer experiments, where pretreated cells are mixed with untreated cells and bystander signaling is determined. These studies allow to conclude that the specific response of tumor cells to generate secondary singlet oxygen is the essential motor for their self-destruction, after a singlet oxygen-mediated triggering process by CAP or PAM.
“…As sole application of nitrite to tumor cells did not cause apoptosis induction, the established interference of nitrite with the catalytic cycle of tumor cell protective catalase [80] is therefore obviously not sufficient to trigger the biochemical steps that lead to apoptosis induction after application of CAP or PAM. As it was confirmed that sole application of H 2 O 2 caused apoptosis induction in nonmalignant cells at much lower concentrations than required for tumor cells, the effect of H 2 O 2 alone can also not explain selective action of CAP or PAM towards tumor cells.…”
Nitrite and H2O2 are long-lived species in cold atmospheric plasma and plasma-activated medium. It is known that their synergistic interaction is required for selective apoptosis induction in tumor cells that are treated with plasma-activated medium. This study shows that the interaction between nitrite and H2O2 leads to the formation of peroxynitrite, followed by singlet oxygen generation through the interaction between peroxynitrite and residual H2O2. This primary singlet oxygen causes local inactivation of few catalase molecules on the surface of tumor cells. As a consequence, H2O2 and peroxynitrite that are constantly produced by tumor cells and are usually decomposed by their protective membrane-associated catalase, are surviving at the site of locally inactivated catalase. This leads to the generation of secondary singlet oxygen through the interaction between tumor cell-derived H2O2 and peroxynitrite. This selfsustained process leads to autoamplification of secondary singlet oxygen generation and catalase inactivation. Inactivation of catalase allows the influx of H2O2 through aquaporins, leading to intracellular glutathione depletion and sensitization of the cells for apoptosis induction through lipid peroxidation. It also allows to establish intercellular apoptosis-inducing HOCl signaling, driven by active NOX1 and finalized by lipid peroxidation through hydroxyl radicals that activates the mitochondrial pathway of apoptosis. This experimentally established model is based on a triggering function of CAP and PAM-derived H2O2/nitrite that causes selective cell death in tumor cells based on their own ROS and RNS. This model explains the selectivity of CAP and PAM action towards tumor cells and is in contradiction to previous models that implicated that ROS/RNS from CAP or PAM were sufficient to directly cause cell death of tumor cells.
“…In addition to the well‐known function of catalyzing the reduction of H 2 O 2 to water and molecular oxygen, CAT can also remove organic hydroperoxides as well as use H 2 O 2 to oxidize toxins including phenols, formic acid, formaldehyde and alcohols. Moreover, CAT may have additional roles such as preventing mitochondrial permeability transitions, modulating the effects of oxidative stress‐induced activation of ion channels and detoxification or activation of toxic and antitumor compounds (Glorieux & Calderon, 2017; Krych‐Madej & Gebicka, 2017; Naziroǧlu, 2012). Therefore, it should not be discarded that some of these processes could be affected in the HC of noise‐exposed rats.…”
Living in big cities might involuntarily expose people to high levels of noise causing auditory and/or extra‐auditory impairments, including adverse effects on central nervous system (CNS) areas such as the hippocampus. In particular, CNS development is a very complex process that can be altered by environmental stimuli. We have previously shown that noise exposure of developing rats can induce hippocampal‐related behavioral alterations. However, noise‐induced biochemical alterations had not been studied yet. Thus, the aim of this work was to assess whether early noise exposure can affect rat hippocampal oxidative state and aminoacidergic neurotransmission tone. Additionally, the effectiveness of an enriched environment (EE) as a neuroprotective strategy was evaluated. Male Wistar rats were exposed to different noise schemes at 7 or 15 days after birth. Upon weaning, some animals were transferred to an EE whereas others were kept in standard cages. Short‐ and long‐term measurements were performed to evaluate reactive oxygen species, thioredoxins levels and catalase activity as indicators of hippocampal oxidative status as well as glutamic acid decarboxylase and a subtype of glutamate transporter to evaluate aminoacidergic neurotransmission tone. Results showed noise‐induced changes in hippocampal oxidative state and aminoacidergic neurotransmission markers that lasted until adolescence and differed according to the scheme and the age of exposure. Finally, EE housing was effective in preventing some of these changes. These findings suggest that CNS development seems to be sensitive to the effects of stressors such as noise, as well as those of an environmental stimulation, favoring prompt and lasting molecular changes.
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