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Publication #SS-AGR-327

Diagnosing Herbicide Injury in Peanut1

S. Morichetti, J. Ferrell, and R. Leon2

1) Photosynthesis Inhibitors

Mechanism of Action: Photosynthesis inhibitors block the electron flow that results after the leaf absorbs light energy. Consequently, the chloroplast is unable to process the absorbed light energy. This massive energy buildup eventually causes cell membranes to rupture and the surrounding plant tissues to die.

Behavior in Plants: Most of these herbicides have significant soil activity and are applied pre-emergence. The herbicide is absorbed by roots and moves upward to the shoots following the water pathway. The herbicide accumulates in the leaf, particularly in the margin of the leaves. Some of these herbicides can be applied post-emergence. In this case, the herbicide only acts on the plant material that it contacts and does not move to other parts of the plant.

Symptoms: When applied pre-emergence, the injury symptoms on susceptible plants begin with chlorosis, or yellowing, of the leaves between leaf veins, then yellowing at the margins followed by tissue death. Older leaves are more affected than newer leaves. When applied post-emergence, the area of the leaf where the herbicide was applied exhibits chlorosis and yellowing, followed by necrosis or a “paper-bag”-type appearance.

Herbicides with this mode of action: Atrazine, Diuron, Bromoxynil, Metribuzin (Lexone/Sencorex), Bentazon, (Basagran), Fluometuron, Prometryn

Figure 1. 

Slight Atrazine injury.

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Figure 2. 

Severe Atrazine injury.

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Figure 3. 

Yellowing followed by marginal necrosis.

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2) Amino Acid Synthesis Inhibitors (ALS Inhibitors)

Mechanism of Action: The ALS-inhibiting herbicides block the acetolactate synthase (ALS) enzyme. The ALS enzyme is responsible for the formation of essential amino acids in the plant (isoluecine, leucine, and valine). Without these amino acids, proteins (complex molecules that control all plant functions) cannot be formed and the plant slowly dies.

Behavior in Plants: These herbicides are absorbed by roots and leaves and are moved extensively in the plant. As these herbicides move in the plant, injury symptoms are most commonly observed in the buds since these areas are the most actively growing. It may take two weeks to develop symptoms depending on weather conditions (temperature, soil moisture, etc.) and the overall rate of plant growth.

Symptoms: Injury on peanut begins with stunted growth and yellowing in the youngest leaves. Leaves take on a “lime” or light green color. The chlorosis is followed by tissue death some days later.

Herbicides with this mode of action:

Imidazolinones: Imazapyr (Arsenal), Imazapic (Cadre)*, Imazethapyr (Pursuit)*, Imazaquin (Scepter)

Sulfonylureas: Chlorimuron*, Halosulfuron, Metsulfuron, Nicosulfuron, Prosulfuron, Primisulfuron, Chlorsulfuron, Trifloxysulfuron

Sulfananilides: Diclosulam*, Cloransulam, Flumetsulam

Pyrimidinylthiobenzoic acid: Staple (Pyrithiobac)

(*) Labeled in peanut.

Figure 4. 

Trifloxysulfuron injury (chlorosis in young leaves).

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Figure 5. 

Metsulfuron injury (chlorosis in young leaves).

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3) Growth Regulators

Mechanism of Action: Auxin is a plant hormone that controls the rate of plant growth. The growth regulator herbicides look very similar to auxin, and the plant is unable to distinguish the difference. This overload of hormone causes the plant to grow in an uncontrollable fashion and results in disruption of numerous essential plant processes (photosynthesis, transpiration, cell division, etc.).

Behavior in Plants: These herbicides are highly mobile in the plant and tend to accumulate in growing points. 2,4-DB is almost identical to 2,4-D but contains additional elements that render it non-herbicidal. Many species quickly remove this protective side-chain and release 2,4-D within the plant. But legumes (peanut, soybean, pea, etc.) are unique in that they do not remove the side-chain from 2,4-DB, leaving this herbicide largely inactive within the plant. The rate of 2,4-DB to 2,4-D conversion is what determines the level of control that will be achieved with a 2,4-DB application.

Symptoms: Symptoms of herbicide injury are uncontrolled growth, resulting in twisting and curling (epinasty) of stems and petioles. Additionally, leaf shape can appear out of proportion (uncharacteristically long and narrow, called strapping) and leaf veins appear abnormal. Bleaching near the base of the leaf is common. With some herbicides (Picloram and Dicamba) we can see leaf cupping, and in some cases it is possible to observe malformed pods.

Herbicides with this mode of action: 2,4-D, 2,4-DB *, Dicamba, Picloram, Triclopyr, Aminopyralid

(*) Labeled in peanut.

Figure 6. 

2,4-D Amine injury (twisting and curling).

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Figure 7. 

Dicamba injury (cupping).

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Figure 8. 

2,4-DB injury (strapping).

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4) Pigment Inhibitors

Mechanism of Action: Chlorophyll absorbs light and directs it to be converted to a chemical that can be used by the plant. But chlorophyll can be damaged if too much sunlight is present, so carotenoid pigments are present to absorb this excess energy and protect chlorophyll. Pigment-inhibiting herbicides act by blocking the formation of carotenoids so that chlorophyll is destroyed by light energy from the sun. These herbicides can be applied pre-emergence or post-emergence.

