In CHO and R1H cells thermotolerance was induced by a pre-incubation at 40 degrees C, by an acute heat shock at 43 degrees C followed by a time interval at 37 degrees C, and during continuous heating at 42 degrees C. Thermotolerance, which was tested at 43 degrees C, primarily causes an increase in D0 of the heat-response curve. The degree of maximum thermotolerance was found to be generally more pronounced in CHO than in R1H cells, but the time interval at 37 degrees C, as well as at 40 degrees C, to reach this maximum level was the same in both cell lines. CHO and R1H cells could be sensitized to 40 degrees C by a pre-treatment at 43 degrees C. When compared for the same survival rate after pre-treatment at 43 degrees C alone the degree of thermosensitization was about the same in both cell lines. In either cell line thermosensitization was found to be suppressed when cells were made thermotolerant by a previous incubation at 40 degrees C for 16 hours.

The development and decay of thermotolerance at pH 6.7, 7.1 and 7.7 was studied after fractionated hyperthermia at 43 degrees C using exponentially growing CHO cells. The maximum of thermotolerance and the time interval to reach this maximum were found to correlate with the survival decrement after the priming heat treatment. Both parameters were only affected by pH in so far as the pH altered survival after the priming treatment. Decay of thermotolerance was exponential. For a given priming heat treatment for the time t1, the half-time of decay, tau 1/2, increased linearly with increasing cell doubling time, tau d, measured for non-heated cells growing at different pH. On the other hand, for a given cell doubling time, tau d, the half-time, tau 1/2, increased exponentially with increasing duration of the priming heat treatment, t1. For all measured data the half-time of thermotolerance decay could be described by the equation tau 1/2 = alpha. tau d.exp(k.t1), with k = 2.2 +/- 0.2 h-1 and alpha = 0.094 +/- 0.009 for all pretreatments applied and all pH conditions tested. This relationship might indicate that the decay of thermotolerance is governed by a single mechanism.