Novakova A A, Davletshina L N, Khval'kovskaya E A, Semin B K, Belevich N P, Ivanov I I, Rubin A B
Department of Biology, Moscow State University, Russia.
FEBS Lett. 1999 Apr 30;450(1-2):135-8. doi: 10.1016/s0014-5793(99)00485-8.
A model description of the Mössbauer spectrum (80 K) of native membranes of the thermophilic cyanobacterium Synechococcus elongatus is suggested on the basis of the known values of quadrupole splitting (deltaE(Q)) and isomer shift (deltaFe) for the iron-containing components of the photosynthetic apparatus. Using this approach, we found that heating the membranes at 70-80 K results in a decrease of doublet amplitudes belonging to F(X), F(A), F(B) and ferredoxin and simultaneous formation of a new doublet with deltaE(Q) = 3.10 mm/s and delta-Fe = 1.28 mm/s, typical of inorganic hydrated forms of Fe2+. The inhibition of electron transfer via photosystem I to oxygen, catalyzed by ferredoxin, occurs within the same range of temperatures. The data demonstrate that the processes of thermoinduced Fe2+ formation and distortions in the photosystem I electron transport in the membranes are interrelated and caused mainly by the degradation of ferredoxin. The possible role of Fe2+ formation in the damage of the photosynthetic apparatus resulting from heating and the action of other extreme factors is discussed.
基于光合装置含铁成分已知的四极分裂(δE(Q))和同质异能位移(δFe)值,提出了嗜热蓝藻细长聚球藻天然膜的穆斯堡尔谱(80K)的模型描述。采用这种方法,我们发现将膜在70 - 80K加热会导致属于F(X)、F(A)、F(B)和铁氧化还原蛋白的双峰振幅降低,并同时形成一个新的双峰,其δE(Q) = 3.10 mm/s,δ-Fe = 1.28 mm/s,这是典型的Fe2+无机水合形式。由铁氧化还原蛋白催化的通过光系统I向氧气的电子转移抑制作用在相同温度范围内发生。数据表明,膜中热诱导Fe2+形成过程与光系统I电子传递中的畸变相互关联,且主要由铁氧化还原蛋白的降解引起。讨论了Fe2+形成在加热及其他极端因素作用导致光合装置损伤中可能的作用。