Induction of arsenite tolerance and thermotolerance by arsenite occur by different mechanisms.
Both V79 and As/R28A cells (an arsenite-resistant Chinese hamster V79 cell variant) show increased resistance to toxic concentrations of arsenite after pretreatment with a nontoxic concentration. The induced tolerance can be completely inhibited by actinomycin D or cycloheximide. Pretreatment with a nontoxic heat shock (45 degrees C, 10 min) resulted in a clear increased thermotolerance in both cell lines but failed to induce arsenite tolerance in either cell line. Pretreatment with arsenite induced a thermotolerance in V79 cells but not in As/R28A cells. These results are consistent with a model whereby the signal for induction of arsenite tolerance involves binding of arsenite to a protein effector which is amplified in the As/R28A line, thereby preventing action of arsenite in the regulation of heat shock factor which induces the heat shock response.
Norton Nelson Institute of Environmental Medicine, New York University Medical Center, New York.
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Rossman
D000818:Animals; D018053:Arsenites / Q000494:pharmacology*; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004351:Drug Resistance; D004361:Drug Tolerance; D006358:Hot Temperature; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D017670:Sodium Compounds / Q000494:pharmacology*
D018053:Arsenites; D012333:RNA, Messenger; D017670:Sodium Compounds; D003609:Dactinomycin; C017947:sodium arsenite; D003513:Cycloheximide