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Herbicides metabolism

The herbicide tolerance of crop species has been found to be based frequently on differential rates of metabolic herbicide detoxification in crop and weed species while rates of herbicide detoxification in the weed species are too low to prevent binding of a lethal herbicide dosage at the target site, the tolerant crop is able to metabolically detoxify the herbicide with such a high rate that binding of the herbicide at the target site in sufficient amounts to cause irreversible herbicidal effects will be prevented. If weed biotypes with an improved ability for herbicide detoxification, comparable to the tolerant crop species, occur in a population they will survive herbicide application and will thus be selected. [Pg.20]

Studies on the mode of inheritance of metabolic herbicide resistance in Mope-curus myosuroides did not result in a uniform picture. It was reported that a single gene was responsible for metabolism-based resistance in a biotype resistant to fenoxaprop and flupyrsulfuron [72], while in another biotype resistance to chloroto-luron was attributed to more than one gene [73]. [Pg.22]

Potentially, a safener could increase the tolerance of the crop by reduction of herbicide uptake and translocation, or by enhancement of metabolic herbicide inactivation in the crop tissue. Furthermore, a safener could counteract the effect of a herbicide at its biochemical target site, with a resultant reduction of crop susceptibility. Evidence for and against these potential modes of action is presented in the following sub-sections. In addition, aspects of safener specificity (crop versus weed) are covered for situations where the safener is applied in tank mix with the herbicide. [Pg.271]

A31 Bispyribac sodium metabolism Herbicide detoxification [191]... [Pg.417]

The lens is an avascular transparent tissue surrounded by an elastic, collagenous capsule. Disturbances in the normal metabolism of the lens and rupture of the lens alter its optical characteristics, and may cause cataract, i.e., reduced transparency of the lens. For example exposure to a herbicide, 2,4-dichlorophenol, may cause cataract. [Pg.293]

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). [Pg.115]

Hassall, K.A. (1990). A readable student text, particularly useful for the metabolism and mode of action of herbicides and fungicides. [Pg.65]

There have been some reports of herbicides disturbing the metabolism of microorganisms in soil. For example, dichlobenil was shown to increase the rate of CO2 formation from glucose in soil (Somerville and Greaves 1987). [Pg.257]

Cl4-DBpD) may occur in trace amounts in the herbicide, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) (I, 2). Radiolabeled preparations of this dioxin are needed to facilitate studies of its degradation chemistry, metabolism, and mode of action. [Pg.7]

The N -Ditroso derivatives of the dinitroaniline herbicides bu-tralinSa and pendimethalin were quite stable in aerobic soils, persisting over several months. An aerobic actinotnycete of the Streptonyces genus was isolated from soil that metabolized N -ni-trosopendimethalin in laboratory culture.e... [Pg.357]

McBride KE, JW Kenny, DM Stalker (1986) Metabolism of the herbicide bromoxynil by Klebsiella pneumoniae subspecies ozaenae. Appl Environ Microbiol 52 325-330. [Pg.85]

Harder PA, DP O Keefe, JA Romesser, KJ Leto, CA Omer (1991) Isolation and characterization of Strepto-myces griseolus deletion mutants affected in cytochrome P-450-mediated herbicide metabolism. Mol Gen Genet 227 238-244. [Pg.328]

Anilide herbicides are metabolized in plants via cleavage of acylamide moiety. [Pg.327]


See other pages where Herbicides metabolism is mentioned: [Pg.25]    [Pg.344]    [Pg.20]    [Pg.20]    [Pg.223]    [Pg.225]    [Pg.25]    [Pg.344]    [Pg.20]    [Pg.20]    [Pg.223]    [Pg.225]    [Pg.35]    [Pg.48]    [Pg.52]    [Pg.52]    [Pg.57]    [Pg.57]    [Pg.569]    [Pg.703]    [Pg.717]    [Pg.283]    [Pg.260]    [Pg.22]    [Pg.82]    [Pg.218]    [Pg.261]    [Pg.356]    [Pg.357]    [Pg.626]    [Pg.626]    [Pg.181]    [Pg.217]    [Pg.208]   
See also in sourсe #XX -- [ Pg.53 , Pg.54 , Pg.55 , Pg.56 , Pg.57 , Pg.58 , Pg.59 , Pg.60 , Pg.61 , Pg.62 , Pg.63 ]




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Effects of Safeners on Herbicide Metabolism

Herbicide enhanced metabolism

Herbicides microbial metabolism

In studies of herbicide metabolism

Metabolic detoxification, herbicides

Metabolic pathway affected herbicides

Metabolism of herbicide

Resistance enhanced herbicide metabolism

Studies of herbicide metabolism

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