Inhibition of photosynthetic oxygen evolution by calmodulin-type inhibitors and other calcium-antagonists.
Several studies have recently implicated a role for Ca2+ in photosynthetic oxygen evolution (9-11). Our previous study indicated that Ca2+ was likely acting at the level of the Cl- cofactor requirement in photosystem II (9). We now demonstrate, through the use of calmodulin-type inhibitors ( calmidazolium and trifluoperazine) and metal Ca2+-antagonists (e.g., Tb+3 and La+3), the function of Ca2+ on the oxidizing side of photosystem II. In addition, the peroxide (H2O2) electron donation site was differentiated from the electron donation site of NH2OH, Mn2+ and diphenyl carbazide in the photosystem II complex.
D002118:Calcium / Q000037:antagonists & inhibitors / Q000502:physiology*; D002147:Calmodulin / Q000494:pharmacology*; D002746:Chlorpromazine / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D008670:Metals / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism*; D010777:Photochemistry; D010788:Photosynthesis / Q000187:drug effects*; D045322:Photosynthetic Reaction Center Complex Proteins; D045332:Photosystem II Protein Complex; D010940:Plant Proteins / Q000378:metabolism; D010944:Plants / Q000378:metabolism; D014268:Trifluoperazine / Q000494:pharmacology
D002147:Calmodulin; D007093:Imidazoles; D008670:Metals; D045322:Photosynthetic Reaction Center Complex Proteins; D045332:Photosystem II Protein Complex; D010940:Plant Proteins; D014268:Trifluoperazine; C031938:calmidazolium; D010100:Oxygen; D002118:Calcium; D002746:Chlorpromazine