Description
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.
Chemical Properties
Pale yellow crystals; forms monohydrate; mp320°C (608 °F) (decomposes); readily solublein water, insoluble in organic solvents; stablein acids or neutral solution.
Uses
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.
Uses
Nonselective contact herbicide used to control broad-leaved weeds in fruit and vegetable crops.
Uses
Diquat Dibromide is a herbicidal desiccant.
Production Methods
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.
Health Hazard
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.
Flammability and Explosibility
Not classified
Mechanism of action
Non-selective, contact absorbed through foliage, some desiccant action. Photosystem I (electron transport) inhibitor.
Safety Profile
Poison by ingestion,
subcutaneous, intravenous, and
intraperitoneal routes. Experimental
teratogenic and reproductive effects. A skin
and eye irritant. Human mutation data
reported. When heated to decomposition it
emits very toxic fumes of NOx, and Br-. See
also PARAQUAT
Environmental Fate
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 welldened, 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).
Toxicity evaluation
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.
