366 Produce Degradation: Reaction Pathways and their Prevention
supply. Diphenyl ethers, oxadiazoles, and triazolines inhibit the mitochondrial mem-
brane-bound enzyme protoporphyrinogen oxidase, thus interfering with chlorophyll
synthesis and causing accumulation of porphyrins in susceptible plants [74]. The
photosensitizing action of porphyrins causes membrane lipid peroxidation, which
results in irreversible damage to the membrane’s function and structure. Other cell
membrane disrupters are clomazone and norflurazon. They block carotenoid biosyn-
thesis, leading to peroxidation and destruction of chlorophyll (chlorosis) and mem-
brane lipids (cell leakage) by singlet oxygen, because the function of carotenoids
consists of dissipation (quenching) of oxidative energy of singlet oxygen produced
during photosynthesis [5,75].
Postemergence herbicides are applied mainly on the weed foliage after seeds
have germinated, thus controlling already emerged and growing plants. Foliage-applied,
systemic herbicides may inhibit protein or lipid synthesis or be synthetic auxins
[1,5]. Various carboxylic acidic compounds, such as (2,4-dichlorophenoxy)acetic
acid (2,4-D), may act like auxin, causing abnormal growth, which results in the
plant’s death. Sulfonylureas and imidazolinones inhibit synthesis of the branched-
chain amino acids valine, leucine, and isoleucine, and glyphosate and its salts prevent
synthesis of aromatic amino acids, leading to disruption of protein and DNA syn-
thesis. Aryloxyphenoxypropionates act as acetyl CoA inhibitors, thus blocking the
biosynthesis of fatty acids.
Foliage-applied, contact herbicides generally interfere with photosynthesis [1,5].
Bentazone, pyridate, and the hydroxybenzonitriles bromoxynil and ionoxynil are
inhibitors of the Hill reaction, whereas glufosinate-ammonium and bilanofos inhibit
glutamine synthetase, leading to accumulation of ammonia and consequently inhi-
bition of photophosphorylation in photosynthesis. Popular postemergence herbicides
and preharvest desiccants, the quartery ammonium (bipyridylium) compounds diquat
and paraquat, need light and oxygen for their action. During photosynthesis, they
can be reduced (by electrons from the photosystem I) to relatively stable radical
cations. In the presence of oxygen, these free radicals are reorganized to the original
ions and superoxide anions are formed, leading to disruption of cell membranes and
cytoplasm (the ultimate toxicant responsible for peroxidation of membrane lipids is
probably hydrogen peroxide originating from the superoxide anion) [76]. Similarly
to glyphosate, the cationic nature of diquat and paraquat causes their inactivation
on contact with soil due to strong interactions with soil colloids.
Herbicides can be applied pre- and postplanting; postplanting treatments may
be termed post- or preemergence depending on whether the crop plant has already
emerged [73]. In all crop planting stages, pre- or postemergence herbicides can be
used depending on the stage of the weed’s growth. For instance, if the crop has
emerged but no weeds are present, the herbicide application is postemergence to the
crop but preemergence to the weeds and herbicides would be applied to the soil
surface. If both the crop and the weeds have emerged, the application is postemer-
gence to both weeds and crops and would usually be directed to the weed foliage
or a selective herbicide would be used to avoid crop losses. With regards to pre-
planting treatments, soil fumigation (e.g., with metam-sodium) is a very effective
preemergence weed control that prevents weed seed germination and also kills other
soil-dwelling pests.