Chinese hamster ovary (CHO) cells became thermotolerant after treatment with either heat for 10 min at 45.5°C or incubation in 100 μM sodium arsenite for 1 h at 37°C. Thermotolerance was tested using heat treatment at 45°C or 43°C administered 6-12 h after the inducing agent. At 45°C thermotolerance ratios at 10-2 isosurvival levels were 4.2 and 3.8 for heat and sodium arsenite, respectively. Recovery from heat damage as measured by resumption of protein synthesis was more rapid in heat-induced thermotolerant cells than in either sodium arsenite-induced thermotolerant cells or nonthermotolerant cells. Differences in inhibition of protein synthesis between heat-induced thermotolerant cells and sodium arsenite-induced thermotolerant cells were also evident after test heating at 43°C for 5 h. At this temperature heat-induced thermotolerant cells were protected immediately from inhibition of protein synthesis, whereas sodium arsenite-induced thermotolerant cells, while initially suppressed, gradually recovered within 24 h. Furthermore, adding cycloheximide during the thermotolerance development period greatly inhibited sodium arsenite-induced thermotolerance (<latex>${\rm SF}<10^{-6}$</latex>) but not heat-induced thermotolerance (<tex-math>${\rm SF}=1.7\times 10^{-1}$</tex-math>) when tested with 43°C for 5 h. Our results suggest that both the development of thermotolerance and the thermotolerant state for the two agents, while similar in terms of survival, differed significantly for several parameters associated with protein synthesis.

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