Carotenoid biosynthesis bleaching herbicides

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... 

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... 

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. 

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]. 

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... 

Most commercial so-called bleaching herbicides inhibit the synthesis of carotenoids by interfering with carotenoid biosynthesis at the level of phytoene desatur-ase [170, 171, 172]. Errzyme kinetics with several inhibitors have revealed a reversible binding to the en2yme and non-competitive inhibition [173],... 

Carotenoids also protect the cell from damage due to photooxidation catalyzed by light-absorbing pigments such as chlorophylls. This effect was noted in comparisons of normal carotenoid-containing bacteria with mutants in which the carotenoids are replaced by the more saturated and colorless carotenoid, phytoene (8) (Ramage, 1972). Many bleaching herbicides inhibit carotenoid biosynthesis the plants usually die because of photooxidation (Britton, 1991). 

The carotenoids fulfill vital functions in green tissues, and so inhibition of their synthesis, or their destruction by peroxidation (see Chapter 5), leads to bleaching of the tissue and subsequent cell death. The purpose of this chapter is to explain the mode of action of bleaching herbicides which inhibit carotenoid biosynthesis in plants. Present and future experimental approaches which should enhance our current understanding of carotenoid biosynthesis and its regulation are also discussed in relation to the development of a new generation of bleaching herbicides. 

A variety of techniques has been used to identify the mode of action of bleaching herbicides on carotenoid biosynthesis and to discover the functional groups on such compounds which are prerequisites for inhibitory activity. The trivial names of herbicides are used in the following sections, and their systematic names are listed in the Appendix at the end of the book. 

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. 

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... 

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