| description abstract | The Arrhenius equation and, similarly, transition state theory (TST) describe well the temperature dependence of the rate of irreversible heating-damage to many biological materials (1234). These equations have been used to correlate the temperature dependence of the rate of damage to proteins (e.g., collagen 56, cells (e.g., HeLa cells 789), and tissues (e.g., burns 1011). The similarity of descriptions of the temperature dependence of heating-damage to proteins, cells, and tissues is unsurprising given the abundance of proteins in cells and tissues. Membrane and nuclear proteins are likely targets in the killing of cells (see, for example, 9121314). Thermotolerance in cells via expression of heat shock proteins (HSPs) also appears to follow denaturation of nuclear proteins 1315. Heating-damage of biological materials manifests many physical and chemical changes, leading to many assays of such damage. Assays for proteins include intrinsic viscosity 616, loss of birefringence 171819, shrinkage 52021, and changes in enthalpy 2223. Hormann and Schlebusch 24 illustrated that the results of gross shrinkage provides much the same information on the kinetics of denaturation as many biochemical assays, although not with the same detail with respect to underlying mechanisms. Damage assays for cells focus on membrane permeability (e.g., 7), nuclear protein aggregation (e.g., 15), and cell survival (e.g., 25). Although the temperature dependence of these has been well described by the Arrhenius equation, the parameters in the Arrhenius equation may vary greatly 26. Furthermore, the response of biological materials to heating may involve multiple reactions and reactions that follow multiple steps 272829. Nevertheless, first-order reaction models have often described the overall process 530. | |
