1384 INDUCTION PHENOMENA CHAP. 33 



terial can also be followed by illuminating the leaf with a flash of strong 

 light and observing the fluorescence in light that is too weak to affect the 

 induction phenomena. In this way, the mean life-time of the inhibitor was 

 found to l)e 2 seconds at room temperature, and 5 seconds at 0° C System- 

 atic polarographic experiments, of the type described in section A2, could 

 perhaps show whether the increase in the photosynthetic gas exchange, 

 after its inhibition by 1 or 2 seconds of illumination, occurs exactly parallel 

 with the decline of fluorescence. 



It may be asked why in light the removal of the inhibition requires at 

 least 1, and often 2 or 3, minutes, while the "survival" experiments in the 

 dark indicate that the inhibitor has a life-time of only a few seconds. 

 Partly, the prolongation of the induction period in light may be caused by 

 the superposition of the "second wave" ; but this cannot be the chief cause, 

 especially in curves of the type in figures 33.19. Probably, the quantity of 

 the "precursor" produced during the dark incul)ation is larger than needed 

 to bring about the first fluorescence wave; consequently, the photochemi- 

 cal activation of the inhibitor continues, at a decreasing rate, even after 

 the peak of fluorescence has been passed, thus slowing down the decay. 

 In the dark, where no activation occurs, the photosynthetic apparatus can 

 be freed from active inhibitor in a few seconds. 



If the formation of the "precursor" means the depletion of a catalyst 

 that, when active, prevents "self-inhil)ition" of photosynthesis by remov- 

 ing the photochemical products, a similar explanation applies. In the first 

 moment of illumination, because of the absence of the protective catalyst, 

 the rate of photochemical production of the inhibitor is much higher than 

 the rate of its metabolic destruction; therefore the rate of photosynthesis 

 declines, and the yield of fluorescence grows. Within a second, however, 

 the reactivation of the catalyst has reduced the rate of formation of the 

 inhibitor, while the rate of removal of the latter has grown proportionately 

 to concentration, causing a reversal of the trend. The rate at which the 

 fluorescence declines is determined by the superposition of the decay of the 

 inhibitor, and its continuous photochemical formation. The steady state 

 thei'efore is approached much more slowly than if the decay were the only 

 relevant process. 



The ascending slope of the first wave AB must depend on the initial 

 amount of the "precursor" (or the initial deficiency of the protective cata- 

 lyst) and on the intensity of illumination. The removal of the inhibitor, 

 on the other hand, is a thermal process (probably related to the intensity 

 of the autoxidative metabolism of the cells), and as such is strongly en- 

 hanced by a rise in temperature. Consequently, for given internal condi- 

 tions, the height of peak B must increase with light intensity, and decline 

 with increasing temperature; while its timing must be delayed by intense 



