Abstract The analysis of electron and proton transport in chloroplasts of higher plants has been carried out on the basis of a mathematical model that takes into account the pH-dependent regulation of electron transport and the operation of the ATP synthase. Numerical experiments aimed at simulation of these processes under pseudocyclic electron transport (water–water cycle) have shown good agreement with experimental data on the kinetics of electron transfer to photosystem 1 (PS1) in class B chloroplasts in metabolic states corresponding to high (state 3) and low (state 4) ATP synthase activity. The simulation of electron transport processes that took into account the Calvin–Benson cycle (CBC), cyclic electron transport around PS1, pH-dependent heat dissipation of energy in photosystem 2 (PS2), and nonphotochemical quenching (NPQ) made it possible to estimate the contribution of these factors to the kinetics of induction phenomena in chloroplasts in situ. It has been shown that the multiphase kinetics of the photooxidation of P 700 (a primary electron donor in PS1) reflects the redistribution of electron flows between cyclic and non-cyclic electron transfer pathways, caused by the activation of CBC due to the alkalization of the stroma, as well as the change of the limiting stage in the electron transport chain, induced by a decrease in the intrathylakoid pH (pH in ). The electron flux between PS2 and PS1 decelerates with pH in decrease, which may be caused by the reduced rate of plastoquinol oxidation and attenuated activity of PS2 due to NPQ.

中文翻译：

---

叶绿体原位和硅中电子和质子传输的 pH 依赖性调节

摘要 高等植物叶绿体中电子和质子传递的分析是基于一个数学模型进行的，该模型考虑了电子传递的 pH 依赖性调节和 ATP 合酶的运行。旨在模拟伪循环电子传输（水 - 水循环）下这些过程的数值实验表明，与 B 类叶绿体中电子转移到光系统 1 (PS1) 的动力学实验数据非常吻合，代谢状态对应于高代谢状态（状态 3 ) 和低 (状态 4) ATP 合酶活性。电子传输过程的模拟考虑了卡尔文-本森循环 (CBC)、PS1 周围的循环电子传输、光系统 2 (PS2) 中依赖于 pH 值的能量散热，和非光化学猝灭 (NPQ) 使得可以估计这些因素对原位叶绿体诱导现象动力学的贡献。已经表明，P 700（PS1 中的主要电子供体）光氧化的多相动力学反映了循环和非循环电子转移途径之间电子流的重新分配，这是由于 CBC 的碱化引起的活化。基质，以及电子传递链中限制阶段的变化，由类囊体内 pH 值（pH in ）的降低引起。PS2 和 PS1 之间的电子通量随着 pH 值的降低而减速，这可能是由于 NPQ 导致 plastoquinol 氧化速率降低和 PS2 活性减弱所致。