PPO Inhibitor (Cell Membrane Disruptor) Herbicides

Crop Insights written by Michael DeFelice, Ph.D.1

Summary

  • The protoporphyrinogen oxidase (PPO) inhibitors are primarily contact-type, postemergence, broadleaf-weed herbicides, but a few have preemergence soil activity.
  • The primary mechanism of action of these herbicides is inhibition of the PPO enzyme which ultimately leads to disruption of cell membranes.
  • The most common visual symptoms of PPO herbicides are leaves that become chlorotic (yellow), then desiccated and necrotic (brown) within 1 to 3 days.
  • The youngest leaves of tolerant plants may show yellow or reddish spotting (called ‘bronzing’). Soil-applied PPO inhibitors can cause yellowing, burning, stunting, girdling and stand loss of seedling plants.
  • A single dominant gene for resistance to PPO herbicides has been confirmed in soybeans that have greater tolerance to these herbicides than varieties without the gene.

Introduction and History of PPO Inhibitor Herbicides

Protoporphyrinogen oxidase (PPO) inhibitors are mainly contact, foliar-applied herbicides that have limited translocation in the xylem. A few are also soil-applied and taken up by the roots. There are several herbicide families classified as PPO inhibitors. Inhibition of the PPO enzyme ultimately leads to accumulation of peroxidative agents that cause the breakdown of cell membranes. For this reason, the PPO inhibitors are also called cell membrane disruptors. The Herbicide Resistance Action Committee and the Weed Science Society of America classify seven herbicide families in this group (Table 1). These families are the diphenylethers, N-phenylphthalimides, oxadiazoles, phenylpyrazoles, thiadiazoles, triazolinones and the triazolopyridinones.

Use of PPO inhibitor herbicides has increased in recent years to manage glyphosate-resistant populations of weeds like common waterhemp.

Figure 1. Use of PPO inhibitor herbicides has increased in recent years to manage glyphosate-resistant populations of weeds like common waterhemp (Amaranthus rudis).

The first PPO inhibitor herbicides were introduced in the 1970’s and early 1980’s. The diphenylethers were the first widely used family of PPO inhibitor herbicides. These herbicides have been labeled primarily for preemergence and postemergence annual broadleaf weed control. However, some of these herbicides also have limited preemergence grass activity. They are widely registered for many agronomic and horticultural crops.

Table 1. PPO families and herbicides*

Herbicide Company Trade Names**
Diphenylethers
    acifluorfen-sodium  United Phosphorus Blazer®, Ultra Blazer®
    bifenox Bayer CropScience Modown
    chlomethoxyfen Syngenta Ekkusugoni
    chlornitrofen Mitsubishi Chemical MO
    ethoxyfen-ethyl Hungarian Chemical Industries Buvirex
    fluoroglycofen-ethyl Dow AgroSciences Compete, Satis
    fomesafen Syngenta Reflex®, Flexstar®
    lactofen Valent Cobra®
    oxyfluorfen Dow AgroSciences Goal®
N-phenylphthalimides
    cinidon-ethyl BASF Lotus
    flumiclorac-pentyl Valent/Sumitomo Resource®
    flumioxazin Valent/Sumitomo Valor®
Others
    flufenpyr-ethyl Valent/Sumitomo  
    pyraclonil Bayer CropScience  
Oxadiazoles
    oxadiargyl Bayer CropScience Raft™, Topstar®
    oxadiazon Bayer CropScience Ronstar®
Oxazolidinediones
    pentoxazone Kaken  
Phenylpyrazoles
    fluazolate Bayer CropScience/Monsanto Twin-Agro
    pyraflufen-ethyl Nichino Milan
Pyrimidindiones
    benzfendizone FMC  
    butafenacil Syngenta Inspire®
    saflufenacil BASF Kixor®
Thiadiazoles
    fluthiacet-methyl Syngenta Action®
    thidiazimin Bayer CropScience  
Triazolinones
    azafenidin DuPont Evoluso
    carfentrazone-ethyl FMC Aim®
    sulfentrazone FMC Authority®

* Heap, I. The International Survey of Herbicide Resistant Weeds. Online. Internet. Thursday, August 27. 2015. Available www.weedscience.org. Herbicide Handbook of the WSSA. 2014. Only commercialized active ingredients are listed.

