Application of target theory to the photoinactivation of Photosystem II in pea leaf discs (Park et al. 1995, 1996a,b) reveals that there is a critical light dosage below which there is complete photoprotection and above which there is photoinactivation (i.e a light-induced loss of oxygen flash yield). The critical dosage is about 3 mol photons m−2 for medium and high light-grown leaves and 0.36 mol photons m−2 for low light-grown leaves. Photoinactivation is a one-hit process with an effective cross-section of 0.045 m2 mol−1 photons which does not vary with growth irradiance, unlike the cross-section for oxygen evolution which increases with decreasing growth irradiance. The cross-section for oxygen evolution increased by about 20% following exposure to 6.8 mol photons m−2 which may be due to energy transfer from photoinactivated units to functional Photosystem II units. We propose that the photoinactivation of PS II begins when a small group of PS II pigment molecules whose structure is uninfluenced by growth irradiance, becomes uncoupled energetically from the rest of the photosynthetic unit and thus no longer transfers excitions to P680. De-excitation of this group of pigment molecules provides the energy which leads to the damage of Photosystem II. Treatment of pea leaves with dithiothreitol, an inhibitor of the xanthophyll cycle, decreases the critical dosage i.e. decreases photoprotection but has no effect on the PS II photoinactivation cross-section. Treatment with 1 μM nigericin increased the photoinactivation cross-section of PS II as did exposure to lincomycin which inhibits D1 protein synthesis and thus the repair of PS II reaction centres.
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