4.13.97
fopsdims.html
ACCase Inhibitors:
Aryloxyphenoxy Carboxylic Acid Sub-Family
General Information
The first commercial herbicide: diclofop-methyl in 1979. Sometimes called the "grass
killers" or the "fops". Developed first in Japan, and later in Germany
Inhibitors of graminaceous plants ("graminicides); exceptions: cultivated oats,
wheat, red fescue and annual bluegrass
Applied postemergence to the crop
Chemistry
Aryoxyphenoxypropionates, a subfamily of the aromatic carboxylic acid family
(including 2,4-D, dicamba)
Some members of this subfamily include:
-Diclofop-methyl (Hoelon)
-Fluazifop-butyl (Fusilade 2000/DX)
-Quizalafop-ethyl (Assure II):
Aryloxyphenoxy herbicides occur as racemic mixes of 2 stereoisomers
("left-handed" and "right-handed" versions with the same chemical
composition). Only the R enantiomer is phytotoxic. The implication of this is that
herbicides like fluazifop have a very specific binding site wherein phytotoxicity is
induced.
Because herbicides in this subfamily have very low water solubility, they are marketed as
esters.
Physiology of the Aryloxyphenoxys
Mode of Aryloxyphenoxy action
Aryloxyphenoxy herbicides have two important modes of action. Primary mode of action
is the inhibition of acetyl Coenzyme A carboxylase (ACCase), a key enzyme(s) in fatty acid
biosynthesis in the chloroplast.
There are 2 different forms of ACCase in higher plants. The different form in dicot
species may be a factor in the selective action difference between dicots and monocots.
Second mode of aryloxyphenoxy action: Depolarization of membranes. Depolarized membranes
have a greater resistance to ion movement.
Antagonistic herbicide mixtures. Mixtures of diclofop and 2,4-D resulted in loss of
diclofop activity but not that of 2,4-D.
Secondary effects: altered chloroplast structure, abnormal plastid membrane development
Mode of Aryloxyphenoxy Lethality
These aryoxyphenoxy herbicides act initially at and near meristems in susceptible
species, sites where considerable cell division and elongation occurs.
To provide necessary components of this growth, fatty acid biosynthesis is very active.
The primary lethal action is the inhibition of this biosynthesis in the meristem, because
of which plant growth ceases. Secondary effects to this cessation of growth include
chlorosis and necrosis.
Uptake and Movement of the Aryloxyphenoxys in Plants
Readily absorbed by both plant root and shoot tissues.
Foliar uptake occurs in hours, and little loss of herbicidal activity will result if
rainfall occurs after 6 hours or more from foliar applications.
These lipophilic ("oil-loving") herbicides strongly absorb into cuticle
epicuticular waxes and slowly desorb into the plant apoplast. Greater absorption into
plants occurs with greater air relative humidity.
Once these aryoxyphenoxy herbicides enter the plant there is a considerable range of
translocation of them in the plant:
-Diclofop translocates only a short distance in plants. This poor ability to translocate
may be due to their rapid uptake into cells nearest the uptake site diclofop which is only
effective on small annual grass seedlings. Spray droplets of diclofop must fall on the
plant near the growing point, or be taken up by roots near growing areas, to be effective.
-Translocation of aryloxyphenoxy herbicides such as fluazifop is also limited, but the
small portions of applied chemical that do move are very toxic in susceptible species. The
1-10% of applied herbicide that translocates is distributed both symplastically and
apoplastically. Apparently, just a few molecules at the active site are very effective.
That portion of the chemical that does translocate, tranlocates rapidly to meristems
(apical and root) and areas of rapid growth in the plant.
Basis of Selectivity between Plant Species
The basis of aryloxyphenoxy (and cyclohexandione) selective action between species follows
the monocot-dicot line with few exceptions. With aryloxyphenoxy herbicides other than
diclofop, uptake, translocation and metabolism are similar in resistant and susceptible
species.
Selectivity between species, except diclofop, is a function of differences in the target
enzymatic site of toxic action, acetyl CoA carboxylase (ACCase).
