Biosynthesis Bleaching

Bleaching Herbicides. Membrane-based modes of herbicidal action relevant to photosynthesis (37) include those of inhibitors of carotenoid biosynthesis, eg, norflura2on, diftmon, y -phenoxyben2amines inhibitors of chlorophyll biosynthesis, eg, oxadia2on, DTP or... 

Nucleophilic catalysts, 10 420 Nucleophibc reagents, 10 389 Nucleophibc substitution in benzene, 3 601 in 1,2-dichloroethane, 6 255 in fullerenes, 12 248 of quinones, 21 261—262 during pulp bleaching, 21 35-38 Nucleosomes, 17 611-612, 613 Nucleotide biosynthesis inhibitors,... 

The molecular target site of triketone herbicides is the enzyme -hydroxyphenylpyruvate dioxygenase (HPPD). Inhibition of this enzyme disrupts the biosynthesis of carotenoids and causes a bleaching (loss of chlorophyll) effect on the foliage similar to that observed with inhibitors ofphytoene desaturase (e.g. norflurazon). However, the mechanism of action of HPPD inhibitors is different. Inhibtion of HPPD stops the synthesis of homogen tisate (HGA), which is a key precursor of the 8 different tocochromanols (tocopherols and tocotrienols) and prenyl quinones. In the absence of prenylquinone plastoquinone, phytoene desaturase activity is interrupted. The bleaching of the green tissues ensues as if these compounds inhibited phytoene desaturase. 

The enzyme p-hydroxyphenylpyruvate dioxygenase is involved in the conversion of p-hydroxyphenylpyruvate into homogentisate, a key step in plastoquinone biosynthesis. Inhibition of this enzyme has an indirect effect on carotenoid biosynthesis as plastoquinone is a co-factor of the enzyme phytoene desaturase. The new maize herbicide isoxaflutole and the triketone herbicides such as sulcotrione (Figure 2.7), inhibit p-hydroxyphenylpyruvate dioxygenase and this leads to the onset of bleaching in susceptible weeds and ultimately plant death.4... 

F, Bleaching inhibition of carotenoid biosynthesis at the phytoene desaturase step (PDS) Pyridazinones Nicotinanilides Others 12... 

Two phytoene desaturase herbicides have been introduced since 2000 picolina-fen (Pico ) [182], introduced in 2001 by BASF, and beflubutamid [183], introduced in 2003 by Ube Industries. The primary mode of action of picolinafen and beflutamid is interference of carotenoid biosynthesis at the phytoene desaturation level, causing bleaching of the plant affected. As in previously developed phytoene desaturase herbicides, a meta-substituted trifluoromethylphenyl group is key for activity in this class of herbicides, pointing to the need for a lipophilic and electron-withdrawing group at this position of the molecule. 

Previously, we determined that the only known mode of action that is selective for grasses/monocots is acetyl CoA carboxylase inhibition.6 This enzyme is the first of two enzymes involved in de novo fatty acid biosynthesis. This mode of action prevents the synthesis of many essential wax compounds. In order to screen our compounds for this mode of action, we used resistant oat (Avena sp.) seeds. The emodin analogues caused dose-dependent bleaching (Fig. 1.7) and a severe decrease in germination for both resistant and nonresistant grasses. 

Because bleaching can also be caused by inhibition of carotenoid biosynthesis, we tested our compounds for effects on carotenoid content. There was a dose-dependent increase in carotenoid content using the series 1 emodin analogues (Fig. 1.8). This was seen in both monocots and dicots and was not observed with the series 2 analogues. 

The first chapter in the herbicide section is devoted to synthetic efforts related to the herbicide Command, currently being developed by FMC Corporation. Here we see detailed the various synthetic and structure-activity relationships of this important group of compounds. These compounds exert their phytotoxic effect by their bleaching action on a wide variety of economic weeds. An important observation was that soybeans were not affected at normal use rates. These compounds act upon the carotene and chlorophyll biosynthesis of the plant. Here are a group of synthetic pathways that are peculiar to plants and a few microorganisms and are susceptible to chemical attack. 

This spectacular bleaching effect is discussed in other chapters of this work, such as the N-benzylideneamino heterocycles of the Shell workers, the nicotinamides of Stauffer, the pyridazines of American Cyanamid and the furanones of Chevron. Various aspects of carotenoid biosynthesis inhibition have been presented in other places (27,31). however, we see here some of the exciting new chemistry associated with these powerful compounds. 

