Allakhverdiev S I, Klimov V V, Carpentier R
Centre de recherche en photobiophysique, Université de Quèbec à Trois-Rivières, Canada.
Biochemistry. 1997 Apr 8;36(14):4149-54. doi: 10.1021/bi962170n.
Organisms that perform oxygenic photosynthesis are subjected to inhibition of their photosynthetic functions when they are exposed to excessive illumination. Photoinhibition occurs mainly at the level of photosystem II, where a cyclic electron transport has often been proposed to be involved in photoprotection. However, a demonstration of direct protection by cyclic photosystem II against photoinhibitory damage has been lacking. In this report, we used the newly characterized compound 4-[methoxybis(trifluoromethyl)methyl]-2,6-dinitrophenylhydrazine methyl ketone (K-15), known to stimulate cyclic electron transport between the acceptor and donor sides of the photosystem [Klimov, V. V., Zharmukhamedov, S. K., Allakhverdiev, S. I., Kolobanova, L. P., & Baskakov, Y. A. (1993) Biol. Membr. 6, 715-732], to verify if photosystem II is significantly protected by cyclic electron transport against aerobic and anaerobic photoinhibitory damage. The photoinhibitory quenching of the maximal level of fluorescence and the decrease of the absorbance change at 685 nm related to pheophytin photoreduction observed during photoinhibitory illumination of untreated or Mn-depleted photosystem II submembrane fractions are significantly attenuated in the presence of K-15. The photodegradation of cytochrome b559 and the photobleaching of beta-carotene and chlorophyll-670 measured in Mn-depleted photosystem II preparations are also strongly retarded when K-15 is present. The detection, by photoacoustic spectroscopy, of the energy stored during the cyclic electron transport is also reported in Mn-depleted photosystem II submembrane fractions and in photosystem II reaction center complexes. This reaction is also gradually photoinhibited due to the progressive photodegradation of the required electron transport intermediates but is significantly more stable in the presence of K-15. It is deduced that cyclic electron transport around photosystem II constitutes an effective protective mechanism against photoinhibitory damage.
进行氧光合作用的生物体在暴露于过度光照时，其光合功能会受到抑制。光抑制主要发生在光系统II水平，人们常认为循环电子传递参与了光保护过程。然而，一直缺乏光系统II循环电子传递对光抑制损伤的直接保护作用的证明。在本报告中，我们使用了新鉴定的化合物4-[甲氧基双（三氟甲基）甲基]-2,6-二硝基苯肼甲基酮（K-15），已知该化合物可刺激光系统受体侧和供体侧之间的循环电子传递[克利莫夫，V.V.，扎尔穆哈梅多夫，S.K.，阿拉赫韦尔季耶夫，S.I.，科洛巴诺娃，L.P.，&巴斯卡科夫，Y.A.（1993年）《生物膜》6，715 - 732]，以验证光系统II是否通过循环电子传递免受需氧和厌氧光抑制损伤的显著保护。在未处理或锰耗尽的光系统II亚膜组分的光抑制光照期间观察到的最大荧光水平的光抑制猝灭以及与脱镁叶绿素光还原相关的685 nm处吸光度变化的降低，在K-15存在时显著减弱。在锰耗尽的光系统II制剂中测量的细胞色素b559的光降解以及β-胡萝卜素和叶绿素-670的光漂白，在K-15存在时也受到强烈抑制。在锰耗尽的光系统II亚膜组分和光系统II反应中心复合物中，还通过光声光谱法检测到了循环电子传递过程中储存的能量。由于所需电子传递中间体的逐渐光降解，该反应也逐渐受到光抑制，但在K-15存在时显著更稳定。由此推断，光系统II周围的循环电子传递构成了一种有效的光抑制损伤保护机制。
