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Diquat (DQ) is a bipyridyl herbicide that has been in use since the 1950s. It is employed as a general use herbicide that is fast acting and nonselective. Additionally, on average, 90% of DQ consumption is reported in North America, Europe, Australia, and Japan.

Pale yellow crystals; forms monohydrate; mp320°C (608 °F) (decomposes); readily solublein water, insoluble in organic solvents; stablein acids or neutral solution.

Diquat Dibromide is a herbicidal desiccant.

DQ is used in a manner similar to paraquat. It is found predominantly as a mixture with paraquat, sold as Weedol and Pathclear. The most widely used formulation of DQ alone, Reglone, is an aqueous solution containing 200 g l-1 DQ dibromide. Besides the use as a general weed control agent on noncrop land, DQ is used as a preharvest desiccant on crops such as cotton, flax, and alfalfa. Additionally, almost one-third of all DQ sold is used to control emergent and subemergent aquatic weeds.

Nonselective contact herbicide used to control broad-leaved weeds in fruit and vegetable crops.

The commercial production of diquat dibromide involves a multi-step process. It begins with the quaternisation of 2,2'-bipyridine with 1,2-dibromoethane in a polar solvent, such as acetonitrile, under controlled temperature and pressure to form the cyclic ethylene-bridged bipyridylium structure. The reaction mixture is then treated with bromide salts to ensure the dibromide form.

The acute toxicity of diquat dibromide ismoderate to high in most species. In domes-tic animals, its toxicity is greater than thatin small laboratory animals. The oral LD50value in cows, dogs, rabbits, and mice is30, 187, 188, and 233 mg/kg, respectively.The symptoms of acute toxicity are somnolence, lethargy, pupillary dilation, and respiratory distress. Prolonged exposure to thiscompound produced cataracts in experimental animals. Intratracheal administration ofdiquat dibromide in rats showed toxic effectsin the lung and caused lung damage (Manabeand Ogata 1986). But when administered byoral or intravenous routes, there was no toxiceffect on the lung.

Notclassified

Non-selective, contact absorbed through foliage, some desiccant action. Photosystem I (electron transport) inhibitor.

Biological. Under aerobic and anaerobic conditions, the rate of diquat mineralization in eutrophic water and sediments was very low. After 65 days, only 0.88 and 0.21% of the applied amount (5 μg/mL) evolved as carbon dioxide (Simsiman and Chesters, 1976). Diquat is readily mineralized to carbon dioxide in nutrient solutions containing microorganisms. The addition of montmorillonite clay in an amount equal to adsorb one-half of the diquat decreased the amount of carbon dioxide by 50%. Additions of kaolinite clay had no effect on the amount of diquat degraded by microorganisms (Weber and Coble, 1968).
Photolytic. Diquat has an absorption maximum of 310 nm (Slade and Smith, 1967). The sunlight irradiation of a diquat solution (0.4 mg/100 mL) yielded 1,2,3,4-tetrahydro1-oxopyrido[1,2-a]-5-pyrazinium chloride (TOPPS) as the principal metabolite.
Chemical/Physical. Decomposes at 320°C (Windholz et al., 1983) emitting toxic fumes of bromides and nitrogen oxides (Lewis, 1990). Diquat absorbs water forming wellde?ned, pale yellow crystalline hydrate (Calderbank and Slade, 1976).
In aqueous alkaline solutions, diquat decomposes forming complex colored products including small amounts of dipyridone (Calderbank and Slade, 1976).

DQ is a dipyridyl compound that is capable of redox cycling. DQ can become reduced to produce a free radical. It can then transfer this electron to molecular oxygen to yield superoxide anion. This redox cycling mechanism allows DQ to generate reactive oxygen species (ROS) resulting in oxidative stress, damage to cellular macromolecules and even cell death. Due to its standard redox potential (E0), DQ is more likely to accept an electron compared to paraquat. Because of this property, DQ is expected to generate greater amounts of ROS compared to paraquat at equivalent concentrations. In vitro studies have shown that DQ is dependent on mitochondrial complex I and III in isolated mitochondria and primarily complex III in midbrain neuronal cultures for ROS production. DQ treatment can lead to NADPH depletion, lipid peroxidation, alteration in intracellular redox status, and liberation of ferritin-bound iron stores.

Herbicide