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[嗜盐菌细胞中光诱导的呼吸抑制与刺激:动力学、作用光谱、与ΔpH光诱导的关系]

[Photoinduced inhibition and stimulation of respiration in cells of Halobacterium halobiums kinetics, action spectra, relationship to photoinduction of deltapH].

作者信息

Litvin F F, Boĭchenko V A, Balashov S P, Dubrovakiĭ V T

出版信息

Biofizika. 1977 Nov-Dec;22(6):1062-71.

PMID:22357
Abstract

Along with the inhibition illumination also causes the stimulation of the respiration of H. halobium R1 cells. When light is switched off photoinhibition of respiration (PIR) decays much faster (tau 1/2=12 sec) than photostimulation (PSR) (tau 1/2=60 sec). This allows the evaluation of the contribution of the each phase into the total change of the respiration rate. PIR prevails in neutral and alkaline media (at pH 6.8 the amplitude ratio of PSR/PIR=0.3). At the same conditions light induced alkalization of the medium is observed, which at high light intensities is followed by acidification. The half rise time of PIR is 0.5 divided by 0.8 sec under excitation with short light flashes at 18C and pH 6.8. When pH of the medium is reduced the rate of dark respiration decreases, PSR amplitude increases, PIR is almost not changed and light-induced alkalinization of the medium decreases. At pH 5.5 PSR prevails: at light of 10(5) erg/(cm(2).s) the ratio PSR/PIR=2. The maximum value of PIR and PSR at 18C reaches 20-30 percent of the dark respiration level. Uncouplers (CCCP, DNF) and inhibitor (DCCD) of phosphorylation suppress PIR and light induced alkalinization of the medium and significantly (5-7 times at Ph 6.8) increase PSR and light induced acidification. The action spectra show that bacteriorhodopsin is responsible for all the observed light induced changes of O2 and H+ exchange; carotinoids do not participate in sensibilization. It is suggested that photophosphorylation is necessary for PIR and that PSR is caused by the rise of internal pH due to light induced efflux of protons mediated by bacteriorhodopsin.

摘要

光照除了会引起抑制作用外,还会刺激嗜盐菌R1细胞的呼吸。当光照关闭时,呼吸的光抑制(PIR)衰减速度(半衰期τ1/2 = 12秒)比光刺激(PSR)(半衰期τ1/2 = 60秒)快得多。这使得能够评估每个阶段对呼吸速率总变化的贡献。在中性和碱性介质中PIR占主导(在pH 6.8时,PSR/PIR的幅度比为0.3)。在相同条件下,观察到介质的光诱导碱化,在高光强度下随后会出现酸化。在18℃和pH 6.8下用短光脉冲激发时,PIR的半上升时间为0.5除以0.8秒。当介质的pH降低时,暗呼吸速率降低,PSR幅度增加,PIR几乎不变,并且介质的光诱导碱化减少。在pH 5.5时PSR占主导:在10(5)尔格/(平方厘米·秒)的光照下,PSR/PIR的比值为2。18℃时PIR和PSR的最大值达到暗呼吸水平的20 - 30%。磷酸化的解偶联剂(CCCP、DNF)和抑制剂(DCCD)抑制PIR和介质的光诱导碱化,并显著(在pH 6.8时增加5 - 7倍)增加PSR和光诱导酸化。作用光谱表明,细菌视紫红质负责所有观察到的光诱导的O2和H+交换变化;类胡萝卜素不参与致敏作用。有人提出,光磷酸化对于PIR是必需的,而PSR是由细菌视紫红质介导的质子光诱导外流导致内部pH升高所引起的。

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