The Physiology and Mode of Action of the Dinitroaniline Herbicides

Publisher Website
Google Scholar
Abstract
The substituted 2,6-dinitroanilines were first reported as herbicides in 1960. At the present time, there are 14 2,6-dinitroaniline herbicides in various stages of product development. Literature on absorption, translocation, and mode of action of the dinitroaniline herbicides refers almost entirely to trifluralin (α,α,α-trifluoro-2,6-dinitro-N,N-dipropyl-p-toluidine) and nitralin [4-(methylsulfonyl)-2,6-dinitro-N,N-dipropylaniline]. These herbicides do not directly inhibit the germination of seed. Inhibition of lateral root development is the most characteristic growth response. Swelling of the root tip is a universally recognized morphological effect caused by these compounds. The cells in this region are multinucleate, indicating that the mitotic process has been disrupted. Examination of these cells shows an increase in the percentage of cells in arrested metaphase due to the disruption of spindle microtubules. Inference is made that the dinitroaniline herbicides affect chromosomes in a manner similar to colchicine, but research with pig brain (Sus scrofa) microtubules has shown that effects of the herbicide on microtubular protein is different. Injury to the top of plants is recognized by stunting, development of dark green color, and swelling and brittleness of the stem or hypocotyl. The major sites of uptake are the shoot of monocots and the hypocotyl or hypocotyl hook for dicots. Exposure of seedling roots to the dinitroaniline herbicides does not kill the plant, but exposure of the young shoot will result in death. Available data indicate that the dinitroaniline herbicides are either absorbed or adsorbed by the roots due to the proximity of the roots to the herbicide, but that translocation from the root to the top is minimal. When a dinitroaniline was found in the plant, the parent compound was the major product present with metabolites equal to 5% or less. Insufficient information is available to accurately describe effects of these herbicides on plant carbohydrates, lipids, and nitrogenous compounds. The effect of trifluralin on RNA and DNA varies with the plant species, treatment time, concentration of herbicide, and plant part investigated, but differences observed do not correlate with dinitroaniline-susceptible and resistant species. Enzyme activity does not appear to be greatly inhibited by the dinitroaniline herbicides. However, the dinitroaniline herbicides interfere with photosynthesis and respiration in vivo and in vitro. The phytotoxic action of trifluralin can be antidoted with the organophosphorus insecticides, phorate [0,0-diethyl-S-(ethylthiomethyl)-phosphorodithioate], disulfoton [0,0-diethyl-S-2-(ethylthioethyl)-phosphorodithioate], and externally applied lipids such as D-α-tocopherol. There is a strong correlation that seeds with a high lipid content are resistant to trifluralin and those with a low lipid content are susceptible. Despite all the work that has been conducted, the mode of action of the dinitroaniline herbicides is still unclear.