Cold shock injury in animal cells.

Cold shock injury (damage to cell structure and function arising from a sudden reduction in temperature) was for many years considered a phenomenon peculiar to certain cell-types. Only in recent years has it become apparent that widely different cell-types manifest cold shock injury. Thus, cold shock appears to be a more general phenomenon, differences between cell-types being quantitative (in the rate of cooling and temperature range at which injury is sustained) rather than qualitative. Loss of particular cell functions depends on cell-type, but reflects the underlying structural and biochemical damage which has been inflicted by rapid cooling. In particular, membranes lose their selective permeability with the result that many cellular components are released including lipids, proteins and ions. Additionally, sodium and calcium gain access to the interior of the cell. Consequent upon this initial disruption, metabolic activities are diminished and further secondary changes ensue. The possible mechanisms of cold shock injury include membrane thermo-tropism and protein denaturation. Susceptibility to cold shock is influenced by membrane composition, and much experimental evidence points to particular involvement of membrane lipids. One hypothesis implicates lipid phase changes in a cooling rate dependent loss of membrane integrity. Other recent hypotheses invoke biophysical concepts and cytoarchitectural features as considerations in a better understanding of cold shock.