Pörtner H O
Alfred-Wegener-Institut für Polar- und Meeresforschung, Okophysiologie, Bremerhaven, Germany.
Naturwissenschaften. 2001 Apr;88(4):137-46. doi: 10.1007/s001140100216.
Recent years have shown a rise in mean global temperatures and a shift in the geographical distribution of ectothermic animals. For a cause and effect analysis the present paper discusses those physiological processes limiting thermal tolerance. The lower heat tolerance in metazoa compared with unicellular eukaryotes and bacteria suggests that a complex systemic rather than molecular process is limiting in metazoa. Whole-animal aerobic scope appears as the first process limited at low and high temperatures, linked to the progressively insufficient capacity of circulation and ventilation. Oxygen levels in body fluids may decrease, reflecting excessive oxygen demand at high temperatures or insufficient aerobic capacity of mitochondria at low temperatures. Aerobic scope falls at temperatures beyond the thermal optimum and vanishes at low or high critical temperatures when transition to an anaerobic mitochondrial metabolism occurs. The adjustment of mitochondrial densities on top of parallel molecular or membrane adjustments appears crucial for maintaining aerobic scope and for shifting thermal tolerance. In conclusion, the capacity of oxygen delivery matches full aerobic scope only within the thermal optimum. At temperatures outside this range, only time-limited survival is supported by residual aerobic scope, then anaerobic metabolism and finally molecular protection by heat shock proteins and antioxidative defence. In a cause and effect hierarchy, the progressive increase in oxygen limitation at extreme temperatures may even enhance oxidative and denaturation stress. As a corollary, capacity limitations at a complex level of organisation, the oxygen delivery system, define thermal tolerance limits before molecular functions become disturbed.
近年来，全球平均气温上升，变温动物的地理分布也发生了变化。为了进行因果分析，本文讨论了那些限制耐热性的生理过程。后生动物与单细胞真核生物和细菌相比耐热性较低，这表明在后生动物中起限制作用的是一个复杂的系统过程而非分子过程。全动物有氧代谢范围似乎是在低温和高温下首先受到限制的过程，这与循环和通气能力逐渐不足有关。体液中的氧气水平可能会下降，这反映了高温下氧气需求过高或低温下线粒体有氧能力不足。当温度超过最适温度时，有氧代谢范围会下降，而当转变为无氧线粒体代谢时，在低温或高温临界温度下有氧代谢范围会消失。在平行的分子或膜调节之上调整线粒体密度，对于维持有氧代谢范围和改变耐热性似乎至关重要。总之，氧气输送能力仅在最适温度范围内与完全的有氧代谢范围相匹配。在这个范围之外的温度下，剩余的有氧代谢范围只能支持有限时间的存活，然后是无氧代谢，最后是热休克蛋白和抗氧化防御的分子保护。在因果层次结构中，极端温度下氧气限制的逐渐增加甚至可能加剧氧化和变性应激。作为一个推论，在组织的复杂层面，即氧气输送系统的能力限制，在分子功能受到干扰之前就定义了耐热性极限。
