Published online by Cambridge University Press: 12 June 2017
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, Fa/Fb. 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 phototoxicity.
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