These symptoms can be found on cotyledons to the newest leaves of susceptible plants. If the insecticide is placed incorrectly or applied at the wrong rate, cotton may be injured. Consult the label for further precautions. Some herbicides act on seedling weeds shortly after they germinate and before they emerge.
These herbicides work beneath the soil so their effects are seldom seen. If overapplied, however, they may inhibit growth of weed or crop seedlings that do emerge through the soil surface.
These herbicides can be divided into two groups—root inhibitors and shoot inhibitors. Root inhibitors. These herbicides interrupt cell division, which stops root growth in seedling weeds. Plants die because they cannot take up enough water and nutrients to sustain growth. The root inhibitors are most effective on small-seeded broadleaf and grass weeds. Large-seeded weeds and crops generally survive normal dosages because their roots and shoots grow through the herbicide treated zone in the soil.
Shoot inhibitors. The seedling shoot growth inhibitors also act on newly germinated weed seeds. They are absorbed by the seedling shoots of grasses and roots of broadleaf plants, and they disrupt cell growth. They are most effective at controlling small-seeded grass and broadleaf weeds. Large-seeded crops and weeds are not usually affected.
Once tolerant or susceptible plants emerge they can generally overcome the effects of the herbicide. Injury to tolerant plants is caused by root damage. Grass crops may be stunted and have a purple discoloration because roots cannot take up enough phosphorus. Root systems appear stubby and thick, especially the lateral roots. Broadleaf plants may have swollen and cracked hypocotyls.
If these herbicides are incorporated shallowly or applied preemergence, they sometimes cause callus tissue tumors to form on the plant stem at the soil surface. This weakens the stem and causes lodging. Dinitroaniline herbicides applied postemergence to broadleaf crops may cause stunting.
Symptoms caused by the shoot inhibitors are much different than those of the root inhibitors. Overapplication or extended periods of cool, wet weather shortly after planting may sometimes cause injury to tolerant crops such as corn or sorghum.
In broadleaf plants, the center vein midrib may draw in the leaf edge in a drawstring effect. Leaf puckering is also a symptom on broadleaf plants.
There may also be stunting that persists until the soil warms enough to promote plant growth. These products are widely used in Texas row crops, turfgrass, and horticultural crops. The growth inhibitor herbicides have no postemergence activity; therefore, the timing of application is critical. Dinitroanilines have various requirements for incorporation into the soil. Consult the individual product label for specific recommendations. The cell membrane disruptor postemergence herbicides control both grasses and broadleaf weeds by destroying cell membranes and causing rapid desiccation of the plant.
There are two types of cell membrane disruptor herbicides: the bipyridylium and the diphenylethers. The bipyridylium herbicides require thorough plant coverage to be effective, and they have no soil activity. The diphenylether herbicides act in a similar way but more slowly. Some of them are more selective between crops and weeds. The herbicides Goal and Reflex have significant soil activity. However, their true mode of action is unknown.
They are used to selectively control wide-leaved grasses such as crabgrass or dallisgrass in narrow-leaved grasses such as bermudagrass lawns. They are also very effective on cocklebur and common ragweed. These herbicides bind tightly to soil clay and organic matter, so they have no residual, preemergence activity. Plants rapidly turn yellow or pale and may look water soaked; then they dry up. The effects of the bipyridylium herbicides are rapid. Even small droplets that drift to nontarget vegetation cause specks of burned tissue.
Roots of perennial weeds are seldom killed because these herbicides do not usually translocate to the roots. The organic arsenicals accumulate in root and leaf tips and symptoms are first seen on leaf tips. They rapidly kill leaf and stem tissue. When applied over cotton to control grasses or cocklebur, they sometimes cause speckled leaf burn and red stems on the cotton plants; however, this has little effect on overall growth.
Be careful to prevent drift during application so that non target plants are not harmed. Applying systemic herbicides shortly after cell membrane disruptors or organic arsenicals is not advised. Paraquat and diquat are generally considered to be nonselective and harmful to both grass and broadleaf vegetation.
In peanuts, however, some selectivity can be achieved by using paraquat at the cracking stage. Lipid synthesis inhibitors are unique because they act only on annual and perennial grasses, not on broadleaf plants.
With the exception of diclofop, these herbicides are applied postemergence and have little or no soil activity. Crop oil concentrate or some other type of adjuvant must be used to increase herbicide uptake into the leaf.
To be most effective, these herbicides should be applied to actively growing grass weeds. If grass weeds are stressed and slow growing, these herbicides will be less effective. These herbicides disrupt lipid biosynthesis in grass plants.
Some herbicides are also prone to chemical reactions which alter their structure and render them non-phytotoxic. These degradation processes all depend upon soil temperature and moisture levels. They increase in direct proportion to soil temperature, and begin when the moisture level rises above the wilting point.
