摘要：

Rimsulfuron, N-((4,6-dimethoxypyrimidin-2-yl)aminocarbonyl)-3-(ethylsulfonyl)-2-pyridinesulfonamide, formerly DPX-E9636, is a sulfonylurea herbicide for postemergence use in maize to control grasses and some broadleaf weeds. Similar to other sulfonylureas, the site of action of rimsulfuron is acetolactate synthase (ALS), an enzyme in branched-chain amino acid biosynthesis. Studies of in vitro inhibition of ALS from sensitive and tolerant species discount differential active site sensitivity as the basis for maize tolerance to this herbicide. However, there was a good correlation between the rate of metabolism of the herbicide and plant tolerance. Plant metabolism studies demonstrated that tolerant maize metabolized rimsulfuron rapidly, with a half-life of < 1 h, while the sensitive species Sorghum halapense, Amaranthus retroflexus, and Digitaria sanguinalis metabolized rimsulfuron slowly, with half-lives of 38, > 48, and 27 h, respectively. The initial metabolic pathway for rimsulfuron in maize primarily involves hydroxylation on the pyrimidine ring followed by glucose conjugation. Both of these metabolites are inactive which results in the detoxification of the herbicide. Rimsulfuron was also metabolized in vitro by maize microsomes in a NADPH-dependent reaction to the same hydroxylated product, suggesting involvement of cytochrome P450. Additional studies with maize leaves demonstrated inhibition of rimsulfuron metabolism by terbufos and piperonyl butoxide, which further supports involvement of a cytochrome P450. Metabolism of rimsulfuron in maize is also temperature dependent, having a maximum rate at 25–30°C and lower rates at higher and lower temperatures. It is concluded that the basis of maize tolerance to rimsulfuron is rapid metabolic inactivation.

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