Do pH and flavonoids influence hypochlorous acid-induced catalase inhibition and heme modification?

Krych-Madej, Justyna; Gębicka, Lidia

doi:10.1016/j.ijbiomac.2015.06.038

Cited by 15 publications

(12 citation statements)

References 45 publications

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“…119 , the multifaceted chemical biology of OCl − /HOCl and dichloride anion radicals (Cl 2 ●− ) as established by Wende et al . 38 , the potential of HOCl to interfere with catalase activity, as shown by Krych-Madej and Gebicka 120 and the generation of ● OH through interaction between HOCl and tumor cell-derived O 2 ●− 80,121 . The major aspects to be addressed for potentially successful application of short-lived CAP-derived species seems to be the relative increase in their concentration, as well as development of regimes of application that are less affected by the short-lived nature of the species discussed above, and that allow a close contact between the plasma source and the tumor.…”

Section: Discussionmentioning

confidence: 97%

Dynamics of Singlet Oxygen-Triggered, RONS-Based Apoptosis Induction after Treatment of Tumor Cells with Cold Atmospheric Plasma or Plasma-Activated Medium

Bauer

Sersenová

Graves

et al. 2019

Sci Rep

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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.

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Section: Discussionmentioning

confidence: 97%

Dynamics of Singlet Oxygen-Triggered, RONS-Based Apoptosis Induction after Treatment of Tumor Cells with Cold Atmospheric Plasma or Plasma-Activated Medium

Bauer

Sersenová

Graves

et al. 2019

Sci Rep

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“…and Jirisek and Lukes 108,109 should encourage further studies on the effects of chlorine/chloride-related compounds in CAP and PAM. Interference of hypochlorous acid with catalase activity discussed by Krych-Madej and Gebicka 110 defines another path of interest in this context.…”

Section: Discussionmentioning

confidence: 99%

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

Bauer¹,

Sersenová²,

Graves³

et al. 2019

Sci Rep

124

144

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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.

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“…In addition, it seems to be very promising to study in detail the effects of chlorine/chloride-related compounds in CAP, based on the connection between atomic oxygen and the formation and biological significance of hypochlorite/hypochlorous acid as shown by Bekeschus et al, [128], the multifaceted chemical biology of hypochlorite/hypochlorous acid and dichloride anion radicals as established by Wende et al [129]. and the potential of hypochlorous acid to interfere with catalase activity, in addition to its potential to generate hydroxyl radicals through interaction with superoxide anions, as discussed by Krych-Madej and Gebicka [130].…”

Section: Discussionmentioning

confidence: 99%

The synergistic effect between hydrogen peroxide and nitrite, two long-lived molecular species from cold atmospheric plasma, triggers tumor cells to induce their own cell death

2019

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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.

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Do pH and flavonoids influence hypochlorous acid-induced catalase inhibition and heme modification?

Cited by 15 publications

References 45 publications

Dynamics of Singlet Oxygen-Triggered, RONS-Based Apoptosis Induction after Treatment of Tumor Cells with Cold Atmospheric Plasma or Plasma-Activated Medium

Dynamics of Singlet Oxygen-Triggered, RONS-Based Apoptosis Induction after Treatment of Tumor Cells with Cold Atmospheric Plasma or Plasma-Activated Medium

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

The synergistic effect between hydrogen peroxide and nitrite, two long-lived molecular species from cold atmospheric plasma, triggers tumor cells to induce their own cell death

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