An Overview of the Mechanisms of Action of Herbicide Safeners

Abstract

Abstract Herbicide safeners are chemicals used for manipulating the tolerance of large-seeded grass crops to selected soil-applied herbicides. The physiological interactions of herbicides and their respective safeners are characterized by the following facts: a) safeners are most effective when applied prior to or simultaneously with the herbicides whose injury they prevent; b) safeners exhibit a high degree of botanical and chemical specificity protecting only certain grasses against injury caused from specific classes of herbicides; and c) protected grass crops are moderately tolerant to the antagonized herbicides. At the biochemical level, safeners may act either as “bioregulators” regulating the amount of a given herbicide that reaches its target site in an active form or as “antagonists” of herbicidal effects at a similar site of action. A safener-induced enhancement of herbicide detoxication in protected plants is currently viewed as the most apparent mechanism for the action of the currently available safeners. Safeners enhance the conjugation of carbamothioate and chloroacetanilide herbicides with glutathione either by elevating the levels of reduced glutathione (GSH) or by inducing the activity of specific glutathione S̱-transferases (GSTs). A safener-induced enhancement of the activity of other degradative enzymes such as the cytochrome P450-dependent mixed function oxidases or UDP-glucosyl transferases seems to be important for the protective action of safeners against injury from aryloxyphenoxypropionate, imidazolinone, and sulfonylurea herbicides. Metabolic processes related to acetyl-CoA metabolism have been implicated as likely target sites for a competitive antagonism between safeners and chloroacetanilide or carbamothioate herbicides. At the molecular level, the “gene activation” and “gene amplification” theories offer a likely explanation for the action of safeners.