Herbicide-Mediated Hormesis - ACS Symposium Series (ACS

Chapter 10

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Herbicide-Mediated Hormesis Regina G. Belz*,1 and Stephen O. Duke2 1Agroecology

Unit, Hans-Ruthenberg-Institute, University of Hohenheim, Stuttgart 70593, Germany 2National Center for Natural Products Research, Agricultural Research Service, United States Department of Agriculture, Oxford, Mississippi, United States *E-mail: [email protected].

Hormesis is the stimulatory effect of a subtoxic level of a toxin. This phenomenon is common with most herbicides on most plant species, although the effect is generally difficult to quantitatively repeat, even under laboratory conditions. The magnitude of and the dose required for hormesis is influenced by many biological and environmental parameters. Hormesis with glyphosate seems to be more consistent than with most other herbicides, perhaps due to its unique mode of action as a herbicide. However, little is known of the mode of action of any herbicide-mediated hormesis. Herbicide-induced hormesis may play a role in the evolution of herbicide resistance. Although subtoxic levels of herbicides are sometimes used to stimulate certain desired crop responses (e.g., sucrose accumulation in sugarcane), the unpredictability of hormesis makes it too risky for general crop production. A better understanding of plant hormetic responses to herbicides is needed.

© 2017 American Chemical Society Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


Hormesis, the stimulatory effect of a subtoxic dose of a toxin or a stress, is a relatively simple concept, yet it is poorly understood (1, 2). Hormesis is observed with almost all toxicants and on almost all organisms. The earliest synthetic herbicides, the auxinic herbicides, have been known to stimulate plant growth at subtoxic levels for many years (e.g., (3)). Meanwhile, hormesis has been reported with almost all herbicide classes and modes of action. These studies have been summarized in several previous reviews (4–11). Hormesis is also common in insects exposed to low doses of insecticides (12) and plant pathogens exposed to low fungicide doses (13). Hormesis is a common phenomenon, and we know that weeds and non-target plants are commonly exposed to a range of herbicide doses, including those that will cause hormesis (14). However, little consideration is given to what the environmental, ecological, and evolutionary implications of hormesis could be. This short chapter will provide a summary of previous work on herbicide hormesis and bring the reader up to date with more recent findings related to this topic.

The General Phenomenon The doses of a toxicant required for hormesis are generally found in a narrow range just before the negative effects of the toxin begin. Hormesis is represented by a biphasic dose-response curve. Most dose-response studies of herbicides have not captured this phenomenon because the concentrations used have not been sufficiently low or have not had concentrations in the often narrow hormetic range. For most herbicides, the effect is 15 to 30% stimulation in the laboratory and slightly less under field conditions (10), although there are cases in which there is no detectable or significant hormesis and others with which the effect is much more than 30% (see ref. (11) and glyphosate section below). Whether one finds hormesis or not and the magnitude of the effect found depends on many factors. One of these is the parameter endpoint measured. For example, the same concentration of a phytotoxin can have no effect on root growth, while increasing shoot growth (15). The hormetic dose can vary for different parameters. Velini et al. (15) reported 2 g ha-1 of glyphosate to stimulate root growth of Pinus caribaea Morelet maximally, whereas for leaf growth, the optimal hormetic dose was 20 g ha-1 (Figure 1). The plant growth stage at the time of herbicide exposure can also have a profound influence on hormesis. For example, De Carvalho et al. (16) found glyphosate hormesis in coffee (Coffea arabica L.) plants exposed at 35 days after transplanting, but not in plants exposed at 10 days (Figure 2). The time after treatment with the herbicide can also be a critical factor in detecting hormesis, since the phenomenon represents a dynamic process. For example, hormesis was easily detectable in barley (Hordeum vulgare L.) treated with a range of glyphosate doses up to seven weeks after spraying, but the effect disappeared thereafter, with no effect on growth or grain yield at doses that had been hormetic to growth of the plants earlier (17) (Figure 3). These dynamics further imply that the hormetic dose range can change with time after treatment. For example, the glyphosate dose that caused increases in growth rate of Bracharia brizantha (Hochst.), was higher at 30 days after application than at 15 days (18). 136 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


Figure 1. Dose-response curves for glyphosate effects on growth of different organs of Pinus caribea. Reproduced with permission from Reference (15). Copyright 2008 John Wiley & Sons.

