hihibition and Retardation of the Oxidation of lAA 163 



system and oxygen was consumed at a slow rate by the system 

 described here. When these systems were illuminated, the production 

 of manganic ions was increased (2) as was also oxygen uptake in 

 our system. 



With respect to the mechanism by which light activates the re- 

 action sequence, tests were made on the effect of light on the oxygen 

 uptake of riboflavin-resorcinol systems (reaction A), and on the spon- 

 taneous oxidation of reduced riboflavin in air (reaction B). In the 

 absence of manganese and enzyme, very little reaction was found 

 to occur between riboflavin and resorcinol in light or darkness, and 

 hence an activation by light of reaction A as proposed by Andreae 

 (2) appears unlikely. On the other hand, white light (980 foot 

 candles) almost doubled the rate of oxygen consumed by solutions 

 of riboflavinphosphate that had been reduced by dithionite. There- 

 fore, we suggest that light activated Andreae's system and the system 

 described herein at the stage of reaction B. 



Oxygen uptake in this system appeared to continue indefinitely 

 and in all probability could exceed the combined theoretical molar 

 equivalence of riboflavin and cofactor. This is possibly due to the 

 cyclical nature of the reaction in which the over-all reaction is an 

 oxidation of Mn+" to Mn+4, but the intermediate valence stage Mn+^ 

 may compete with oxygen for reduced riboflavin as follows: 



Rb-2H + 2Mn-3 _^ Rb ^ 2Mn-2 ^ 9h- 



When the system is ilkmiinated, reduced riboflavin reacts prefer- 

 entially with oxygen owing to light activation at this stage (reaction 

 B). This would explain the increased production of manganipyro- 

 phosphate as found by Andreae (2) and the increased oxygen uptake 

 of our system under illumination. 



The significant points emerging from the experiments of Andreae 

 (2) and those reported here are that riboflavin can indirectly generate 

 manganic ions in this system and that reduced riboflavin may pos- 

 sibly react with Mn+3. This would provide an explanation not only 

 for the retardation of the indole-3-acetic acid system by riboflavin, 

 but also for the alleviation of this retardation by light. Evidently 

 the reduced form of the retarder which is a necessary product of 

 manganigenesis must be the immediate cause of retardation by be- 

 ing involved in a second redox system with an essential oxidized 

 intermediate. The degree of retardation would depend on the 

 equilibrium established between the oxidized and reduced forms of 

 riboflavin, the latter diverting an oxidized intermediate from its 

 normal function as a chain reactant in indole-3-acetic acid autoxida- 

 tion. 



The intermediate with which reduced riboflavin reacts is most 



