Understand the mode of action and persistence of ornamental herbicides
Herbicides perform a vital role in the management of weeds in ornamentals. As the name indicates, herbicides are chemicals that kill or control weeds. Although the ultimate effect of most herbicides is the same (usually weed death), the way they control weeds is vastly different. Physiologists use the term mode of action to describe the way herbicides affect weeds. It includes the entire sequence of events that occur from the time the weed absorbs the herbicide to the final plant response (usually death). Thus, mode of action includes absorption, translocation to an active site, inhibition of a specific biochemical reaction, degradation or breakdown of the herbicide in the plant and the effect of the herbicide on plant growth and physiology.
Large differences exist in the length of time for which specific herbicides provide acceptable levels of control. Persistence refers to the length of time that a herbicide remains active in the soil. Depending on the herbicide, persistence can vary from a matter of days to a few years. Long persistence is desirable in terms of weed control but may be undesirable if new plantings are scheduled for a site or if the herbicide poses a risk of contamination to ground or surface water.
Modes of action Normal plant growth and development involves complex biochemical reactions. A herbicide will adversely affect some of these reactions, but not all of them. Therefore, we can place herbicides into several general mode-of-action categories based on their biochemical effects. Also keep in mind that many herbicides act in more than one way. *Photosynthesis. In the presence of light, green plants produce sugar (C6H12O6) from carbon dioxide (CO2) and water (H2O) in a process called photosynthesis. Photosynthesis is a two-phase process that occurs in the leaf chloroplasts. During the light-dependent phase of photosynthesis, the plant transforms light energy from the sun into biological energy in the form of ATP (adenosine triphosphate) and NADPH2 (nicotinamide adenine dinucleotide phosphate). In the light-independent phase of photosynthesis, ATP and NADPH2 supply energy for the conversion of CO2 into sugars. Plants subsequently convert sugars into longer-chain carbohydrates, which represent the major stored portion of biological energy in the plant.
Herbicides that directly inhibit photosynthesis interfere with or block electron transport and prevent ATP and NADPH2 production. This leads to decreased sugar or food formation. However, the visual injury symptoms (chlorosis, desiccation or browning of plant tissue) occur too rapidly to be the result of starvation of the plant. Instead, chlorosis of leaf tissue may be due to the photo-destruction (damage from excessive light) of chlorophyll and other plant pigments. When herbicides block electron transport, chlorophyll continues to absorb light energy but cannot pass this energy on to make ATP and NADPH2. Thus, chlorophyll either self-destructs from the energy it is absorbing or passes this absorbed energy on to oxygen. This forms radical oxygen, which is highly destructive to cell membranes and other cell structures. Cell-membrane destruction causes leakage of the cellular contents and results in the desiccation of plant tissue.
Ornamental herbicides that inhibit photosynthesis include simazine and bentazon. Additionally, the modes of action of oxyfluorfen, diquat, oxadiazon and glufosinate relate to the photosynthetic process.
* Amino-acid and protein synthesis. Plants use proteins in functional, storage and structural roles. Functional proteins are called enzymes. Enzymes catalyze thousands of chemical reactions necessary for plant growth and development. Storage proteins commonly occur in seeds and supply essential amino acids to young, developing seedlings. Both enzymes and seed proteins consist of long chains of interconnected amino acids. Commonly, just l7 to 20 different amino acids occur in plants. However, the amino-acid composition between different plant proteins varies greatly.
In the absence of amino-acid and protein synthesis, plants cannot complete the chemical reactions necessary for growth. Imazaquin, halosulfuron and glyphosate inhibit the synthesis of specific amino acids. Without them, protein synthesis decreases, certain metabolic reactions cease and the plant gradually dies over a period of one to several weeks.
Protein synthesis is under the direct control of DNA (deoxyribose nucleic acid) and RNA (ribonucleic acid). DNA is located in the nuclei and chloroplasts of plant cells and contains the genetic information that determines the sequence of amino acids in the various plant proteins. RNA (messenger RNA) transports the genetic information that is contained in DNA and is involved in the assembly (transfer RNA) of amino acids into proteins. Metolachlor and napropamide interfere with nucleic-acid synthesis, which in turn decreases protein synthesis.
* Cell division. Plant growth includes the process of cell division, or mitosis, which the nucleus initiates and regulates. During cell division, a mother cell divides into two identical daughter cells. (Strictly speaking, mitosis is the division of the nucleus, not the whole cell. However, in common use, "mitosis" often refers to the entire act of cell division, not just nuclear division.)