Extra moisture increases the rate of degradation but not by as much as higher temperatures. All other things being equal, imidazolinones will be more persistent on acid soils and sulphonyl ureas on alkaline soils. Triazines are very slightly more persistent on alkaline soils.
Any paddock where any of these products were applied in June or later especially in a year with low rainfall after application should be regarded as having potentially damaging levels of residues, and so should areas of earlier applications if there were significant periods when the soil surface was dry.
Triazine residues will vary in the damage they cause according to the seasonal conditions. Residue effects will be much less when the season start is uniform and rainy compared to dry. Root disease will exacerbate the effect of triazine residues as the young seedlings cannot grow away from the residues which are concentrated in the cultivation layer.
Sulfonyl urea and imidazolinone residues are less affected by soil moisture as they are more soluble. The first effect of the sulfonyl ureas is to prune roots.
Be careful in duplex soils that have sand over alkaline clay. The sulfonyl ureas can leach down to the clay where they will be more persistent due to the high pH. Herbicide drift is the movement of pesticide away from the target area in the atmosphere.
The three main forms of drift are droplet drift, vapour drift and particulate drift. Droplet drift is the main cause of off-target damage. Spray emerging from a boom breaks up into droplets of varying size. Larger droplets fall onto the target area, while the smallest droplets may remain in the air.
Because droplet drift usually disperses as it moves away from the sprayed area, the type of crop damage it causes in adjoining areas is easily recognised. That part of the sensitive crop which is closest to the sprayed area is severely damaged but damage decreases away from the severe zone. Vapour is produced by evaporation from the droplets when they leave the boom and from the target surface after spraying. Like droplets, vapour disperses rapidly as it is carried away from the target area.
The vapour will remain suspended in the air unless the contaminated air is forced back to ground level where it may damage growing plants. Vapour can drift for long distances, and the characteristic feature of vapour drift damage is that no clear damage gradients can be seen. Damage, which is generally mild but widespread, is usually caused by a large body of contaminated air several square kilometres in size.
To understand damage caused by drift of herbicides there are four key aspects that require understanding:. The smaller droplets provide better coverage which is important when the target plant is small, when the herbicide is poorly translocated or when low carrier volumes are used.
The larger droplets result in greater interception or less drift, but the poorer coverage may need to be compensated for by using translocated herbicides or higher carrier volumes.
Most commercially available nozzles produce a range of droplet sizes so there is usually a proportion of very fine droplets that may drift. Also, shear stresses in recirculating pumps especially centrifugal pumps can reduce the effect of polymer drift reducing agents. Under the influence of gravity, all droplets fall at a speed called sedimentation rate. Large droplets fall faster than small droplets.
Within a few centimetres of the nozzle the movement of most droplets is determined by gravity, their buoyancy and wind. The higher the droplet is released, the further it will move away from the target area because the wind speed is slower close to the ground and there is more time for the wind to move the droplet before it lands.
Therefore, the amount of pesticide that drifts off target is closely related to the boom or flying height. In situations where drift can cause problems the boom should be operated at the lowest height possible for the nozzles and spacing. Decreasing the nozzle spacing will allow the boom to be operated at a lower height.
Large droplets contain more herbicide but they tend to land close by, whilst small droplets contain less herbicide but are moved over greater distances by the wind and are more likely to be affected by turbulence that may carry them upwards.
Emulsifiable formulations of herbicides will produce about twice as many droplets in this size range with the same equipment.
The size of the area sprayed also affects the amount of herbicide leaving the target area because successive runs contribute to drift. As small droplets drift away from the sprayed area they normally disperse to non toxic concentrations within metres downwind. These herbicides are nonselective in nature and are applied usually prior to harvesting the crop.
These herbicides are represented by the bipyridilium chemical family and are also known as PSI electron diverters as they accept electrons from PSI and, in the process, generate herbicide radicals.
Upon interacting with O 2 , the herbicide radicals form superoxide radicals, which, in the presence of the superoxide dismutase enzyme, form hydrogen peroxide H 2 O 2 and hydroxyl radicals [ ]. These radicals disrupt the unsaturated fatty acids, chlorophyll, lipids, and proteins in the cell membrane. As a result, the cell membrane is disrupted beyond repair causing leakage of the cell cytoplasm, which leads to wilting and eventual plant death. Due to the overuse of herbicides, agricultural weeds and other undesirable plants develop resistance, which must be contained or eliminated in order for the maximum output of the harvest.
Herbicide resistance occurs due to the overuse of herbicides over the years. It is important to follow the lead in developing a proactive and robust herbicide resistance management strategy for minimizing the agricultural loss.
Similar techniques can be extrapolated to the land management, ornamental, and other related industries to minimize the evolution of the herbicide-resistant varieties of weeds and other pests. Based upon the available body of knowledge, recent advances in agricultural research, and latest techniques, it is advisable to use different herbicides different modes of action at different times of the year and with different crops so that the weeds do not develop resistance to the herbicides as quickly as that have been reported.
Deciding which herbicide is the most effective and the most environmental friendly option for a specific crop can be a daunting task particularly with so many products competing for attention in the multibillion dollar herbicides market.
Most of these herbicides are developed based upon similar weed control and pest management strategies and are designed based upon their mode of action. Rearranging various chemical groups within the chemical family, which most of the companies tend to do while developing their key products, may not be the best strategy as the weeds tend to develop a quick resistance to such chemicals or groups of chemicals.
Therefore, it is imperative that the herbicides be designed to obtain the maximum effect with regard to their mode of action so as to control or eliminate weeds and destroy their capacity to acquire the herbicide resistance. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications.
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Sherwani, Ibrahim A. Arif and Haseeb A. Downloaded: Abstract The mode of action of herbicides is important for understanding the management, classification, organization, and hierarchy of the herbicides.
Keywords Herbicides mode of action resistance translocation regulator. Introduction Herbicides or weedkillers belong to a class of pesticides that are used in the management of undesired plants in the areas of agriculture, landscaping, forestry, gardening, and industry [ 1 , 2 ]. Group 1: Acetyl Coenzyme A Carboxylase ACCase inhibitors Also known as lipid biosynthesis inhibitors, these herbicides inhibit the ACCase enzyme activity and are used typically for controlling grass during the cultivation of broadleaf crop varieties or crop rotation.
Group 2: Acetolactate Synthase ALS inhibitors Also known as amino acid synthesis inhibitors, these herbicides inhibit the action of the acetolactate synthase ALS enzyme. Group 3: Root growth inhibitors Also known as the seedling root growth inhibitors, these herbicides inhibit cell division as part of their mode of action, which, ultimately, blocks root extension and growth.
Group 4: Plant growth regulators Also known as synthetic auxins, this group includes hormone-based herbicides and is used to keep broadleaf weeds out during the cultivation of corn, wheat, and sorghum.
Groups 8 and Shoot-growth inhibitors Also known as seedling shoot growth inhibitors, the herbicides designed with this mode of action are applied as part of the soil preparation and act effectively before the grass and broadleaf weeds emerge.
Group 9: Aromatic amino acid inhibitors The mode of action of these herbicides is as an amino acid synthesis inhibitor. Group Glutamine-synthesis inhibitors The mode of action is nitrogen metabolism-based and is specific to glufosinate, which is nonspecific in nature.
Groups 12, 13, and Pigment synthesis inhibitors Also known as carotenoid biosynthesis inhibitors, these herbicides destroy the green pigment, chlorophyll, which is necessary for photosynthesis in the plants.
Group PPO inhibitors The PPO inhibitors act by disrupting the cell membranes and hence their mode of action is categorized as cell membrane disrupters and their site of action is the cell membrane. Group Photosynthesis inhibitors — Photosystem I PSI inhibitors Upon contact with the plant foliage, these herbicides act by penetrating and destroying the cell lipid bilayer leading to the breakdown of the cell membranes and hence their mode of action is categorized as cell membrane disrupters.
Table 1. Modes of action of different classes of herbicides. More Print chapter. How to cite and reference Link to this chapter Copy to clipboard. Cite this chapter Copy to clipboard Shariq I. Khan December 2nd Available from:. Over 21, IntechOpen readers like this topic Help us write another book on this subject and reach those readers Suggest a book topic Books open for submissions.
More statistics for editors and authors Login to your personal dashboard for more detailed statistics on your publications. Access personal reporting. More About Us. Mode of Action. Site of Action. Chemical Family. Lipid-Synthesis Inhibitors. ACCase Inhibitor. Amino-Acid Synthesis Inhibitors. Imidazolinones, pyrimidinylthiobenzoates, sulfonylaminocarbonyltriazolinones, sulfonylureas, triazolopyrimidines. Root-Growth Inhibitors. Microtubule Inhibitors. Benzamide, benzoic acid DCPA , dinitroaniline, phosphoramidate, pyridine.
Plant-Growth Inhibitors. Site of Action Unknown. Benzoic acid, phenoxycarboxylic acid, pyridine carboxylic acid, and quinoline carboxylic acid. Photosynthesis Inhibitors. Photosystem II Inhibitors. Triazine, triazinone, phenylcarbamates, pyridazinones, and uracils.
Nitriles, benzothiadiazinones, and phenylpyridazines. Phenyl, urea, and amides. Shoot-Growth Inhibitors. Phosphorodithioates and thiocarbamates. Not designated by any specific chemical family. Nitrogen-Metabolism Inhibitors. Glutamine-Synthesis Inhibitors. Pigment-Synthesis Inhibitors. HPPD Inhibitors.
Amides, anilidex, furanones, phenoxybutan-amides, pyridiazinones, and pyridines. Diterpene-Synthesis Inhibitors. Cell-Membrane Disrupters. PPO Inhibitors.
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