** All herbicides are Trademarks or Registered Trademarks of their respective manufacturers. Only a representative sample of the trade names containing these active ingredients are listed.

Mode of Action

The primary mechanism of action of the PPO inhibitor herbicides is inhibition of the protoporphyrinogen oxidase enzyme (also called Protox). The Protox enzyme controls the conversion of protoporphyrinogen IX to protoporphyrin IX. The result of inhibiting the Protox enzyme is accumulation of singlet oxygen in the presence of light. This leads to a light-induced breakdown of cell components. Cell membranes are destroyed by this light peroxidation reaction which results in cell leakage, inhibited photosynthesis, and finally bleaching of chloroplast pigments. The primary site of action is cellular membranes where Protox is mainly located.

The PPO inhibitor herbicides are absorbed mostly by leaves, with some limited root absorption. These are mainly contact-type herbicides that are translocated primarily in the xylem, although movement within the plant from leaf absorption is very limited. Herbicide degradation in the plant is through conjugation with glutathione and/or glucose. The mechanism of selectivity in tolerant plants appears to be breakdown of the herbicide to inactive metabolites. Metabolic breakdown is much slower in susceptible weed species than in tolerant plant species. A resistance gene has also been discovered in resistant weeds that involves a unique codon deletion in the PPX2 gene. It is suspected that metabolic degradation may also play a role in weed resistance to PPO herbicides.

Physical and Chemical Properties

Many of the PPO inhibitors are foliar-applied, contact-type herbicides. Plant absorption is increased with high relative humidity. Most of these herbicides require spray additives to improve foliar coverage and leaf absorption. Spray additive recommendations should be followed closely because using the wrong additive can lead to greater crop response. The PPO-inhibiting herbicides have low volatility, low toxicity to mammals, and very favorable environmental impact profiles. Most of the herbicides in these families are fairly immobile in soil through strong adsorption to soil organic matter and clay. These herbicides are primarily degraded by sunlight (photodegradation) and microbial action. The soil-active members of these herbicide families have somewhat short half-lives with short to moderate residual activity in the four to six week range.

Symptoms

The PPO inhibitor herbicides are primarily foliar-applied and have limited soil activity. They are contact-type herbicides that primarily affect only the sprayed plant tissues. The leaves of susceptible plants will quickly become chlorotic (yellow), then desiccated and necrotic (brown) within one to three days. The youngest leaves of tolerant plants may show yellow or reddish spotting (called ‘bronzing’) and plants can be temporarily stunted. Soil-applied PPO inhibitors cause rapid yellowing, necrosis, stunting, and death of germinating susceptible plants.

Soybean leaf bronzing due to acifluorfen.

Figure 2. Soybean leaf bronzing due to acifluorfen.

The degree of plant response will vary with application rate, stage of plant growth, plant species, plant (or crop) variety, and environmental conditions. Plant response tends to be more severe and common with high humidity, and extremely cool or hot temperatures.

Plant response to the soil-applied PPO inhibitors tends to be greater with saturated soils or following high intensity rainfall that splashes treated soil onto young seedlings. These herbicides can cause yellowing, burning, girdling, stunting and stand loss of plant seedlings under severe environmental conditions.

Soybean seedling showing sulfentrazone splash injury.

Figure 3. Soybean seedling showing sulfentrazone splash injury, resulting in burning of the hypocotyl and cotyledon tissue.

