Hyperthermic Toxicity and the Modulation of Heat Damage to Cell Protein Synthesis in HeLa Cells

Abstract

The possibility that heat shock proteins (hsps) might be involved in the development of thermotolerance is suggested by a number of experimental approaches, including mutational analysis of hsp genes (Craig and Jacobson 1984) and kinetic analysis of hsp levels and thermotolerance development (Landry et al. 1982; Li and Werb 1982; Li and Mak 1985; Laszlo and Li 1985). Nevertheless, one finding of experiments aimed at determining the cytotoxic effects of hyperthermia on cultured mammalian cells was that tolerance to hyperthermic toxicity could be achieved by depletion of calcium ions from the culture medium (Lamarche et al. 1985). Moreover, addition of the protein synthesis inhibitor cycloheximide did not prevent the development of thermotolerance after hyperthermia (Hall 1983; Widerlitz et al. 1986). The fact that both calcium depletion and cycloheximide addition can block heat-induced hsp gene activation casts some doubt on the possible role of hsps in thermotolerance development.

This work was partly supported by grants made available by the Cancer Research Campaign and the Scottish Home and Health Department.