Heat death in poikilotherms: Is there a common cause?

Abstract

The primary aim of this contribution is to make the case for membrane impairment as the outcome of the exposure of poikilotherms to damaging high temperatures that result in organism heat death. The paper emphasises that heat death points are not fixed but are altered by acclimation, acclimatization, heat shock and hardening. The definition of these terms is revisited as there is confusion in their usage in the literature. That poikilotherm heat death points depend on acclimation temperature is one of the most demonstrated outcomes. However, fewer studies have been made into the underlying cause(s) of heat death. Most studies have clearly shown that membrane function is impaired early in heat treatment, leading to knock-on effects at the physiological level. As heat death points are subject to acclimation status, then what is changed by acclimation must be directly related to what fails in heat death. Many comparative studies have shown that acclimation in a variety of species changes the phospholipid (PL) profile of membranes, such that cold acclimation results in an increase in the fluidity of membrane lipids. This increase in membrane fluidity would also lower the heat death point as membrane damage would occur at a lower temperature. This is consistent with the premise that membrane structure/function is changed by acclimation and that this is the site of the primary lesion in heat death. Breakdown in cellular homeostasis will have consequences at the physiological level that will depend on the life style of the organism. I therefore propose that heat death is a cellular membrane event common to poikilotherms.