Selectivity of diclofop within different species is a function of metabolism. Diclofop
selectivity follows the monocot-dicot line, with the notable exception of diclofop
tolerance in wheat, cultivated oats (but not wild oat), and several important pasture
fescue grasses.
Crop resistance in maize. Research at the University of Minnesota has produced several
corn genotypes resistant to sethoxydim and, to a lesser extent, some aryloxyphenoxy
herbicides.
Resistance in Weeds.
Resistance in natural populations to aryoxyphenoxy and cyclohexanedione herbicides has
been found in several species at this time. Both cases possess cross resistance to several
other different herbicide families.
-Lolium rigidum (annual ryegrass). Populations have been found in Australia with
high levels of resistance to herbicides in over seven different families:
aryloxyphenoxypropionates, cyclohexanediones, sulfonylureas, dinitroanilines, s-triazines,
triazinones and phenylureas. Many of the herbicides Lolium is resistant to have
never been applied in the fields they were found in.
-Alopecurus myosuroides (slender foxtail; blackgrass). Populations have been found
in England with high levels of resistance to several different chemical groups:
sulfonylureas, s-triazines, aryloxyphenoxypropionates, phenylureas, triallate,
cyclohexanediones, barban and pendimethalin. The resistance in both countries seems to be
based on herbicide metabolism.
Others: giant foxtail, large crabgrass resistant to both aryloxyphenoxy's and
cyclohexenones (Wisconsin). Johnsongrass resistant to aryloxyphenoxy's (Mississippi)
Fate of the Aryloxyphenoxys in the Environment
Soil
Most aryoxyphenoxy herbicides have some soil activity on plants after postemergence
applications, but their ability to inhibit weeds from soil residues is limited. Reliable
weed control from soil applications of these herbicides is not significant.
Most are degraded microbially in the soil in a matter of days or weeks.
Aryloxyphenoxy herbicides have low solubility in water and are stable in the soil.
Losses due to volatility, photodegradation or leaching are negligible.
They are strongly adsorbed by the soil colloidal fraction.
Ester forms of these chemicals are rapidly deesterified, hydrolyzed, in the soil.
Aryloxyphenoxy herbicides in racemic mixes undergo stereochemical transformation in the
soil. Soil mediated racemization reactions favor the phytotoxic R enantiomer. The
conversion of the S to R stereoisomer has a half-life in the soil of 1-2 days.
Animal toxicology
Several experimental chemicals in this subfamily were not developed commercially due to
preliminary unfavorable toxicology problems.
Some members in this subfamily have been found to be mammalian liver toxicants.
Animals rapidly deesterify ester forms of these herbicides enzymatically with
monooxygenases.
Plant Injury Symptomology of the Aryloxyphenoxys in Plants
Often, the first symptom is very rapid cessation of growth, which is hard to see at
first. Herbicide translocation to apices and meristems stops growth very fast, and is
followed over a longer time period by leaf chlorosis, leaf tip "die-back", and
necrosis.
Leaf chlorosis, especially the youngest leaves, is often the first visible symptom. It is
followed by necrosis and leaf death.
Aryloxyphenoxy symptom development in susceptible species occurs slowly, often over days.
Phytotoxicity in seedlings with ample herbicide doses can occur more rapidly.
One of the best diagnositic symptoms is to pull the youngest leaf from a treated grass
plant days after treatment, the leaf may still appear green but the base of the leaf that
was inside the culm will be blackened and necrotic. This is due to the primary killing of
the growing point inside the grass culm.
Often the area around a droplet will have a water-soaked spot with disruption of internal
cellular membranes, chlorosis and possible necrosis. This spotting can occur on both
susceptible and resistant species.
Other symptoms can include leaf distortion, puckered or bunched leaves, and leaf cupping.
Occasionally leaf color can become mottled or speckled in chlorosis pattern.
Maize injury often is first seen in the whorl as chlorosis on leaves near the shoot apex.
BackTo:
