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Toxicity of the quinalphos metabolite 2‐hydroxyquinoxaline: Growth inhibition, induction of oxidative stress, and genotoxicity in test organisms
10.1002/tox.20231.abs
The quinalphos metabolite 2‐hydroxyquinoxaline (HQO), previously shown to photocatalytically destroy antioxidant vitamins and biogenic amines in vitro, was tested for toxicity in several small aquatic organisms and for mutagenicity in Salmonella typhimurium. In the rotifer Philodina acuticornis, HQO caused the disappearance of large individuals and increased hydroperoxide concentration. The latter effect was not only observed in animals kept in a light/dark cycle, but also in constant darkness, indicating that HQO can assume a reactive state and/or form reactive intermediates under the influence of either light or redox‐active metabolites, in particular, free radicals. Cell proliferation was inhibited in the ciliate Paramecium bursaria. In the dinoflagellate Lingulodinium polyedrum, which allows early detection of cellular stress on the basis of bioluminescence measurements, strong rises in light emission became apparent on the 2nd day of exposure to HQO and continued until cells died between 12 and 18 days of treatment. Oxidative damage of protein by HQO was demonstrated by measuring protein carbonyl in L. polyedrumin vivo as well as in light‐exposed bovine serum albumin in vitro. In an Ames test of mutagenicity, HQO proved to be genotoxic in both light‐ and dark‐exposed bacteria. HQO appears as a source of secondary quinalphos toxicity, which deserves further attention. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 33–43, 2007.
Toxicity of the quinalphos metabolite 2‐hydroxyquinoxaline: Growth inhibition, induction of oxidative stress, and genotoxicity in test organisms
10.1002/tox.20231.abs
The quinalphos metabolite 2‐hydroxyquinoxaline (HQO), previously shown to photocatalytically destroy antioxidant vitamins and biogenic amines in vitro, was tested for toxicity in several small aquatic organisms and for mutagenicity in Salmonella typhimurium. In the rotifer Philodina acuticornis, HQO caused the disappearance of large individuals and increased hydroperoxide concentration. The latter effect was not only observed in animals kept in a light/dark cycle, but also in constant darkness, indicating that HQO can assume a reactive state and/or form reactive intermediates under the influence of either light or redox‐active metabolites, in particular, free radicals. Cell proliferation was inhibited in the ciliate Paramecium bursaria. In the dinoflagellate Lingulodinium polyedrum, which allows early detection of cellular stress on the basis of bioluminescence measurements, strong rises in light emission became apparent on the 2nd day of exposure to HQO and continued until cells died between 12 and 18 days of treatment. Oxidative damage of protein by HQO was demonstrated by measuring protein carbonyl in L. polyedrumin vivo as well as in light‐exposed bovine serum albumin in vitro. In an Ames test of mutagenicity, HQO proved to be genotoxic in both light‐ and dark‐exposed bacteria. HQO appears as a source of secondary quinalphos toxicity, which deserves further attention. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 33–43, 2007.
Toxicity of the quinalphos metabolite 2‐hydroxyquinoxaline: Growth inhibition, induction of oxidative stress, and genotoxicity in test organisms
Riediger, Sonja (Autor:in) / Behrends, Andreas (Autor:in) / Croll, Björn (Autor:in) / Vega‐Naredo, Ignacio (Autor:in) / Hänig, Nils (Autor:in) / Poeggeler, Burkhard (Autor:in) / Böker, Jutta (Autor:in) / Grube, Sascha (Autor:in) / Gipp, Juliane (Autor:in) / Coto‐Montes, Ana (Autor:in)
Environmental Toxicology ; 22 ; 33-43
01.02.2007
11 pages
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
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