Herbicides antagonism

Compounds that affect activities of hepatic microsomal enzymes can antagonize the effects of methyl parathion, presumably by decreasing metabolism of methyl parathion to methyl paraoxon or enhancing degradation to relatively nontoxic metabolites. For example, pretreatment with phenobarbital protected rats from methyl parathion s cholinergic effects (Murphy 1980) and reduced inhibition of acetylcholinesterase activity in the rat brain (Tvede et al. 1989). Phenobarbital pretreatment prevented lethality from methyl parathion in mice compared to saline-pretreated controls (Sultatos 1987). Pretreatment of rats with two other pesticides, chlordecone or mirex, also reduced inhibition of brain acetylcholinesterase activity in rats dosed with methyl parathion (2.5 mg/kg intraperitoneally), while pretreatment with the herbicide linuron decreased acetylcholine brain levels below those found with methyl parathion treatment alone (Tvede et al. 1989). 

Herbicide resistance was also bred into com lines to permit the use of sethoxydim herbicide. Although these hybrids were widely available to growers, their acceptance was limited by sethoxydim s narrow spectrum of weed control and by concerns over antagonism between the sethoxydim and tank-mixed broadleaf herbicides. Sethoxydim-resistant hybrids are no longer grown. 

Premix and tank-mix compatibility Atrazine is an excellent mixing partner with many herbicides. Compatibility and antagonism problems are rare. In fact, its premix compatibility is so good that atrazine is used more often than any other herbicide as a premix component in com herbicide products. Furthermore, because of the tremendous margin of com safety, mixes do not typically pose a risk for increased crop injury. 

Atrazine use in ecofallow usually is supplemented with other herbicides. For example, the first herbicide application to wheat stubble often uses glyphosate and 2,4-D or dicamba, with the atrazine application postponed until later in summer to coincide with the emergence of volunteer wheat, cheat, and downy brome. Atrazine can be applied with glyphosate, but antagonism with some atrazine formulations is associated with this tank mixture (Stahlman and Phillips, 1979 Wicks and Hanson, 1995) because of physical binding of inert components in the atrazine formulation with glyphosate (Ahmadi et al., 1980). Farmers know that if rainfall does not move atrazine off the wheat residue and into the soil, control of weeds, and volunteer wheat will be unsatisfactory. 

Research on chemical antidotes or safeners has been summarized in several reviews and published symposia (3.-9). Most of the major developments (Table I) have resulted from impirical screening programs by Industry that may have been stimulated by observations of herbicide antagonism in plants (3, 10). However, some of the research on mode of action of antidotes has been directed at finding new ways to protect crop plants from herbicides (3). The research to be discussed in this text, namely the use of subtoxic herbicide pretreatments to improve crop tolerance to selected herbicides, arises in part from research on the mode of action of R-25788 as a selective antidote for EPIC or butylate in corn. 

Diclofop-methyl is a postemergence grass herbicide whose action is not related to photosynthetic electron transport. Its herbicidal effect, still not well known, probably involves an antagonism of auxin-mediated processes and an increase in membrane permeability (1,2). Its physiological effects have not been described. 

Auxin inhibitor herbicides include the so-called wild oat herbicides shown in Figure 5.22. Their classification as auxin inhibitors is based on their inhibition of auxin-induced responses in auxin bioassays and their antagonism of auxin herbicides. " This anti-auxin activity of diclofop-methyl is almost certainly secondary in importance to its inhibition of acetyl-CoA carboxylase (see Chapter 3). 

Antagonism cooperative action of two herbicides such that the observed response of a test plant to their joint application appears... 

A bentazon-induced reduction in the foliar absorption of sethoxydim by goose grass Eleusine indica L.) has been proposed by Rhodes and Coble as a likely mechanism for the observed antagonism between these two herbicides. However, Retzlaff et aV suggested that the site of the antagonistic interaction between bentazon and sethoxydim is located in biomembranes such as the chloroplast envelope or the plasmalemma. The... 

D, the activity of 2,4-D on broadleaf weeds is not affected by DM. Other auxinlike herbicides such as dicamba and MCPA also antagonize the action of DM on wild oats. " The timing of the application of DM and auxin herbicides appears to be critical for their antagonistic interaction on wild oats. In oat coleoptiles, 2,4-D reverses the action of DM when applied within 2 h after exposure to DM, " whereas in whole plants, antagonism occurs even when auxin herbicides are applied within 8 h following the application of DM. " ... 

The following mechanisms have been proposed to explain the antagonism of DM by 2,4-D on wild oats a 2,4-D-induced reduction of DM absorption and translocation a 2,4-D-induced decrease in the rate of hydrolysis of DM to diclofop acid, the active form of this herbicide a... 

D-induced increase in the rate of herbicide detoxification by conjugation of diclofop to water-soluble metabolites a competitive antagonism between DM and 2,4-D on a common receptor site and a 2,4-D-induced reversal of the DM effects on transmembrane proton gradient. " ... 

The antagonism of bactericidal sulfanilamides by p-aminobenzoic acid (PABA), a precursor of the vitamin folic acid, has been well documented in the pharmacological literature. More recently, it was shown that the phytotoxic activity of asulam, a herbicidal sulfanilamide derivative, also results from an inhibition of the biosynthesis of the vitamin folic acid. " In particular, asulam inhibits competitively the enzyme 7,8-dihydropteroate synthase, which catalyzes the conversion of 2-amino-4-hydroxy-6-hydroxy-methyl-7,8-dihydropteridine and PABA to dihydropteroic acid, leading to folate depletion. A consequence of the depletion of folic acid derivatives is the buildup of intermediates of the de novo synthesis of purine nucleo-tides. ° Such intermediates include 5 -phosphoribosyl glycineamide (GAR) or 5 -phosphoribosyl-5-amino-4-imidazole (AICAR). The accumulation of GAR and AICAR in asulam-treated pea seedlings has been reported. 

The reversal of the inhibitory action of asulam on wheat, wild oats, and carrots by exogenous applications of folic acid and p-aminobenzoic acid has been demonstrated by a number of investigators. The antagonism of asulam by 2.4-D on bracken fern [Pteridium aquilinum (L.) Kuhn] appeared to be linked to an interaction of the two herbicides on protein synthesis rather than the biosynthesis of folic acid. ... 

A number of studies have demonstrated that the phytotoxic action of trifluralin and of other dinitroaniline herbicides can be antidoted with the use of compensation-type antagonists (for a review, see Ref. 121). Ascorbic acid, cysteine, 2,3-d-mercaptoethanol, and D-a-tocopherol acetate have all been reported to reduce growth inhibitions induced by trifluralin or other dinitroaniline herbicides.It is evident, however, that the antagonism of dinitroaniline herbicidal activity by these compounds does not seem to be related to the primary mechanism of action of these herbicides. As mentioned in Section 6.3.2, dinitroaniline herbicides act by interfering with the function and polymerization of plant microtubules. ... 

Finally, exogenous application of ascorbate or galactonolactone, a direct precursor of ascorbate in plants, has been reported to antagonize the activity of herbicides generating toxic oxygen species, such as paraquat and... 

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