Bowler Ken
Emeritus Professor Department of Biosciences University of Durham, Durham DH13LE United Kingdom.
J Therm Biol. 2018 Aug;76:77-79. doi: 10.1016/j.jtherbio.2018.06.007. Epub 2018 Jun 18.
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.
本文的主要目的是论证膜损伤是变温动物暴露于导致机体热死亡的有害高温下的结果。本文强调热死亡点不是固定不变的，而是会因驯化、气候适应、热休克和硬化而改变。由于这些术语在文献中的使用存在混淆，因此重新审视了它们的定义。变温动物的热死亡点取决于驯化温度，这是最得到证实的结果之一。然而，对热死亡的潜在原因进行的研究较少。大多数研究清楚地表明，在热处理早期膜功能就会受损，从而在生理水平上产生连锁反应。由于热死亡点受驯化状态的影响，那么驯化所改变的因素必然与热死亡中出现故障的因素直接相关。许多比较研究表明，多种物种的驯化会改变膜的磷脂（PL）组成，因此冷驯化会导致膜脂流动性增加。膜流动性的这种增加也会降低热死亡点，因为膜损伤会在较低温度下发生。这与以下前提一致，即膜结构/功能会因驯化而改变，且这是热死亡中主要损伤的部位。细胞内稳态的破坏将在生理水平上产生后果，这取决于生物体的生活方式。因此，我认为热死亡是变温动物共有的细胞膜事件。