Behavior in Plants: With no carotenoid pigments produced, the chlorophyll is destroyed, and the leaf turns white since there are no leaf pigments of any kind.

Symptoms: Injury is noted in bleached-white foliage. Varying levels of bleaching can occur, depending on the herbicide dose. Affected plants often recover from light bleaching while total bleaching is rapidly followed by tissue death.

Herbicides with this mode of action: Norflurazon*, Mesotrione, Clomazone, Isoxaflutole, Tembotrione (Laudis)

(*) Labeled in peanut.

Figure 9. 

Norflurazon injury (bleaching).

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Figure 10. 

Severe Norflurazon injury (bleaching).

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Figure 11. 

Severe Tembotrione injury (bleaching).

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5) Cell Membrane Disruptors

Mechanism of Action: The cell membrane disruptor herbicides (also called the PPO herbicides) inhibit an enzyme that manufactures chlorophyll. Consequently, accumulation of a pre-chlorophyll molecule occurs that is capable of accepting light energy, but cannot pass it along to the photosynthesis process. As a result, energy builds up in the leaf until cell membranes are destroyed. Rapid burning and death of leaves occurs within 1–3 days, depending on light and weather conditions.

Behavior in Plants: Although many herbicides in this group are labeled for pre-emergence applications only, all of these herbicides possess foliar activity as well.

Symptoms: When applied pre-emergence, these herbicides can cause burning of tissue or failed emergence. Bronzing and burning in a speckled pattern are characteristic of these herbicides when applied post-emergence. Injury from cell membrane disruptor herbicides can be easily confused with paraquat injury except that no bronze coloration will be associated with paraquat applications.

Herbicides with this mode of action: Flumioxazin*, Fomesafen, Sulfentrazone, Lactofen*, Carfentrazone, Acifluorfen

(*) Labeled in peanut.

Figure 12. 

Cobra injury (necrosis).

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Figure 13. 

Necrosis (speckling).

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Figure 14. 

Valor injury after rainfall followed by cool temperature.

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6) Lipid Synthesis Inhibitors (ACCase Inhibitors)

Mechanism of Action: The herbicides inhibit an enzyme (ACCase) that produces lipids, which are used to build cell membranes. Although all plants contain an ACCase enzyme, broadleaf and grass plants have distinctly different types of this enzyme. ACCase-inhibiting herbicides cannot bind to this enzyme in broadleaf plants, rendering these plants totally immune to the herbicide. Conversely, almost all grasses are sensitive and these herbicides are used for post-emergence grass control. These herbicides do not have soil activity.

Behavior in Plants: ACCase inhibitors move throughout the plant, although they only affect grasses.

Symptoms: Peanut is very tolerant of these herbicides, and ACCase inhibitors do not cause injury on peanuts. However, under hot and humid weather conditions, the crop oil adjuvants used for these applications can cause transient leaf burning on tolerant broadleaf plants.

Herbicides with this mode of action: Sethoxydim*, Clethodim*

(*) Labeled in peanut.

7) Seedling Growth Inhibitors

There are two types of seedling growth inhibitors: root inhibitors and shoot inhibitors. They have different modes of action, but both control plants at the seedling stage below the ground.


Mechanism of Action: These herbicides (also known as the DNAs or the yellow herbicides) inhibit root formation in susceptible plants. Root inhibition occurs when the herbicide blocks the process of mitosis (cell division) in the root tip. Affected plants eventually die of drought stress, regardless of soil water status, because of the inability to develop sufficient root structure to support the water needs of the leaf and shoot. There is a correlation between oil content of seeds and sensitivity to these herbicides; the higher the seed oil content (peanut, soybean, etc.), the more the plant has tolerance to these herbicides. As peanut seeds have a high oil content, it is difficult to see injury from these herbicides. Besides, peanut taproot is much less affected than lateral roots. The peanut taproot may elongate sufficiently to place the apical meristems below the zone of treated soil where lateral roots develop. Therefore, herbicide placement is another factor in plant selectivity.

Behavior in Plants: The yellow herbicides do not move in plants and only work at the root tip. Roots that extend beyond the treated zone will regain normal growth and development.

Symptoms: Peanut symptoms from these herbicides are short, club-like roots. These symptoms are often associated with high rates of herbicides, improper incorporation (placement), or shallow planting followed by excessive rainfall.

Herbicides with this mode of action: Pendimethalin*, Trifluralin**, Oryzalin, Ethalfluralin*

(*) Labeled in peanut.

(**) Labeled only in peanuts grown in Texas, Oklahoma and New Mexico.


Mechanism of Action: These herbicides inhibit several plant processes such as lipid and protein formation.

Behavior in Plants: Chloroacetamides are absorbed into the shoots of emerging plants. The herbicide must be present during emergence to be effective. No activity will be observed from later applications to emerged weeds.

