Difenoxuron (commercially known as Lironion) is a phenylurea herbicide used to control annual broad-leaved weeds and grasses in allium crops (predominantly onions),[3][4] carrots, jojoba, and celery.[5][6][7]
Difenoxuron is a member of the phenylurea class of herbicides. Phenylureas inhibit photosynthesis at photosystem II by binding to the serine 264 residue of the D1 protein, occupying the Qb (secondary plastoquinone) binding site and hence halting electron transfer from the primary acceptor Qa to the secondary acceptor Qb.[10] This prevents CO2 fixation and energy production.[11]
Moreover, this blockade prevents chlorophyll from transferring energy to Qa, increasing production of triplet-state chlorophyll, which reacts with molecular oxygen to form singlet oxygen, a highly reactive species that oxidatively damages the pigments, lipids and proteins of the photosynthetic thylakoid membrane.[11]
Herbicidal activity
Liming in Boddington soil has been shown by a 1976 study to increase the herbicidal toxicity of difenoxuron by two to three times compared to soil without the additional level of liming.[12]
Toxicology
Difenoxuron's hazards include acute toxicity caused by oral ingestion, and acute toxicity of inhalation. There are very few studies about the genotoxicity of difenoxuron and these studies are inconcordant but there appears to be a dose dependent relationship between the concentration of difenoxuron and rate of observed chromosomal aberrations.[4]
^ abRoberts TR, Hutson DH, Lee PW, Nicholls PH, Plimmer JR, Roberts MC, Croucher L, eds. (2007). "Ureas". Metabolic Pathways of Agrochemicals: Part 1: Herbicides and Plant Growth Regulators (1st ed.). Cambridge: Royal Society of Chemistry. pp. 705–772. doi:10.1039/9781847551382-00705. ISBN9780854044948.