Sicora Cosmin, Máté Zoltán, Vass Imre
Institute of Plant Biology, Biological Research Center, 6726, Szeged, Temesvári krt. 62, Hungary,
Photosynth Res. 2003;75(2):127-37. doi: 10.1023/A:1022852631339.
In order to understand the mechanism of photodamage induced by solar radiation under natural conditions, we studied the interaction of visible and ultraviolet-B light in the inactivation and repair of the Photosystem II complex by using oxygen evolution and flash-induced chlorophyll fluorescence measurements. In isolated spinach thylakoids and Synechocystis 6803 cells, in which de novo protein synthesis is blocked by lincomycin, photodamage of Photosystem II by visible and UV-B light is characterized by linear semilogarithmic inactivation curves for both separate and combined illumination protocols. The extent of PS II inactivation obtained after combined illumination can be well simulated by assuming independent damaging events induced by visible and UV-B photons. In intact Synechocystis cells capable of protein repair, simultaneous illumination by visible and UV-B light impairs Photosystem II activity to a smaller extent than expected from the independent damaging events. This protective effect is pronounced at low visible light (130 muE m(-2) s(-1)), but becomes negligible at high intensities (1300 muE m(-2) s(-1)). Exposure of intact Synechocystis 6803 cells to direct sunlight leads to a rapid inactivation of PS II, accompanied by the accumulation of donor side inhibited centers. This phenomenon, which shows the impairment of the manganese cluster of water oxidation was not observed when the ultraviolet components of sunlight were filtered out. We conclude that visible and UV-B photons inactivate PS II via non-interacting mechanisms, which affect different target sites. In intact cells, the two spectral regions do interact, and results in synergistically enhanced protein repair capacity when UV-B radiation is accompanied by low intensity visible light, which provides protection against photodamage. However, this ameliorating effect becomes insignificant at high light intensities characteristic of direct sunlight.
为了了解自然条件下太阳辐射引起光损伤的机制，我们通过氧释放和闪光诱导叶绿素荧光测量，研究了可见光和紫外线B光在光系统II复合物失活和修复过程中的相互作用。在分离的菠菜类囊体和集胞藻6803细胞中，林可霉素可阻断其蛋白质的从头合成，可见光和紫外线B光对光系统II的光损伤在单独和联合光照方案下均表现为线性半对数失活曲线。通过假设可见光和紫外线B光子诱导的独立损伤事件，可以很好地模拟联合光照后PS II失活的程度。在能够进行蛋白质修复的完整集胞藻细胞中，可见光和紫外线B光同时照射对光系统II活性的损害程度小于独立损伤事件预期的程度。这种保护作用在低强度可见光（130 μE m(-2) s(-1)）下很明显，但在高强度（1300 μE m(-2) s(-1)）下可忽略不计。完整的集胞藻6803细胞暴露在直射阳光下会导致PS II迅速失活，并伴有供体侧抑制中心的积累。当滤除太阳光中的紫外线成分时，未观察到这种表明水氧化锰簇受损的现象。我们得出结论，可见光和紫外线B光子通过非相互作用机制使PS II失活，这些机制影响不同的靶位点。在完整细胞中，这两个光谱区域确实相互作用，当紫外线B辐射伴有低强度可见光时，会协同增强蛋白质修复能力，从而提供抗光损伤保护。然而，在直射阳光的高光强度下，这种改善作用变得微不足道。