Herbicides that interfere with cell division are called mitotic poisons. When these products block cell division, new cell production decreases and eventually growth stops. Herbicides that inhibit cell division are the dinitroanilines (for example, oryzalin, prodiamine, pendimethalin and trifluralin), pronamide and dithiopyr. * Cell membranes. A cell wall and a membrane (the plasma membrane) enclose plant cells. Contact herbicides cause a breakdown of the cell membrane and leakage of the cellular contents. The plant then undergoes rapid wilting and desiccation, often within hours of the herbicide application. Plant tissues appear burned. However, the mode of action of most contact herbicides is not due to actual burning or caustic action of the herbicide; contact herbicides affect specific physiological processes. For example, diquat intercepts electrons during the light-dependent phase of photosynthesis, creating free radicals. These pass electrons to other compounds that form superoxide radicals and hydrogen peroxide, which are toxic and break down the cell membrane. Oxyfluorfen and oxadiazon are other herbicides that cause massive membrane disruption through the process of free-radical formation.
Fatty acids are critical components of cell membranes. If fatty-acid synthesis is blocked or inhibited, plants are unable to form the cell membranes necessary for normal growth. The post-emergence grass herbicides sethoxydim, fluazifop, fenoxaprop and clethodim inhibit fatty-acid synthesis in susceptible grassy weeds. Tolerant plants (that is, broadleaf and non-grass ornamentals) have a different structure of the enzyme that these herbicides do not affect. * Cell-wall biosynthesis. As I mentioned, a cell wall (in addition to a membrane) composed of cellulose, hemicelluloses, pectin and other compounds encloses all plant cells. Cell-wall biosynthesis begins during the process of cell division and continues during the growth of the cell. The primary purpose of the cell wall is to impart rigidity and structure to the plant. The mode of action of isoxaben is inhibition of cell-wall biosynthesis. * Pigment synthesis. Carotenoids (yellow in color) and chlorophyll (green in color) are plant pigments located in the chloroplasts of leaf cells. Both carotenoids and chlorophyll absorb light during photosynthesis. An additional function of carotenoids is that they protect chlorophyll molecules from photo-oxidation (damage from excessive light). Norflurazon inhibits carotenoid synthesis. In the absence of the protective carotenoids, chlorophyll breaks down in sunlight and susceptible plants become bleached or white in color due to photo-oxidation. Plant death occurs slowly due to the eventual depletion of stored food reserves and the inability of the plant to manufacture new sugars. * Growth regulation. Auxins are natural plant hormones that regulate plant growth and are under direct metabolic control by the plant. At low concentrations, auxins promote normal growth and development. However, at abnormally high concentrations, auxins inhibit plant growth. Several herbicides, such as 2,4-D and related compounds, mimic the activity of heavy doses of auxins and thereby cause abnormal plant growth.
The exact mode of action of auxin-type herbicides is unknown. The first apparent symptom after application is a downward twisting or curvature of the leaves and stems of susceptible plants, often within hours of application. Although other symptoms are slower to develop, plants also undergo rapid, uncontrolled cell division and enlargement. Vascular tissues responsible for the transport of food materials and water become plugged or broken, and the plant slowly dies over a 2- to 4-week period.
Recent evidence indicates that auxin-type herbicides stimulate the production of excessive amounts of ribonucleic acids (DNA and RNA). This induces uncontrolled cell enlargement and division and results in the abnormal growth of susceptible plants.
Herbicides that have auxin-type activity include 2,4-D and related phenoxy herbicides, and dicamba. While these herbicides are not good choices for weed control in ornamentals (most ornamentals are susceptible to broadleaf herbicides), they are common ingredients in many products for controlling broadleaf weeds in turfgrasses.
* Growth inhibition. Although all herbicides inhibit the growth of plants in some manner, the specific mechanism of action of some herbicides is unknown. Metolachlor, a substituted amide, is one such product. It inhibits the synthesis of fatty acids and lipids, proteins and gibberellins. It also inhibits both shoot or root growth of susceptible weeds. * Nitrogen metabolism. Glufosinate inhibits an essential enzyme involved in nitrogen metabolism. This enzyme helps convert inorganic nitrogen, in the form of ammonia, into amino acids. Glufosinate interferes with the activity of this enzyme, which causes toxic levels of ammonia to accumulate in plant cells. This, in turn, directly inhibits photosynthesis. The result is rapid tissue necrosis and death of the treated plants.
