1224 THE TEMPERATURE FACTOR CHAP. 31 



fig. 31.5). Kennedy argued that if this heat injury were caused by the 

 inactivation of an enzyme, as suggested by Blackman, its influence could 

 be balanced, in flashing light experiments (c/. chapter 34) by longer dark 

 intervals between flashes (as is actually possible in the case of cyanide 

 poisoning; cf. chapter 12, page 307). However, he found that the reduc- 

 tion in oxygen yield per flash, caused by 15 minutes preheating to 45°, was 

 the same, whether the dark intervals lasted 0.0175 or 0.37 second. (The 

 cyanide effect would disappear in the latter case; cf. fig. 34.12.) 



Progressive heat injury is not a specific property of the photosynthetic ap- 

 paratus, but is common to all biochemical functions, as well as to many en- 

 zymatic reactions in vitro. However, photosynthesis is more sensitive to 

 heat than most other life processes. Respiration of yeast, for example, 

 shows the first signs of inhibition at 46° C. and is rapidly destroyed only 

 by temperatures in excess of 50° {cf. van Amstel and van Iterson 1911). 

 A comparison between the temperature curves of photosynthesis and 

 respiration of the lichen Rantalina farinacea was given in figure 31.2; 

 figure 31.6 gives a similar comparison for four unicellular algae. 



Sooner or later, all vital functions of the cell become totally inhibited 

 by heat. What ensues is known as "heat coma." In its first stages, it is 

 still reversible, but finally it leads to "thermal death." With most leaves 

 and algae, this happens at 55-60° C, although for organisms adapted to 

 extreme cold (or heat) the lethal temperatures may be considerably lower (or 

 higher) . 



The comparatively early onset of the thermal injury of photosynthesis 

 seems to indicate that its origin lies in an impairment of the photosjmthetic 

 apparatus itself, rather than in the general decline in the "vitality" of the 

 protoplasm. The fact that, with short exposures, the ascending tempera- 

 ture curve can be followed for some distance above the optimum indicates 

 that the thermal inhibition is caused by a destructive process (e. g., slow 

 deactivation of an enzyme), and is not associated with an intrinsic property 

 of the kinetic mechanism of photosynthesis (such as thermal dissociation 

 of the ACO2 complex, as was suggested by Willstatter and StoU). 



Attempts have been made to calculate the activation energy Ea of the 

 process responsible for heat injury, by measuring its rate at difterent tem- 

 peratures {cf. Belehradek 1935, page 174). Values between 51 and 95 kcal 

 have been calculated for the heat inhibition of photosynthesis between 20 

 and 65° C, with the smaller values derived from measurements at the 

 lower temperatures. Several hypotheses have been suggested as to the 

 nature of the process to which this remarkably high activation energy may 

 correspond. Denaturation and coagulation of proteins was the first explana- 

 tion; and it finds much credence despite the fact that the "heat inhibition" 

 of photosynthesis occurs at temperatures considerably below those usually 