Symptoms: Peanut is generally tolerant to these herbicides, but injury can be observed under certain conditions. The primary symptoms in peanut are root deformation or curling (J-rooting). Symptoms are mostly observed when peanuts are emerging in cool and wet soil conditions. Severely affected plants rarely make full recovery from initial injury. There is also a leaf burning associated with post-emergence application of these herbicides, but this is due primarily to the solvents in the herbicide formulation.The burning from these applications can be quite obvious, but usually doesn’t impact peanut growth or development.

Herbicides with this mode of action: Metolachlor*, Alachlor* (not for use in Florida), Dimethenamid*, Acetochlor

(*) Labeled in peanut.

Figure 15. 

Dual injury (root curling).

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Figure 16. 

Dual injury: Severe injury (left), slight injury (middle), and no injury (right).

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8) Glufosinate

Mechanism of Action: Glufosinate inhibits the activity of the enzyme that converts glutamate and ammonia into glutamine. Inhibiting this enzyme leads to accumulation of toxic levels of ammonia within the cell. The buildup of ammonia quickly leads to multisystem failure within the photosynthesis pathway and causes irreversible cell damage.

Behavior in Plants: Glufosinate has no soil activity. It only affects plant tissue if glufosinate comes into contact with it.

Symptoms: This is a foliar-applied herbicide with contact activity (no movement within the plant). Yellowing and leaf wilting are general symptoms, followed by tissue death. Lesions or burning can be present on affected tissue. Peanut is very sensitive to glufosinate, but injury can be easily mistaken for paraquat or cell disrupter herbicides.

Herbicides with this mode of action: Glufosinate

Figure 17. 

Glufosinate injury.

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Figure 18. 

Glufosinate injury.

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Figure 19. 

Glufosinate injury.

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9) Glyphosate

Mechanism of Action: Glyphosate inhibits an enzyme (EPSP) that is responsible for the production of aromatic amino acids (tryptophan, tyrosine, and phenylalanine). Proteins regulate all activity that occurs within a cell, and no proteins can be formed without these essential amino acids. Halting amino acid production slowly starves the plant, and several days or weeks are required before symptoms or plant death is observed.

Behavior in Plants: Glyphosate moves within the plant and accumulates in growing points and young leaves.

Symptoms: The most common symptom of glyphosate injury is generalized chlorosis (leaf yellowing) that begins in the newest leaves and progresses to the entire plant. Bleaching can even occur. The degree and type of injury observed will depend on application rate and peanut growth stage. Distinguishing glyphosate injury from ALS herbicide injury is difficult if not impossible. Unless glyphosate injury is severe and persists for several weeks, peanuts generally make full recovery with peanut yield only slightly affected.

Figure 20. 

Severe Glyphosate injury.

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Figure 21. 

Slight Glyphosate injury. See chlorosis at the margins of the leaflets.

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Figure 22. 

Slight Glyphosate injury in a newer leaf. See the older leaf with no injury.

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Figure 23. 

Slight Glyphosate injury. See chlorosis at the margins of the leaflets.

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Figure 24. 

Glyphosate injury. Well-defined pattern.

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Figure 25. 

Old symptoms of Glyphosate injury.

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Figure 26. 

Slight Glyphosate injury. See chlorosis at the margins of the leaflets.

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10) Paraquat*

Mechanism of Action: Paraquat is a post-emergence herbicide with contact foliar activity. It is rapidly absorbed by green tissue and inhibits photosynthesis. The specific site of action is different from that of atrazine, and the results are a much more rapid onset of leaf death. Regardless, paraquat causes the formation of radical oxygen, which is toxic to plant cell membranes, within the chloroplast.

Behavior in Plants: Paraquat does not move within the plant and only acts on tissue that it contacts.

Symptoms: Paraquat causes rapid leaf burning on all species present at the time of application. Injury can be confused with the cell membrane disruptors or glufosinate. Paraquat can be separated from the cell membrane disruptors since paraquat does not result in bronzing around the burned lesion. However, injury symptoms of paraquat and glufosinate are almost indistinguishable. The only difference between the two is that paraquat injury will generally appear within 1 day of application, while glufosinate may require 3–4 days to develop symptoms.

Herbicides with this mode of action: Paraquat*

(*) Labeled in peanut.

Figure 27. 

Paraquat injury.

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Figure 28. 

Paraquat injury.

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Figure 29. 

Paraquat injury.

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This document is SS-AGR-327, one of a series of the Agronomy Department, UF/IFAS Extension. Original publication date December 2009. Revised January 2012. Reviewed October 2015. Visit the EDIS website at


S. Morichetti, former graduate assistant, Agronomy Department; J. Ferrell, professor, Agronomy Department; and R. Leon, assistant professor, Agronomy Department, West Florida Research and Education Center; UF/IFAS Extension, Gainesville, FL 32611.

Use herbicides safely. Read and follow directions on the manufacturer's label.

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U.S. Department of Agriculture, UF/IFAS Extension Service, University of Florida, IFAS, Florida A & M University Cooperative Extension Program, and Boards of County Commissioners Cooperating. Nick T. Place, dean for UF/IFAS Extension.