Herbicide persistence The ideal soil-applied herbicide is one that controls weeds for a desired period and then rapidly degrades or breaks down in the soil to non-phytotoxic levels. Understanding the residual life, or soil persistence, of a herbicide is extremely important. It not only determines the length of weed control that you can expect but also influences the plant selection of succeeding plantings. Physical, chemical and microbial processes affect the persistence of herbicides in the soil (see figure, page 40) with regard to their breakdown. Volatility, leaching and soil erosion by wind and water are physical processes that also affect herbicide persistenceby determining how much moves from the application site. * Volatility. This is the process by which a herbicide changes from a liquid or solid state to the gaseous (vapor) state. Once in the vapor state, the herbicide rapidly leaves the area of application, and poor weed control or injury to non-target plants can occur if enough of the herbicide volatilizes.
Chemical characteristics, soil moisture, temperature and adsorption of the herbicide to soil colloids all affect herbicide volatility. For example, under hot, dry conditions, pronamide volatility is high. The dinitroaniline herbicides (oryzalin, trifluralin, prodiamine, benefin and pendi-methalin) vary in their volatility characteristics. Oryzalin and prodiamine are perhaps the least volatile, followed by pendimethalin, benefin and trifluralin. Mechanical incorporation, rainfall or irrigation within 1 to 2 days of application will prevent or dramatically reduce the volatility losses of dinitroaniline (and other) herbicides, resulting in better control as well as reduced risk of non-target effects. * Leaching. The movement of herbicides in soil by water is called leaching. Leaching of herbicides can occur in any direction in the soil, but the most common direction is downward. Soil texture, the adsorption of the herbicide to soil colloids, the water solubility of the herbicide and the amount of water movement through the soil all affect the amount of herbicide lost to leaching. Herbicides such as the salt forms of 2,4-D have a low tendency to adsorb to soil colloids and readily leach in fine-sand or silt-loam soils. In contrast, the dinitroaniline herbicides and most other pre-emergence herbicides readily adsorb to soil colloids and resist leaching. * Adsorption. Adsorption is the attraction of ions or molecules to the surface of a solid. After application, many herbicides adsorb (bind) to the clay and organic-matter fractions of soils. However, herbicides adsorb poorly to the sand and silt fractions of soil. Therefore, the extent of herbicide adsorption increases as the percentage of organic matter and clay increases. The dinitroaniline herbicides, dithiopyr, oxadiazon and most other pre-emergence herbicides readily bind to soils. * Photo-decomposition. Herbicides break down or degrade in sunlight. Specifically, the ultraviolet (UV) portion of sunlight is responsible for photo-decomposition. Several herbicides, such as most dinitroanilines herbicides, are photo-degradable. Therefore, they require incorporation into soil with tillage, rainfall or irrigation to retain their herbicidal activity. Herbicide labels generally supply information about incorporation, including methods and time limitations. Be sure to consult this information whenever you use a herbicide that requires incorporation. * Microbial processes. Microbial decomposition is one of the most important processes by which herbicides break down in the soil. Microorganisms use many organic herbicides as a food source. Thus, soil temperature, aeration, pH, organic matter and moisture levels that favor microbial growth also promote rapid herbicide breakdown. Herbicides that microbes can affect include the dinitroanilines, metolachlor, napropamide, prona-mide, bentazon, dithiopyr, glufosinate, glyphosate and isoxaben.
A commonly used term for describing the persistence of herbicides is T1/2, or half-life. T1/2 indicates the average length of time (days, weeks or months) it takes a herbicide to reach one-half of the originally applied dosage (see table, page 44). Pre-emergence herbicides usually have a longer T1/2 in the soil than post-emergence herbicides. Long half-lives are desirable in terms of residual weed control but can be a problem if you've scheduled a renovation or new plantings for a site you previously treated with a pre-emergence herbicide. You'll find replanting restrictions and related information on pre-emergence-herbicide labels, which you should consult before conducting renovations.
A basic understanding of the behavior of herbicides in weeds and soils is paramount to their safe andeffective use. If you understand and can discuss the mode of action and persistence characteristics of landscape herbicides, it will make you a more effective grounds manager and improve the credibility and professionalism of your company and the industry as a whole.
Landscape-maintenance personnel use herbicides directly under the scrutiny of the public eye. Often, pesticide opponents accuse this industry of using "poisons" or "sterilizing the soil." However, the herbicides we use in the landscape industry are not general poisons, nor do they sterilize the soil. They work in specific ways on specific biochemical processes. The ability to communicate this to the public is increasingly important in helping ease fears about these products.
Dr. Tim Murphy is an extension weed specialist with the University of Georgia (Griffin).
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