Binding to the Same Target Site

Competitive binding for an active site occurs when an antagonist acts reversibly on the same target site as the herbicide this mechanism has been 

Specific data on the binding affinity of these two sulfonylureas for ALS were not provided.  

In other studies, it was shown that pretreatment with the safeners dichlormid and naphthalic anhydride (NA) increased significantly the activity of ALS in treated corn seedlings. The in vitro inhibition of ALS by chlorsulfuron, however, was either unaltered or increased by pretreatment with the safeners. Rubin and Casida proposed that the dichlormid-induced elevation in ALS activity in vivo is sufficient to offer partial protection to corn against injury from the herbicide chlorsulfuron. In similar studies on the interactions between safeners and imidazolinone herbicides, Barrett failed to detect any measurable effects of the safeners NA, dichlormid, oxabetrinil, and flurazole on extractable ALS activity in shoots or roots of corn and sorghum seedlings. 

A bentazon-induced reduction in the foliar absorption of sethoxydim by goose grass Eleusine indica L.) has been proposed by Rhodes and Coble as a likely mechanism for the observed antagonism between these two herbicides. However, Retzlaff et aV suggested that the site of the antagonistic interaction between bentazon and sethoxydim is located in biomembranes such as the chloroplast envelope or the plasmalemma. The 

The antagonism of diclofop-methyl(DM) by 2,4-D is reciprocaf and has been demonstrated in coleoptiles or whole plants of wild oat as well as in corn and soybean tissue culture. DM and 2,4-D are structural analogues with different biological activities. DM is phytotoxic to grasses but inactive against broadleaf weeds, whereas the activity of 2,4-D is just the opposite. While the effects of DM on wild oat are much reduced by 

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Cross-resistance means that a single resistance mechanism causes resistance to several herbicides. The term target-site cross-resistance is used when these herbicides bind to the same target site, whereas nontarget-site cross-resistance is due to a single nontarget-site mechanism (e.g., enhanced metabolic detoxification) that entails resistance across herbicides with different modes of action. 

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