Abstract
Epichlorohydrin (ECHH) highly inhibited the tritiated thymidine uptake by human lymphocytes cultured in vitro, although the corresponding cell viability was unaffected. Furthermore, it elicited unscheduled DNA synthesis, acting as a DNA-damaging agent after its metabolic activation. ECHH also showed a clear toxic and mutagenic activity toward a human epithelial-like cell line, causing a decrease in cell viability and an increase in mutants resistant to 0.05 Lf/ml of diphtheria toxin.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Cell Survival / drug effects
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Cells, Cultured
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Chlorohydrins / toxicity*
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DNA / metabolism*
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DNA Replication / drug effects
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Diphtheria Toxin / antagonists & inhibitors
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Drug Resistance
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Epichlorohydrin / toxicity*
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Epithelial Cells
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Epithelium / drug effects
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Humans
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Lymphocytes / drug effects
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Mutagens / toxicity*
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Mutation
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Thymidine / metabolism
Substances
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Chlorohydrins
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Diphtheria Toxin
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Mutagens
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Epichlorohydrin
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DNA
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Thymidine