Electron donation to photosystem II by diphenylcarbazide is inhibited both by the endogenous manganese complex and by exogenous manganese ions.

Abstract

Diphenylcarbazide (DPC) is an efficient electron donor to the inactive oxygen-evolving complex of photosystem II (PSII). We investigated the role of manganese on the rate of electron donation from DPC to PSII in both Mn-depleted (Tris washed) and Mn-retaining (NaCl washed) PSII preparations. The rate of electron donation from DPC to PSII was significantly higher in Mn-depleted than in Mn-retaining preparations, indicating a negative role of native Mn complex on DPC electron donation. The apparent Km values for DPC were found to be 0.11 and 0.17 mM for Mn-depleted and Mn-retaining PSII preparations, respectively. This difference in the Km values also indicates an antagonistic effect of endogenous Mn cluster on electron donation from DPC, which was markedly inhibited by exogenous Mn2+. However, the magnitude of inhibition was greater in Mn-depleted than in Mn-retaining PSII preparations. This indicates a higher accessibility to DPC to PSII in the absence of native Mn complex. Our results suggest (i) that Mn, either endogenous or added, acts as an accessibility barrier for DPC to donate electrons to PSII and (ii) that the native Mn complex not only functions as an accumulator of oxidizing equivalents but may also protect PSII from exogenous reductants.