Abstract
Several commercial and experimental herbicides such asp-nitrodiphenyl ethers, oxadiazoles, and cyclic imides inhibit protoporphyrinogen IX oxidase (Protox), the enzyme that converts protoporphyrinogen IX to protoporphyrin IX (Proto). This leads to uncontrolled autooxidation of the substrate and results in accumulation of Proto. Blockage of the porphyrin pathway at this site inhibits synthesis of both chlorophylls and heme. Heme is a feedback regulator of the porphyrin pathway. Thus, inhibition of Protox also deregulates the pathway, causing increased carbon flow to the accumulating pool of Proto. Proto is a potent photosensitizer that generates high levels of singlet oxygen in the presence of molecular oxygen and light. In plants treated with these herbicides, damage is light dependent and closely correlated with the level of Proto that accumulates. Proto accumulation is apparently largely extraplastidic, resulting in rapid photodynamic damage to the plasmalemma and tonoplast. After high levels of Proto accumulate in response to these herbicides, protochlorophyllide (PChlide) levels can increase also; however, Proto appears to be the primary photodynamic pigment responsible for the herbicidal activity.
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