This family of herbicides are translocated through the transpiration stream (xylem; apoplastic translocation) with initial symptoms occuring on old growth. Susceptible seedlings will have green cotyledons, chorotic to necrotic first true leaves, and progressively less injury occurring further up the plant. Death can occu early as a few days to as late as two weeks or more.
Inhibition of photosynthesis
in photosystem II (PS II) is caused by a block in the transfer of electrons
from plastiquinone and cytochromes. Since the electrons are not converted
to stored chemical energy (ATP and NADPH) in PS II, they form free radicals
that result in cell membrane destruction. Cell membrane disintegration result in plant death.
Photosynthesis is the process by which plants use light energy to convert carbon dioxide (CO2) and water to glucose and oxygen (O2). Photosynthesis occurs within the chloroplasts of plant cells. A single chloroplast is made up of many layers of thylakoid membranes (granum) that are surrounded by a liquid medium called the stroma. Embedded within the thylakoid membranes are photosystem complexes.
The photosystem complexes are composed of energy absorbing pigments (chlorophyll A and B, xanthophylls, and carotenoids) capable of harnessing light energy from the sun and funneling the energy through a pathway capable of creating energy rich compounds (ATP and NADPH+). The light energy is transferred to a P680 reaction center, creating an excited state electron. This electron is passed to pheophytin and then to a protein-bound plastoquinone molecule called QA. QA, in turn, passes the electron to a protein-bound plastoquinone called QB via a nonheme iron. When a second electron is passed to QB from QA, the fully reduced quinone then becomes protonated (two hydrogen ions are added) to form a bound plastohydroquinone (QBH2). The binding affinity of the QBH2 is low, thus another plastoquinone molecule from the plastoquinone pool in the membrane can easily displace it. The function of the reduced QBH2 is to transfer electrons between PS II and a cytochrome b6f complex, which in turn transfers electrons to PS I via plastocyanin.
This reaction center (specifically the D1 protein), is the site of action for the Triazines (e.g. atrazine and simazine) and Phenlyureas (e.g. linuron). These herbicides inhibit photosynthesis by binding to the D1 protein at the binding site for QB. When electron flow is blocked, the singlet chlorophyll energy cannot be transferred to the PS II reaction centers. The singlet energy state of chlorophyll molecules (including the P680 dimer) can be transformed to a longer-lived, triplet state. Some triplet-state chlorophyll is formed during normal photosynthesis and is dissipated by carotenoids, however, because of the mass of triplet chlorophyll molecules produced by blocking electron flow through PS II, the carotenoid quenching system is overloaded. The excess triplet chlorophyll causes initiation of lipid peroxidation by two mechanisms. The first, although not unequivocally proven, is the direct formation of a lipid radical in unsaturated fatty acids. The second is triplet chlorophyll, with a lifetime sufficiently long to react with oxygen, forms reactive singlet oxygen from ground state oxygen. Some singlet oxygen is produced during normal photosynthesis and is dissipated by carotenoids on PS II, but as in the case of carotenoid quenching of triplet chlorophyll, the carotenoid system becomes overloaded in the presence of photosynthesis inhibitors.