Resistance of human tumor cells in vitro to oxidative cytolysis

Nine human cell types, six of them malignant, displayed a marked resistance to lysis by hydrogen peroxide (LD50, 2-20 mM). Of the reactive oxygen intermediates generated extracellularly, only H2O2 lysed all the cell types. OH was lytic to one of four, OI- to one of one, and O-2 to none of four cell...

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Bibliographic Details
Published in:The Journal of clinical investigation 1985-07, Vol.76 (1), p.80-86
Main Authors: O'Donnell-Tormey, J, DeBoer, C J, Nathan, C F
Format: Article
Language:English
Subjects:
Catalase - metabolism
Cell Line
Cell Survival - drug effects
Free Radicals
Glutathione - metabolism
Humans
Hydrogen Peroxide - metabolism
Hydrogen Peroxide - toxicity
Hydroxides - toxicity
In Vitro Techniques
Neoplasms, Experimental - pathology
Oxygen - toxicity
Superoxides - toxicity
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Summary:Nine human cell types, six of them malignant, displayed a marked resistance to lysis by hydrogen peroxide (LD50, 2-20 mM). Of the reactive oxygen intermediates generated extracellularly, only H2O2 lysed all the cell types. OH was lytic to one of four, OI- to one of one, and O-2 to none of four cell types tested. Resistance to oxidative lysis did not correlate with specific activity of catalase, glutathione (GSH) peroxidase, other peroxidases, or glutathione disulfide reductase, or with specific content of GSH. Resistance to H2O2 seemed to occur via mechanisms distinct from those responsible for cellular consumption of H2O2. Consumption was inhibitable by azide and was probably due to catalase in each cell type. In contrast, resistance to oxidative lysis occurred via distinct routes in different cells. One cell type used the GSH redox cycle as the primary defense against H2O2, like murine tumors previously studied. Other cells seemed to utilize catalase as the major defense against H2O2. Nonetheless, with both catalase and the GSH redox cycle inhibited, all the human cells tested exhibited an inherent resistance to oxidative lysis, that is, resistance independent of detectable degradation of H2O2.
ISSN:0021-9738
DOI:10.1172/JCI111981