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Achim Trebst, Herbert Eck and Sieglinde Wagner 



This might best be explained by a competition of o-hydroquinone and ascorbate 

 for the same site of oxidation. Since no autoxidizable hydroquinone is formed 

 (as it is from anthraquinone) the system is blocked. 



6. Th e action of salicylaldoxime on photosynthetic reactions 



Salicylaldoxime is a copper chelating agent, which inhibits copper con- 

 taining enzymes, like phenoloxydase^'^^) and cytochromeoxydasev'*'*). It also 

 inhibits photosynthesis in intact Chlorella^'*^' . Table 9 shows the influence of 

 salicylaldoxime on various photosynthetic activities in broken chloroplasts . All 

 reactions involving oxygen evolution (ferricyanide and TPN reduction) as well 

 as cyclic photophosphorylation (vitamin Kj as cofactor) are inhibited by lo" m 

 salicylaldoxime. The only photosynthetic reaction possible in the presence of 

 salicylaldoxime is the reduction of TPN at the expense of DCPIP/ascorbate. 



For comparison the behavior of DCMU, as worked out by Vernon and 

 others^^^''^^''*^) is included in table 9. The difference between DCMU and sali- 

 cylaldoxime is, that DCMU does not inhibit cyclic photophosphorylation, whereas 

 salicylaldoxime does. In the DCMU experiments, the addition of DCPIP/ascor- 

 bate restores TPNH and ATP formation, whereas in the salicylaldoxime exper- 

 iments coupled ATP formation does not reappear, when TPN is reduced by 

 DCPIP/ascorbate. 



According to Vernon and Witt^ reduced DCPIP reacts with cyto- 



chrome f . Since salicylaldoxime does not influence photosynthetic TPN reduc- 

 tion at the expense of DCPIP/ascorbate, the site of inhibition of salicylaldoxime 

 must be before cytochrome f. But since salicylaldoxime inhibits cyclic photo- 

 phosphorylation, its site of inhibition would be after plastoquinone and the sec- 

 ond light reaction (see scheme). The phosphorylation site (either in cyclic or 

 non-cyclic photophosphorylation) cannot be between cytochrome f and TPN, 

 since the reaction sequence: ascorbate - DCPIP - cytochrome f - light - TPN 

 is not coupled in the presence of salicylaldoxime. Witt already argued for rea- 

 sons of redoxpotential that the phosphorylation site has to be between plastoqui- 

 none and cytochrome f^^^). In the DCMU experiments, where the reduction of 

 TPN by DCPIP/ascorbate is coupled to ATP formation^^") , one has to assume, 

 that DCPIP does not react with cytochrome f but with a compound, located in 

 the electron transport chain before the phosphorylation site, possibly plastoqui- 

 none or even with a compound (Y) before the second light reaction, as suggested 

 by Witt(42). 



The inhibition of photosynthetic reactions in chloroplasts by salicylald- 

 oxime seems interesting; for if it is accepted that salicylaldoxime as copper 

 chelating agent inhibits a copper enzyme in these experiments with chloroplasts, 

 then the site of salicylaldoxime inhibition would indicate the location of this 

 copper enzyme in the electron transport chain of photosynthesis. 



Such a copper enzyme has already been isolated from chloroplasts. 

 Katoh named it plastocyanine and drew attention to its possible significance in 



