Anomalous uncoupling of photophosphorylation by palmitic acid and by gramicidin D.

Anomalous uncoupling of photophosphorylation by palmitic acid and by gramicidin D.
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棕榈酸和短杆菌肽 D 引起的光磷酸化异常解偶联。

DOI:
10.1021/bi00399a041
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发表时间:
1987
期刊:
影响因子:
2.9
通讯作者:
Rottenberg,H
Rottenberg,H
中科院分区:
生物学3区
文献类型:
--
作者:
Pick,U;Weiss,M;Rottenberg,H

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魏茨曼科学研究所生物化学系,雷霍沃特 76100,以色列,以及哈内曼大学医学院病理学和实验医学系,费城,宾夕法尼亚州 19102 收稿日期:1987 年 5 月 5 日;修订稿于 1987 年 6 月 29 日收到摘要:棕榈酸和短杆菌肽 Dat 低浓度解偶联光磷酸化的机制与经典解偶联的以下特性不一致:(1) H+ 摄取或跨膜电位不受抑制。(2) 02 演化在非磷酸化条件下受到刺激,但在腺苷 S'-二磷酸+无机磷酸盐存在下略有抑制(P¡)。(3) 光触发的腺苷S'-三磷酸(ATP)-P¡交换几乎不受影响,并且ATP酶活性仅受到轻微刺激。(4) ATP诱导的形成被选择性抑制。仅当电子传输系统的天然偶联位点用于供能(例如甲基紫精偶联磷酸化)时,才会观察到这种特征性解偶联。使用产生人工偶联位点的绿脓青,需要高1000倍的短杆菌肽D和更高的棕榈酸浓度才能抑制,并且抑制作用伴随着光系统1和光系统2电子传递的减少以及膜解堆积的影响,低短杆菌肽D优先抑制光系统2,而棕榈酸更有效地抑制光系统1偶联位点。当链长减少到 16 个烃以下或在烃链中引入单个双键时,脂肪酸的抑制能力显着下降。有人认为,棕榈酸和短杆菌肽 D 会干扰特定电子传递和 ATP 合酶复合物之间的直接 H+ 转移,这提供了与批量到批量 µ+ 并行的替代偶联机制。抑制位点似乎位于叶绿体 ATP 合酶、光系统 2 和细胞色素 b¿ f 复合物中。
Department of Biochemistry, The Weizmann Institute of Science, Rehovot 76100, Israel, and Department of Pathology and Laboratory Medicine, Hahnemann University School of Mediciné, Philadelphia, Pennsylvania 19102 Received May 5, 1987; Revised Manuscript Received June 29, 1987 abstract: Palmitic acid and gramicidin Dat low concentrations uncouple photophosphorylation in a mechanism that is inconsistent with classical uncouplingin the following properties:(1), H+ uptake, or the transmembrane electric potential is not inhibited.(2) 02 evolution is stimulated under non-phosphorylating conditions but slightly inhibited in the presence of adenosine S'-diphosphate+ inorganic phosphate (P¡).(3) Light-triggered adenosine S'-triphosphate (ATP)-P¡ exchange is hardly affected, and ATPase activity is only slightly stimulated.(4) ATP-induced formation is selectively inhibited. This characteristic uncoupling is observed only when the native coupling sites of the electron transport system are used for energization such as for methylviologen-coupled phosphorylation. With pyocyanine, which creates an artificial coupling site, 1000-fold higher gramicidin D and higher palmitic acid concentrations are required for inhibition, and the inhibition is accompanied by a decrease in. Moreover, comparison between photosystem 1 and photosystem 2 electron transport and the effects of membrane unstacking suggest that low gramicidin D preferentially inhibits photosystem 2, while palmitic acid inhibits more effectively photosystem 1 coupling sites. The inhibitory capacity of fatty acids significantly drops when the chain length is reduced below 16 hydrocarbons or upon introduction of a single double bond in the hydrocarbon chain. It is suggested that palmitic acid and gramicidin D interfere with a direct H+ transfer between specific electron transport and the ATP synthase complexes, which provides an alternative coupling mechanism in parallel with bulk to bulk µ+. The sites of inhibition seem to be located in chloroplast ATP synthase, photosystem 2, andthe cytochrome b¿ f complexes.