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.
Wang
Z
Z
Norton Nelson Institute of Environmental Medicine, New York University Medical Center, New York.
Hou
G
G
Rossman
T G
TG
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