Figure 2. Coffee (Coffea arabica) plant height at 60 days after being exposed to glyphosate applied to plants at 10 days (A) and 45 days (B) after transplanting. Reproduced from Reference (16) and used under a Creative Commons Attribution-NonCommercial 3.0 license. Published 2013 by Academia Brasileira De Ciencias. 137 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


Figure 3. Barley (Hordeum vulgare) plant weights at different times after spraying a range of glyphosate doses. The one week results show results of a second experiment. Reproduced with permission from Reference (17). Copyright 2008 Elsevier Applied Science Publishers. Nutrient status can affect herbicide-induced hormesis. Cedergreen et al. (19) found that nitrogen, but not phosphorus limitation, can allow and/or enhance glyphosate-mediated hormesis in hydroponically-grown barley. In duckweed (Lemna minor L.), glyphosate-mediated hormesis was seen on both nitrogen- and phosphorus-deficient plants, and the authors hypothesized that glyphosate might act as a source of phosphorus. Atmospheric CO2 levels, light intensity, and temperature can have profound effects on hormesis (11). Pre-stressing a plant with another chemical or with the same chemical can influence hormesis as well. For example, glyphosate hormesis was only found in lettuce root length in plants that had been pre-stressed with a pelargonic acid or methanol exposure (20). Pre-exposure to a hormetic dose of glyphosate affects a later dose-response curve. Silva et al. (21) found a greater stimulation of growth by a hormetic dose of glyphosate in soybean plants that had received a preconditioning hormetic dose of glyphosate 14 days earlier. Calabrese (22) reported that such preconditioning effects on hormesis are common in nonherbicide studies of hormesis. We have mentioned only a few of the many parameters, both environmental and plant aspects that can influence whether herbicide-mediated hormesis is found and the magnitude of the effect. Hormesis is influenced by almost every parameter that has been tested, which makes it a phenomenon that is sometimes difficult to reproduce with even slight changes in an experiment.

What Causes Herbicide Hormesis? The mechanism(s) of hormesis is (are) poorly understood. If the mode of action of the stimulation at lower doses is unrelated to that of the inhibition at higher doses, one could expect a relatively wide hormetic peak if the stimulatory effect occurs at a sufficiently low dose. But, the stimulatory peak is generally a rather narrow dose range just before inhibition begins, which 138 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


supports the hypothesis that hormesis is caused by responses to very mild stress caused by a toxin, presumably as a secondary effect of the toxin affecting its target. In animals, hormesis has been associated with the production of cellular increases in cytoprotective and restorative proteins such as growth factors and antioxidants (23). If all of this is the case, the phenomenon of hormesis is due to secondary and tertiary effects of mild stress resulting from the target site of the toxicant being affected. There is some evidence for this “mild stress” hypothesis in the case of glyphosate, a case in which we can easily see a biomarker for the herbicide affecting its target site. Shikimic acid accumulates to high levels in glyphosate-treated plants as a result of inhibition of 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), a key enzyme of the shikimate pathway (24, 25), and even at hormetic doses, shikimate levels increase in most plants (i.e., (15)). Neither hormesis nor shikimate was found in glyphosate-resistant soybean at glyphosate doses that cause hormesis in glyphosate-susceptible soybean (15). Thus, glyphosate hormesis seems to be tied to the stress caused by the herbicide at the herbicide target site, and not to an effect by some other mechanism. In rare cases, a herbicide can be transformed to a plant growth-stimulating compound, so that, under some conditions, one might mistake the effect for a direct hormetic effect of the herbicide. For example, sulcotrione can be phototransformed to a compound that is further converted to a mimic of salicylic acid (26). This compound is a root growth enhancer. So, this process might explain the mechanism of some of the sulcotrione-mediated hormesis.

Glyphosate-Mediated Hormesis – A Special Case? Glyphosate is the most important herbicide in history (27). Thus, any aspect of its biological activity has importance. It is a relatively high use rate herbicide that is normally recommended to be used at 0.29 to 2.16 kg ha-1, depending on the weed species. Early in its use, it was found to enhance sucrose levels in sugarcane at low (40 to 180 g ha-1) doses (28), but these doses are normally quite phytotoxic, if not lethal to other plant species. Hormetic growth effects of glyphosate on sugarcane were observed with doses of 7 to 36 g ha-1 (29). Hence, the glyphosate-mediated sucrose accumulation may be in part or entirely caused by reduced sucrose movement to metabolic sinks that have reduced growth because of glyphosate toxicity. There have been more reported cases of hormesis with glyphosate than any other herbicide, with hormetic doses of 0.2 to 20 g ha-1 (11, 15, 21). The magnitude of the effect is sometimes much higher than that found with other herbicides. For example, in Commelina benghalensis L., a 100% increase was reported for shoot dry weight in response to ca. 0.2 g ha-1 glyphosate (15). In addition to the list of cases of glyphosate hormesis in our earlier review (14), there are several new reports. Cochavi et al. (30) found that glyphosate significantly enhanced Egyptian broomrape-infested carrot growth at ca. 100 g ha-1, apparently due to killing the broomrape. However, as it involves the interaction with another organism for an effect, it could be argued that this is not true hormesis. Pokhrel and Karsai (31) found 1% of the recommended 139 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


dose of commercially formulated glyphosate to promote biomass of Bryophyllum pinnatum (Lam.) Oken more than 50%. The magnitude of stimulation of some woody plants under certain environmental conditions and growth stages is quite high. For example, root dry weights of Eucalyptus grandis and Pinus caribea were increased to 210 and 153%, respectively, of the control value by ca. 2 g ha-1 glyphosate (15). However, the response of woody plants to glyphosate depends on many factors, and this magnitude of hormetic response is not always found. For example, Schrübbers et al. (32) found that although coffee plant height was increased by as much as 35% by 10-86 g ha-1 of glyphosate, no hormesis was found with leaf area and total biomass. The 86 g ha-1 dose caused increases in shikimic acid. But, this study did not include lower doses that might have maximized hormesis. Could glyphosate-mediated hormesis have additional direct mechanisms that add to the “mild stress” hypothesis? Hormetic doses of glyphosate can enhance photosynthesis (21, 33), but there is no evidence as to whether this is a direct effect or a secondary effect of mild stress from inhibition of the herbicide target site. Cedergreen et al. (19) speculated that glyphosate might be a plant phosphorous source in some cases, but this is unlikely to occur unless glyphosate is rapidly metabolized, which may not be the case in most plant species (34). Another hypothesis is that at hormetic doses, all or part of the carbon in the shikimate that accumulates would have been channeled into lignin, a product of the shikimate pathway. If so, stiffening of cell walls would be delayed, resulting in larger cells before growth stops, as suggested by Velini et al. (15). This could account for taller plants or longer roots, but it would not necessarily account for increased dry weight. Because the magnitude of the hormetic effect of glyphosate is generally greater than with most other herbicides, the question of whether sub-toxic doses of glyphosate can increase yield arises. Abbas et al. (35) reported that potted chickpea (Cicer arietinum L.) grain yield was increased 34% by a glyphosate dose of 7.2 g ha-1 applied at 4 weeks after seedling emergence. Number of seeds per plant was increased in four weed species (Chenopodium album L., Rumex dentalus L., Coronopus didymus (L.) Smith, and Lathyrus aphaca L.) by low (8-31 g ha-1) doses of glyphosate (36).

Can Herbicide Hormesis Be Harnessed? Considering population growth and global climate change, there is a dire need to improve crop productivity and stress tolerance (37). Low doses of many herbicides or other plant toxins are known to increase harvestable crop yield or other desired plant traits such as stress tolerance, and the use of herbicide hormesis for desired agronomic effects has been proposed in publications and patents. Furthermore, the potential for crop improvement by herbicide hormesis has been considered to be similar or greater than what can be achieved by breeding or modern biotechnology (10). Despite this tempting potential to enhance plant productivity and health and, thus, to provide a significant economic benefit for a farmer, harnessing herbicide hormesis has succeeded in only a few 140 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


cases. Examples of commercial exploitation of hormesis are the use of low doses of glyphosate and other herbicides as ripeners in sugarcane to enhance sugar production (38), the use of herbicide safeners to induce tolerance in crops to a followup herbicide treatment (39), and the use of low doses of several auxins and antiauxins as bioregulators for yield improvement (40–42). Furthermore, plant stimulatory responses to certain commercial biostimulants may also represent a hormetic response since some of these low-toxicity compounds may be phytotoxic at higher doses. This may especially apply for hormone containing products or substances extracted from plants (43). A fairly new effort in this regard is the restoration of crop yield losses caused by herbicides using such plant growth biostimulants. First reports show recovery rates of nearly 100% from herbicide injury causing yield losses up to 30% (44). Applications targeting preconditioning hormesis and, thus, the induction of hormesis before plants are exposed to stress may also be envisioned, e.g. young transplants or during bloom in order to protect highly stress sensitive growth stages. However, none of these few actual or proposed uses are labelled under the term (herbicide) hormesis, and few of the compounds mentioned are actually registered as a herbicide. What is it that makes the herbicide hormesis phenomenon so difficult to use commercially for general crop production? According to the current state of knowledge, its unpredictability makes it simply very risky. The examples given above and discussed in our earlier reviews (10, 11) show that hormesis varies quantitatively with many environmental and plant aspects and with time. Furthermore, since hormesis is at the low end of the dose-response curve and is followed by the negative effect as the dose increases, only a slight change in the dose reaching the molecular target site(s) can dramatically change the resulting response from no effect to a considerable negative effect if the dose range for hormetic responses is narrow. Figure 4 illustrates this practical constraint in the form of a spray application of the phytotoxin parthenin, a metabolite of the invasive weed Parthenium hysterophorus L., in two independent experimental runs conducted under semi-natural conditions (45). A parthenin dose of 0.23 kg ha-1 lead to a maximum stimulation of 38% over control in leaf area of Sinapis arvensis L. in one experiment, while the same dose applied in another experiment inhibited leaf area growth by 21%. The reasons for this may be manifold, however, looking at the untreated controls it is indicated, that the absence of hormesis in the one experiment may have been partly caused by unfavourable climatic conditions preventing S. arvensis plants from enhanced growth (45). Such an interference of hormesis formation with growth factors seems to widely apply in plant biology such that hormesis is unlikely to manifest itself under conditions preventing plants from enhanced growth, i.e. conditions leading to retarded/no plant growth or optimum growth (46). Plants under field conditions are inevitably exposed to multiple stressors at once or in sequence and, therefore, a low-dose application rate that reproducibly elicits a stimulatory response under all circumstances is highly unlikely. Or vice versa, the final outcome of a hormetic application under the conditions encountered in the field is hard to predict (10). Hence, finding the ‘ideal application window’ and predicting a reliable hormetic dose for a desired increase in final yield of economically relevant plant parts under particular field conditions seem to be the major reasons for the previous 141 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


failure to harness hormetic herbicides for crop growth and/or stress tolerance improvement (37). At the moment it seems unfeasible to overcome these practical problems in a field situation and, therefore, herbicide hormesis may continue to be economically worthwhile only in rare cases or under the more controlled conditions of a greenhouse or a floriculture setting of higher value crops.

Figure 4. Dose-response relationships for the effect of the phytotoxin parthenin applied as spray application under seminatural conditions on leaf area of wild mustard (Sinapis arvensis) in two independent experiments. Adapted from Reference (45) and used under a Creative Commons Attribution-NonCommercial 3.0 license. Published 2008 by Sage Publications. As it may never be possible to widely use the hormetic phenomenon as hitherto intended, Gressel and Dodds (37) proposed to change the strategy from direct field applications of hormetic herbicides to unraveling the genetic processes triggering and regulating hormesis and using this knowledge for transgenic breeding of improved crops as well as for screening more reliable hormetic compounds.

