iQig] ROSE— BLISTER CANKER II7 



brings oxidation to an end. It seems more reasonable to suppose, 

 however, that the time factor is of importance here; that is, that 

 an acidity of Ph = 4.29 is more effective when reached gradually 

 than when established as a starting point. Looking at the situa- 

 tion from another angle, we may say that inhibition is total if the 

 initial hydrogen ion concentration is high enough, but will be only 

 partial if the concentration is lower; but since partial inhibition 

 means some oxidation, which in itself increases acidity, the process 

 in time necessarily comes to an end. The hydrogen ion concen- 

 tration at that point will depend on what it was in the beginning, 

 but will never be equal to that which causes total inhibition. 



That this theory fits the facts is shown by table VII. Oxidation 

 took place in all the mixtures, the amount depending on the initial 

 hydrogen ion concentration, except where diseased bark was used 

 with buffer no. 4. Acidity increased in all the mixtures but one, 

 diseased bark with buffer no. 6 (see tables VI and VII). The 

 increase in acidity is shown graphically in fig. 2. It is unexpectedly 

 small for diseased bark except where the 3 most alkaline buffers 

 were used, a condition which suggests the need of further experi- 

 ments. 



In figs. 3 and 4 are shown graphically the oxidation data given in 

 table VII, representing the final amounts of oxidation for each set 

 of tests (healthy and diseased bark with the different buffer solu- 

 tions) . In addition there are shown graphs for several earlier stages 

 in each experiment. These graphs show that below i X io~^ (Ph = 4) 

 for healthy bark, and 2.5X10"^' (Pa = 4. 39) for diseased bark, 

 oxidation drops rapidly as acidity increases. Above these points 

 the changes are not so marked. The hydrogen ion concentration 

 for total inhibition, estimated by extrapolation to the base line, 

 lies between 3.55 and 3.80X10"-* for healthy and between 3.55 

 and 4. 27X10"^ for diseased bark. All these figures closely approxi- 

 mate those found by Bunzell (12) for potato oxidase, 2 . i- 

 2.8Xio~'*, and by Reed (28) for apple oxidase, 5.0-7.0X10"^ 



The results given in table VII show that hydrogen ion con- 

 centration is not the only factor effective in controlling oxidation 

 in the apparatus, and consequently that the lower hydrogen ion 

 concentration of diseased bark cannot account entirely for its 



