The nuclear matrix (NM) has been identified as a potential target for heat-induced cell killing. Previous studies have shown that heat-shock may significantly modulate lamin B content. Since changes in NM structure have often been accompanied by changes in protein composition, we investigated whether hyperthermia induced changes in nuclear lamina (NL) structure in non-tolerant and thermotolerant cells, and the implications of these changes on cell survival. Using indirect immunofluorescence techniques and confocal microscopy, we found that heating cells at 42 or 45.5 degrees C caused invaginations and other distortions of the peripheral NL. While hyperthermia did not alter the number or structure of internal lamin B foci, heat-induced alterations to the peripheral NL were dose-dependent. Interestingly, NL structure recovered with time after heating in cells that were destined to live or die. Thermotolerant cells heated at 45.5 degrees C showed similar initial changes in the NL compared to non-tolerant cells, but recovery occurred much faster. Taken together, these results suggest that the amount of initial damage to the peripheral NL is not correlated with heat-induced cell killing. However, the possibility that an increased rate of recovery might confer a survival advantage cannot be discounted.