Influence on Evolution of Herbicide Resistance? Herbicide hormesis can also be associated with undesirable effects in an agricultural context and of particular importance seems to be the promotion of weeds by regular applications of herbicides for which they have evolved resistance (10, 11). Reports of growth stimulation in herbicide-resistant weeds by the herbicide to which they have evolved resistance are available for target-site (TSR) and non-target-site resistant (NTSR) biotypes. For example, at doses that severely damage the sensitive biotype, growth of acetyl-CoA carboxylase (ACCase)-TSR biotypes of Alopecurus myosuroides Huds. was stimulated 54% over the control by ACCase-inhibiting herbicides (10, 47), growth of acetolactate synthase (ALS) TSR biotypes of Matricaria inodora L. and Lolium perenne L. 142 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


were stimulated 31% (Figure 5) and 64%, respectively, by ALS-inhibitors (48, 49), and a psbA-TSR biotype of Chenopodium album L. showed a 37% maximum stimulation by terbuthylazine, a PSII inhibitor (Figure 5) (48). Furthermore, growth of triazine-NTSR annual bluegrass (Poa annua L.) was enhanced by 25 and 95% at simazine doses of 2.24 and 1.12 kg ha-1, respectively (50), and growth of glyphosate-resistant Eleusine indica (L.) Gaertn. proved much more responsive to low-dose stimulation by glyphosate than the wildtype (Figure 5) (48). The dose causing maximum stimulation of resistant weeds does not always match the field rate, but resistant weeds may still be considerably promoted by regular herbicide applications (10). This does not directly cause a selection pressure for evolution of resistance, but may indirectly promote the development of resistance by making hormetically enhanced resistant weeds more competitive, more resistant to a second weed control measure, or even more reproductive (10, 11). While early growth stimulation by herbicide hormesis is well documented for resistant weeds, an impact on competitive ability, repeated herbicide applications, or reproduction especially under practical field conditions is still to investigate. For glyphosate hormesis, however, results with sensitive plants have shown hormetic effects on reproduction (36, 39) as well as enhanced hormesis with a sequential low glyphosate dose (21), both of which could facilitate the evolution of resistance.

Figure 5. Dose-response relationships for sensitive and herbicide-resistant weed biotypes in germination assays. A: sensitive and glyphosate resistant Eleusine indica exposed to glyphosate; D: sensitive and ALS target-site resistant (TSR) biotypes of Matricaria inodora exposed to the ALS-inhibitors iodo-/mesosulfuron; I: sensitive and PSII-TSR Chenopodium album exposed to the PSII-inhibitor terbuthylazine. Reproduced from Reference (48) and used under a Creative Commons Attribution-ShareAlike 4.0 International license. Published 2014 by Julius-Kühn-Institut. Besides these obvious effects that herbicide hormesis may have on resistance evolution, Cutler and Guedes (51) hypothesized in connection with insecticide-induced hormesis in insects that hormetic doses may also be able to induce mutations that might support resistance or tolerance. Such an increase in mutation frequencies was assumed by Gressel (52) for sublethal pesticide doses and so it may also be conceivable that low-dose herbicide hormesis is a driver of resistance or tolerance endowing mutations. The phenomenon has so far been neither addressed in insects (51) nor weeds. Moreover, selective effects of low herbicide doses on individuals within a weed population may 143 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


be a further long-term aspect impacting herbicide sensitivity or resistance by undesired changes in population composition. Studies investigating herbicide hormesis usually consider the population level in the form of mean values without taking into account possible differences in responses of individual plants (e.g., (6, 7, 16, 45)). A weed population within an agricultural field, however, can be a very heterogeneous group of individual plants of the same species due to genetic variation or non-genetic variability. This variation substantiates the ubiquitous ability of a population to adapt to local stress factors, including herbicide exposures (53). It is, thus, likely that by ‘selective hormesis’ parts of a population are hormetically boosted, while others are not affected or are adversely affected by herbicides, which may lead to changes in population composition and ultimately in herbicide sensitivity. A very good example to demonstrate this ‘selective hormesis’ hypothesis are TSR populations of diploid species where the resistance appears heteroand homozygous. For example, a TSR field population of blackgrass (A. myosuroides) typically represents a mixed population of sensitive, heteroand homozygous resistant individuals with varying sensitivity to the selecting herbicide (54). A preliminary study with an ACCase-TSR blackgrass biotype indicated that splitting-up the monophasic response of the entire population to an ACCase-inhibitor into selective responses of individual genotypes gives considerable differences in efficacy and hormesis (Figure 6). An application rate of 25 g a.i. ha-1 clodinafop for instance completely controlled the sensitive individuals, while the heterozygous individuals were stimulated by 69% over control, and the homozygous individuals remained unaffected.