Herbicidal Activity. As with FMC 55626, all of the active 3-isoxazolidinones cause bleaching of the emerging weed seedlings. Results observed to date indicate that these compounds affect carotene and chlorophyll biosynthesis (8. 9). Typical greenhouse activity data for preemergence application of FMC 57020 (8, X-2-C1) on some representative weed species are shown in Table VII. The... 

A great diversity in molecular structure is observed among herbicides which inhibit carotene biosynthesis as is exemplified by the structures of norflurazon, fluridone and difunone (shown below). Nonetheless, many of these compounds, which comprise a subset of the larger group known as bleaching herbicides, appear to inhibit the same step in the biosynthetic pathway to the carotenoids (1 ). The inhibited step is the desaturation of 15-cis phytoene to 15- cis phytofluene (Figure 1) and the build-up of phytoene in plants and in cell-free systems which have been treated with these herbicides is well documented (2-4). 

Herbicides have several different mechanisms of action. Carotenoid biosynthesis inhibitors (Norflurazon, Fluridone, Flurochoridone, Diflufenican) block the formation of antioxidants which protect the photosynthetic apparatus in plants [3]. Plants treated with this class of substance are bleached and become unable to photo-synthesize [4]. 

The chemistry and biochemistry of wood have been summarized in several monographs. Numerous reviews of the chemistry of the hemi-celluloses are also available. " The chemistry of the polysaccharides associated with wood cellulose and the structural chemistry of the hemi-celluloses have previously been discussed in this Series. In the following, the structures and properties of all wood hemicelluloses will be considered in detail, and brief reference will also be made to their location in the wood. Topics not reviewed are evolution of wood hemicelluloses, their biosynthesis, their possible association with lignin in the wood, and their behavior in the technical pulping and bleaching processes. The hemicelluloses occurring in the bark of trees have also been omitted. 

A number of other herbicides interfere with photosynthesis in specific ways. Amitrole inhibits biosynthesis of chlorophyll and carotenoids. The affected plants present a bleached appearance before they die because of the loss of their characteristic pigments. Another herbicide, atrazine, inhibits the oxidation of water to hydrogen ion and oxygen. Still other herbicides interfere with electron transfer in the two photosystems. In photosystem II, diuron inhibits electron transfer to plastoquinone, whereas bigyridylium herbicides accept electrons by competing with the electron acceptors in photosystem I. The inhibitors active in photosystem I include diquat and paraquat. The latter substance attained some notoriety when it was used to interfere with an... 

Data on herbicides are presented and reviewed, which allows the distinction between two different modes of bleaching. The first mode is caused by inhibited carotene biosynthesis exhibited by particular phenylpyridazinones, substituted phenylfuranones or amitrole. Decrease of carotenes leads to subsequent photodestruction of chlorophyll, peroxidation of other membrane components, and decay of electron transport activity. The second mode, represented by p-nitrodl-phenylethers, is associated with peroxidation of membrane-bound polyunsaturated fatty acids concurrently with the breakdown of carotenes, chlorophylls, and decay of photosynthetic electron transport. Short-chain hydrocarbon gases are reliable markers. The action of peroxidizing diphenylethers appears to be related to that of bipyridylium salts, although no light-induced oxygen uptake can be measured. 

In Pennisetum seedlings treated with difunon in higher concentration (>10 iM), the bleaching of pigments was reported to be paralleled by a decrease of the porphobilinogenase level whereas the contents of -aminolevulinic synthetase and dehydratase were not lowered ( 4). This proposed mode of action of difvinon upon chlorophyll biosynthesis could not be confirmed with the microalga Chlorella (23). 

Primary herbicidal effects are followed by secondary ones that show up before death of the plant cell. The 70-S ribosomes of wheat chloroplasts are decreased by bleaching pyridazinones in the light, but not in the dark ( 9) A prominent mode of action is observed upon the composition of fatty acids by, e.g., BAS 13338 (SAN 9785) (24, 5), which does not substcuatially interfere with carotenoid biosynthesis. Good direct inhibition of photosynthetic electron transport (I50 3 x 10 7m) is observed with the phenylpyridazinone BAS 100822 electron transport inhibition of other phenyl-pyridazinones is less than with BAS 100822 (28). 

Carotenoid Biosynthesis and Phytotoxic Effects of Bleaching Herbicides 4.1.2.1 Targets for Bleaching Herbicides... 

Bleaching may be a result of photooxidative events generated within the plant cell or chloroplast, leading to the destruction of the plant pigments or direct inhibition of pigment biosynthesis, whereby carotenoid and chlorophyll formation is prevented [5]. 

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