INTERACTIONS OF HERBICIDES WITH PHOTOSYNTHETIC ELECTRON-TRANSPORT
INTERACTIONS OF HERBICIDES WITH PHOTOSYNTHETIC ELECTRON-TRANSPORT
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DOI：
10.1017/s0043174500073227
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发表时间：
1991-07-01
期刊：
影响因子：
2.5
通讯作者：
NORMAN, MA
中科院分区：
文献类型：
--
作者：
FUERST, EP;NORMAN, MA
除草剂在光合电子传递中的两个主要作用位点是抑制光系统II（PS II）电子传递和转移通过光系统I（PS I）的电子流。 PS II电子传递抑制剂与PS II反应中心的D1蛋白结合，从而阻止电子传递到质体醌。 PS Ⅱ电子传递的抑制阻止了吸收的光能转化为电化学能，并导致三重态叶绿素和单线态氧的产生，从而诱导膜脂过氧化。 PS I电子受体可能从铁硫蛋白F（a）/F（B）接受电子。 除草剂的自由基形式导致羟基自由基的产生，从而导致脂质过氧化。 除草剂诱导的脂质过氧化破坏膜的完整性，导致细胞解体和植物毒性。
The two primary sites of herbicide action in photosynthetic electron transport are the inhibition of photosystem II (PS II) electron transport and diversion of electron flow through photosystem I (PS I). PS II electron transport inhibitors bind to the D1 protein of the PS II reaction center, thus blocking electron transfer to plastoquinone. Inhibition of PS II electron transport prevents the conversion of absorbed light energy into electrochemical energy and results in the production of triplet chlorophyll and singlet oxygen which induce the peroxidation of membrane lipids. PS I electron acceptors probably accept electrons from the iron-sulfur protein, F(a)/F(b). The free radical form of the herbicide leads to the production of hydroxyl radicals which cause the peroxidation of lipids. Herbicide-induced lipid peroxidation destroys membrane integrity, leading to cellular disorganization and phytotoxicity.