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The Master Gardener Journal


W H A T   Y O U   N E E D   T O   K N O W


How Herbicides Work
by Angela O'Callaghan, Ph.D.

In agriculture and landscape, herbicides (weed killers) are among the most widely used pesticides. While common sense would lead anyone to treat this kind of chemical with respect, many herbicides are labeled "caution" and apparently pose low risk to human health. When it comes to plants, however, they are capable of killing both targets (usually weeds) and non-targets (usually desirable plants), and they cannot distinguish between them.

Some of these chemicals are transported within a plant ("systemic" or "translocated"), while others affect only the tissue on which they land ("contact"). This will determine when and how the compound gets applied. For instance, a contact herbicide that kills leaf tissue won't be terribly effective if it doesn't touch and cover the leaf tissue. Applying it as a pre-emergent to the soil will probably be useless for weed control.

The movement of theses chemicals within the plant occurs in one or both of the two components of its vascular system. The xylem carries raw materials — water and mineral nutrients, mainly — from the soil solution through the roots, up the stems and into the leaves. Xylem-translocted herbicides are frequently soil applied. The created products of photosynthesis are taken from the leaves and distributed to the rest of the plant via the phloem. Phloem-translocated herbicides are usually applied to the emerged plant.

There is a host of herbicides with many different modes of action. This term refers to the sequence from uptake of the chemical through plant death. It also describes what plant process is affected.

Herbicides fall into one of eight modes of action, although there are several subdivisions within most of these categories. Some have an effect on grassy plants (monocots), while others are generally only effective on broadleaved ones (dicots). Some are toxic to both kinds of plants.

Among the oldest herbicides are growth regulators, mainly used for broadleaf weed control. These behave in plants as if they were auxin, a plant hormone responsible for cell and stem elongation. Because they cause the contents of plant cells to grow uncontrollably, they cause a range of deformities. Frequently leaves become misshapen — elongated or cupped (up or down) — petioles swell, and stems may become swollen and twisted.

Dicamba and 2,4-D are very common and found in many commercial preparations, although there are many more members of this class. Many of them are translocated through both the xylem and phloem.

Seedling growth inhibitors kill the young plant before it breaks through the soil. They do not prevent seeds from germinating, rather they attack either the developing shoot or root, or both, underground. Obviously, they are applied to the soil before weeds emerge. Some, like dinitroanilides, are generally used to control grasses, but others, such as EPTC, are effective on both grasses and broadleaves. If a seedling is not killed by a third type of seedling inhibitor, acetochlor, it will show some tissue deformity, but will probably survive, since herbicides of this type are only effective on seedlings.

Photosynthesis inhibitors (e.g. atrazine, linuron, bentazon) are used both individually and in commercial mixtures. These herbicides attack the process where, in the presence of light, a plant takes carbon dioxide and water and converts it into sugar. Without the ability to create sugars, the plant will die. First, however, it will develop interveinal chlorosis, and may look like it has an iron deficiency. There are many herbicides, from a range of different chemical families, which inhibit photosynthesis. Many are xylem-transported, hence are applied to the soil, but not all. Bromoxinil (e.g. Buctril) is applied to, and absorbed into, leaves, where it remains without translocating (contact herbicide).

Because most of these have little effect on grasses, these are applied to kill broadleaved weeds in grassy areas, although bentazon (Basagran®), which is also a contact herbicide, is used to control nutsedge (a monocot) foliage.

The category of cell membrane disruptors contains two sets of herbicides, attacking two different plant systems, but they result in the same symptoms. They cause leaves to appear as if they had been sunburned, and scorching is actually what happens. Most require light in order to be active, and are used for broadleaved weeds.

One group inhibits a particular step in photosynthesis, with the result that the plant tissue accumulates oxidants, which burn it. These affect only the tissue where they are applied, although there are reports of some instances where paraquat and diquat will move out of leaves and on to roots of certain plants.

Another group attacks the process that manufactures cell components required for photosynthesis. The outcome here again is the build-up of oxidants, which burn the leaf tissue. Although mostly applied post emergence, and usually considered contact herbicides, some, like fomasafen, are also translocated in the xylem.

Amino acid synthesis inhibitors interfere with protein production, causing the plant to die. Again, two different sets of chemicals, working on two different plant process for manufacturing of amino acids (protein building blocks), come under this heading. They are used for both grassy and broadleaved weeds.

The first works on what are called the branched-chain amino acids. Symptoms on plants include stunted growth, followed by foliage becoming pale, yellow to white, and ultimately dying. These chemicals have names that start with "ima-" (e.g. imazaquin) or end in one of two suffixes: "sulfuron" (e.g. halosulfuron) or "sulam", (e.g. flumetsulam). Many are translocted in both the xylem and the phloem, which permits them to be applied to foliage or to the soil.

The other set contains glyphosate (Roundup®, Rodeo® and Touchdown®). This compound interferes with production of the aromatic amino acids and causes stunted or deformed growth and chlorosis before plants die. Glyphosate needs to be applied to foliage because it is translocated in the phloem, and because it becomes tightly bound to soil particles.

Lipid synthesis inhibitors are used to control grasses by interfering with fat production, essential for all membranes in plant cells. Older leave frequently turn colors — purple, orange or red — before becoming necrotic. The central growing point becomes easy to remove from plants treated with lipid synthesis inhibitors. Those compounds with chemical names ending in "fop" are phloem translocated; hence they are applied to emerged plants. The other group of these herbicides have chemical names ending in "dim" and these are translocated in both xylem and phloem. As a result, these can be applied both pre- and post- emergence (soil or foliar).

Nitrogen metabolism inhibitors (glufosinate) prevent plants (both grasses and broadleaves) from using nitrogen, a nutrient involved in virtually all plant functions. When nitrogen-using processes are interrupted, ammonium accumulates within the cells and causes cell death. Other toxic events also occur, all of which result in plant death. The first symptoms are chlorosis and wilting. These proceed most rapidly when there is bright sunlight, high humidity and moist soil. Glufosinate does not translocate well in either the xylem or the phloem, hence it is used as a contact herbicide.

Pigment inhibitors (e.g. Zorial® or Callisto®) prevent plants from creating the compounds that protect from excess sunlight (carotenoids). Many of these pigments are the reds, oranges and purples, which appear in leaf tissue and they serve as antioxidants, Leaves of plants (usually broadleaved) treated with these herbicides develop interveinal chlorosis and may even become bleached white before turning necrotic. Most pigment inhibitors are translocated in the xylem, although some also move through the phloem.

If an herbicide is not applied in a manner where it's most effective — systemic vs. contact, grass control vs. broadleaf, xylem vs. phloem translocated — then the result is a waste of money and possible risk to the environment. Recognizing what's in a formulation allows the applicator to make intelligent choices with herbicides.

Angela O'Callaghan, Ph.D. is a horticulture specialist with the University of Nevada Cooperative Extension.

Article reprinted from Southwest Trees & Turf, January 2004. Photo by Candice Sherrill.


Maricopa County Master Gardener Volunteer Information
Last Updated November 21, 2004
Author: Lucy K. Bradley, Extension Agent Urban Horticulture, University of Arizona Cooperative Extension, Maricopa County
© 1997 The University of Arizona, College of Agriculture and Life Sciences, Cooperative Extension in Maricopa County
Comments to Maricopa-hort@ag.arizona.edu 4341 E. Broadway Road, Phoenix, AZ 85040,
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