PPO Inhibitor (Cell Membrane Disruptor) Herbicides

• 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.

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.

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*

* 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.

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.

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.

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.

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.

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.

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.

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.

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