- ^ Kollmeyer, Willy D.; Flattum, Roger F.; Foster, James P.; Powell, James E.; Schroeder, Mark E.; Soloway, S. Barney (1999). «Discovery of the Nitromethylene Heterocycle Insecticides». In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 71–89. ISBN 978-4431702139.
- ^ Yamamoto, Izuru (1999). «Nicotine to Nicotinoids: 1962 to 1997». In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 3–27. ISBN 978-4431702139.
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- ^ Tomizawa, Motohiro; Latli, Bachir; Casida, John E. (1999). «Structure and Function of Insect Nicotinic Acetylcholine Receptors Studied with Nicotinic Insecticide Affinity Probes». In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 271–292. ISBN 978-4431702139.
Imidacloprid is effective against sucking insects, some chewing insects, soil insects and fleas on domestic animals. It is systemic with particular efficacy against sucking insects and has a long residual activity. Imidacloprid can be added to the water used to irrigate plants. Controlled release formulations of imidacloprid take 2–10 days to release 50% of imidacloprid in water.
It is applied against soil pests, seed, timber and animal pests as well as foliar treatments.
As of 2013 neonicotinoids have been used In the U.S. on about 95 percent of corn and canola crops, the majority of cotton, sorghum, and sugar beets and about half of all soybeans. They have been used on the vast majority of fruit and vegetables, including apples, cherries, peaches, oranges, berries, leafy greens, tomatoes, and potatoes, to cereal grains, rice, nuts, and wine grapes.
Imidacloprid is possibly the most widely used insecticide, both within the neonicotinoids and in the worldwide market.
In agriculture, usefulness of neonicotinoid seed treatments for pest prevention depends upon the timing of planting and pest arrival. For soybeans, neonicotinoid seed treatments typically are not effective against the soybean aphid, because the compounds break down 35–42 days after planting, and soybean aphids typically are not present or at damaging population levels before this time. Neonicotinoid seed treatments can protect yield in special cases such as late-planted fields or in areas with large infestations much earlier in the growing season.
Overall yield gains are not expected from neonicotinoid seed treatments for soybean insect pests in the United States, and foliar insecticides are recommended instead when insects do reach damaging levels.
Health Canada estimated that neonicotinoids provide benefits equivalent to over 3% of the national farm gate value of corn and 1.5% to 2.1% of the national farm gate value of soybean in 2013 .
Neonicotinoids have been registered in more than 120 countries. With a global turnover of €1.5 billion in 2008, they represented 24% of the global market for insecticides. After the introduction of the first neonicotinoids in the 1990s, this market has grown from €155 million in 1990 to €957 million in 2008. Neonicotinoids made up 80% of all seed treatment sales in 2008.
As of 2011, seven neonicotinoids from different companies are on the market.
|Name||Company||Products||Turnover in million US$ (2009)|
|Imidacloprid||Bayer CropScience||Confidor, Admire, Gaucho, Advocate||1,091|
|Thiamethoxam||Syngenta||Actara, Platinum, Cruiser||627|
|Clothianidin||Sumitomo Chemical/Bayer CropScience||Poncho, Dantosu, Dantop, Belay||439|
|Acetamiprid||Nippon Soda||Mospilan, Assail, ChipcoTristar||276|
|Dinotefuran||Mitsui Chemicals||Starkle, Safari, Venom||79|
|Nitenpyram||Sumitomo Chemical||Capstar, Guardian||8|
Mode of action
Neonicotinoids, like nicotine, bind to nicotinic acetylcholine receptors (nAChRs) of a cell and trigger a response by that cell. In mammals, nicotinic acetylcholine receptors are located in cells of both the central nervous system and peripheral nervous systems. In insects these receptors are limited to the central nervous system.
Nicotinic acetylcholine receptors are activated by the neurotransmitter acetylcholine.
While low to moderate activation of these receptors causes nervous stimulation, high levels overstimulate and block the receptors,
causing paralysis and death. Acetylcholinesterase breaks down acetylcholine to terminate signals from these receptors. However, acetylcholinesterase cannot break down neonicotinoids and their binding is irreversible.
Basis of selectivity
R-nicotine (top) and desnitro-imidacloprid are both protonated in the body
Mammals and insects have different composition of the receptor subunits and the structures of the receptors. Because most neonicotinoids bind much more strongly to insect neuron receptors than to mammal neuron receptors, these insecticides are more toxic to insects than mammals.
The low mammalian toxicity of imidacloprid has been explained by its inability to cross the blood–brain barrier because of lack of a charged nitrogen atom at physiological pH. The uncharged molecule can penetrate the insect blood–brain barrier.
Other neonicotinoids have a negatively charged nitro or cyano group, which interacts with a unique, positively charged amino acid residue present on insect, but not mammalian nAChRs.
However, the breakdown product desnitro-imidacloprid, which is formed in a mammal’s body during metabolism as well as in environmental breakdown of imidacloprid, has a charged nitrogen and shows high affinity to mammalian nAChRs. Desnitro-imidacloprid is quite toxic to mice.
The precursor to nithiazine was first synthesized by Henry Feuer, a chemist at Purdue University, in 1970;Shell researchers found in screening that this precursor showed insecticide potential and refined it to develop nithiazine. In 1984 nithiazine’s mode of action was found to be as a postsynaptic acetylcholine receptor agonist, the same as nicotine. Nithiazine does not act as an acetylcholinesterase inhibitor, in contrast to the and insecticides. While nithiazine has the desired specificity (i.e. low mammalian toxicity), it is not photostable—that is, it breaks down in sunlight, thus is not commercially viable.
In 1985, Bayer patented imidacloprid as the first commercial neonicotinoid.
During the late 1990s, primarily, imidacloprid became widely used[specify]. Beginning in the early 2000s, two other neonicotinoids, clothianidin and thiamethoxam, entered the market[where?]. As of 2013, virtually all corn planted in the United States was treated with one of these two insecticides. As of 2014, about a third of US soybean acreage was planted with neonicotinoid-treated seeds, usually imidacloprid or thiamethoxam.