Figure 6. Dose-response relationships for the ACCase-inhibitor clodinafop applied as spray application in a greenhouse study on the aboveground biomass of the entire population of an ACCase target-site resistant biotype of Alopecurus myosuroides as well as the sensitive, hetero- and homozygous-resistant sub-populations. Data are from Reference (54). 144 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


‘Selective hormesis’ was, furthermore, observed in sensitive populations if exposed to low doses of herbicides. This may be relevant whenever low herbicide doses appear in practice, e.g. drift deposition, run-off, errors in application, leaf contact of treated and untreated plants, protection by taller plants or mulch, or absorption of low doses from soil (10, 28). For a sensitive, high-density population of M. inodora exposed to the ALS-inhibitors iodo-/mesosulfuron (55) as well as for a model-population of lettuce (Lactuca sativa L.) exposed to the antiauxin PCIB [2-(p-chlorophenoxy)-2-methylpropionic acid] (53), selective stimulation of individual plants depending on the individual growth rate could be observed (Figure 7). The slow-growing individuals within the population (represented by the ≤10% percentile) were more sensitive and were more strongly stimulated than the total population, while the fast-growing individuals (represented by the ≥90% percentile) were less responsive both at being stimulated and inhibited. Hence, depending on the dose, such selective effects will change the size distribution within an exposed population. Figure 7 illustrates this selectivity for root and shoot length responses. Very low doses of PCIB of around 0.1 mM selectively promoted root elongation of the more sensitive slow-growing individuals with a maximum of 134% stimulation and, thus, lead to a decrease in overall size variation. The same PCIB dose selectively enhanced shoot elongation at a maximum of 53% stimulation, although shoot length was not promoted by PCIB at the population level and at the fast-growing individuals. At higher PCIB doses of around 0.5 mM root length of the less sensitive fast-growing individuals was promoted at most, while root growth of the slow-growing individuals was already severely inhibited. The same PCIB dose also severely inhibited shoot growth of the slowgrowing individuals, while shoot growth of the fast-growing individuals remained unaffected (Figure 7). Especially doses that selectively promote less sensitive, fast-growing individuals or leave them unaffected may shift a population towards less sensitive individuals which may in the long-run affect the herbicide sensitivity of a population.

Figure 7. Dose-response relationships for the antiauxin PCIB [2-(p-chlorophenoxy)-2-methylpropionic acid] in a germination assay on root length of the 10 and 90% percentile (%ile) of a population of Lactuca sativa (Left) and on shoot length of the 10 and 90%ile (Right). Data are from Reference (53). 145 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.

The relevance and ecological implications of selective effects of low doses of herbicides under field conditions are yet unknown. However, the examples point to the possibility that herbicide hormesis may have the potential for a hitherto underestimated factor in the development of weed resistance.


Parting Thoughts The implications of herbicide hormesis are many. Almost any plant growth or development parameter can be stimulated or enhanced by a low dose of almost any herbicide under the right conditions. The phenomenon is, however, too difficult to predict in the field for its use in yield or crop quality improvement for most crop/herbicide combinations. Nevertheless, unpredictable herbicide hormesis almost certainly occurs in crops. The economic impact of this is unknown. New information indicates that the variable hormesis parameters for subpopulations of the same weed species within a field results in selection for and against certain subpopulations by low herbicide doses. This phenomenon deserves more study to understand its full impact on the evolution of weed resistance to herbicides.

Acknowledgments The authors acknowledge the German Research Foundation for funding RG Belz’s research on herbicide-induced hormesis (Individual grant BE4189/1-2).

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