ArticleBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine1996
Peroxidase deficiency of nickel-transformed hamster cells correlates with their increased resistance to cytotoxicity of peroxides.
Article in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 1 citations in OpenAlex.
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4 authors at 2 institutions in 2 countries.
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Abstract
Using a procedure aimed at isolation of genes that are inactivated during nickel-induced carcinogenesis in Chinese hamster cells, a homolog of genes encoding human and mouse heme containing peroxidases has been cloned. Northern blot analysis of normal cultured fibroblasts and two nickel-transformed cell lines confirmed that this gene was expressed in normal but not in transformed cells. Nickel-transformed cells also tested negative for peroxidase activity using a sensitive fluorescence assay. Cultured embryo cells or fibroblasts that express peroxidase activity and their nickel-transformed peroxidase-deficient counterparts were employed to investigate the role of peroxidase-catalyzed processes in cytotoxicity induced by tert-butyl hydroperoxide or cumene hydroperoxide. It has been found that peroxidase-deficient cells were significantly more resistant to cytotoxic effect of these compounds suggesting that cytotoxic effect of hydroperoxides may be mediated in part by free radicals generated in the course of peroxidase-catalyzed reactions.
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