Differential Response in Soybean Varieties

University of Arkansas and Auburn University researchers discovered differences in susceptibility among soybean varieties to sulfentrazone. Their research indicated susceptible varieties lacked a gene for tolerance to PPO-inhibiting herbicides. Additional research conducted by Pioneer and the University of Arkansas confirmed that the gene for resistance was a single dominant trait. Pioneer has published charts that identify Pioneer® brand soybean varieties that have lower tolerance to PPO herbicides with more potential for exhibiting crop injury. Screening for PPO tolerance is an on-going program at Pioneer.

Guidelines for Using PPO Inhibiting Herbicides in Soybean and Corn Production

The PPO-inhibiting herbicides are valuable broadleaf weed control tools in soybean and corn production systems. Important herbicides in this group can provide quick control of many difficult-to-control broadleaf weed species including morningglory, Palmer amaranth, waterhemp and velvetleaf. The contact-type herbicides require good foliar coverage. The soil-applied herbicides require rainfall for good “activation.” Herbicide performance is enhanced by using higher spray volumes to maximize coverage. Weed control is also improved under good growing conditions and higher relative humidity.

Carfentrazone herbicide symptomology - corn plant leaves.

Figure 4. Carfentrazone herbicide symptomology on corn.

The level of crop tolerance to PPO-inhibiting herbicides varies with the specific herbicide, crop genetics and environmental conditions. Most crop responses to these herbicides occur during extended periods of high humidity, very low or high temperatures and/or wet soils. Crop response is mostly cosmetic and short-lived since there is very little translocation within the plant. Applying these herbicides at the correct growth stage, using only recommended spray additives, and avoiding conditions of crop growth stress will minimize crop response and provide the greatest level of weed control.

References

Anonymous. 2014-2015. EPA- approved herbicide labels produced by their respective manufacturers.

Anderson, W. P. 1996. Weed Science: Principles and Applications, 3rd ed. West Publishing Company. Minneapolis/St. Paul. 388 p.

Duke, S. O., J. Lydon, J. M. Becerril, T. D. Sherman, L. P. Lehnen, and H. Matsumoto. 1991. Protophyrinogen oxidase-inhibiting herbicides. Weed Sci. 39:465-473.

Gonsolus, J. L. and W. S. Curran. 1998. Herbicide Mode of Action and Injury Symptoms. North Cent. Reg. Ext. Pub. No. 377. Univ. of Minnesota. 17 pp.

Heap, I. M. 2015. International Survey of Herbicide-Resistant Weeds. Web site: http://www.weedscience.com, Weed Science Society of America and the Herbicide Resistance Action Committee, Corvallis, OR.

Patzoldt, W. L., A. G. Hager, J. S. McCormick, and P. J. Tranel. 2006. A codon deletion confers resistance to herbicides inhibiting protoporphyrinogen oxidase. Proc. of the Nat. Acad. of Sci. of the United States of America. 103:329–334.

Retzinger, E. J. and C. Mallory-Smith. 1997. Classification of herbicides by site of action for weed resistance management strategies. Weed Technol. 11:384-393.

Schmidt, D. H., M. D. Vogt, M. S. DeFelice, D. K. Steiger, G. L. Morelock, G. A. Lubich, B. R. Millard, J. D. Hicks, and P. W. Handley. 1998. Response of soybean genotypes to sulfentrazone. Proc. South. Weed Sci. Soc. 51:4.

Shaner, D. L. (ed). 2014. Herbicide Handbook, 10th Ed. Weed Science Society of America. Manhattan, KS. 513 p.

Swantek, J. M., C. H. Sneller, and L. R. Oliver. 1998. Evaluation of soybean injury from sulfentrazone and inheritance of tolerance. Weed Sci. 46:271-277.

1 Former Senior Manager: Herbicide, Ag Traits & Seed Treatments; Pioneer

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The foregoing is provided for informational use only. Please contact your Pioneer sales professional for information and suggestions specific to your operation. Product performance is variable and depends on many factors such as moisture and heat stress, soil type, management practices and environmental stress as well as disease and pest pressures. Individual results may vary.