O xygenic photosynthetic organisms grow under an everchanging sunlight environment. Fluctuations of solar energy input can be accommodated by a tradeoff between energy utilization in photosynthetic carbon assimilation and energy dissipation by various photoprotective mechanisms that modulate absorption and dissipation of excess light energy (1-3). Despite the complex suite of strategies for photoprotection, however, photooxidative damage inevitably occurs to photosystem (PS) II, in which P680 ϩ (a special Chl in the PSII reaction center), the strongest biological oxidant, is generated to split water to molecular oxygen, protons, and electrons (4). The consequent loss of PSII photochemical efficiency measured under low light, termed photoinhibition or photoinactivation (5), depends inter alia on the number of absorbed photons during the light exposure (6-8). That is, PSII photoinactivation can occur with a light-dosage-dependent probability under any light environment in nature, ranging from limiting to saturating irradiances. Over a sunny day, the entire population of PSII in a leaf may undergo photoinactivation.Yet, effects of photoinactivation on PSII efficiency are not always obvious; they are noticeable only when the rate of inactivation exceeds the capacity for rapid and efficient repair of nonfunctional PSII reaction centers by de novo synthesis of D1 protein (psbA gene product in PSII reaction center) (9). The operation of the PSII repair cycle involves coordinated regulation of degradation and synthesis of D1 protein (10). When the supply of newly synthesized D1 protein is insufficient, such as under high light and͞or low temperature, the degradation process also slows down (11,12), resulting in the accumulation of nonfunctional PSII reaction centers in stacked grana domains of the thylakoid membranes of higher plants (13). These nonfunctional PSII centers, capable of light absorption but not of photosynthetic electron transfer, reduce the PSII quantum efficiency of leaves or leaf segments.An important implication of PSII photoinactivation is that nonfunctional PSII centers, still embracing pigment molecules, can exacerbate photooxidative damage to the thylakoid membranes unless light energy absorbed by the pigments is dissipated safely. Thus, it has been hypothesized that photoinactivated PSII complexes are able to efficiently dissipate excitation energy harmlessly (14), and further, may contribute to photoprotection of their functional neighbors by acting as sinks for excitation energy (13,15).Experimental results consistent with this hypothesis have emerged from recent studies using leaves of Capsicum annuum L (16, 17). In leaves of C. annuum in the presence of lincomycin (an inhibitor of chloroplast-encoded protein synthesis), the functional fraction of PSII ( f ), determined from the oxygen yield per single-turnover flash or from chlorophyll (Chl) a fluorescence, decreased monoexponentially from 1.0 (ϭ the original level) to Ϸ0.3 under illumination (16). However, the decrease in f thereafter proceed...