Resistance to substituted urea herbicides in Lolium rigidum biotypes

Two populations of Lolium rigidum (R-1 and R-2) from a monoculture of winter wheat were treated with diclofop-methyl, whereas another population of L. rigidum (R-3) was treated with diclofop-methyl plus chlorotoluron or diclofop-methyl plus isoproturon. The R-1 biotype is resistant to chlorotoluron and isoproturon (ED50 R-1/ED50 S values of 6.5 and 4.2, respectively), while the R-3 also exhibits resistance to chlorotoluron and isoproturon (ED50 R-3/ED50 S values of 9.26 and 5.53, respectively). The diclofop-methyl-resistant R-2 biotype was similarly sensitive to both substituted ureas, as was the susceptible (S) biotype. The resistance mechanism in the R-1 and R-3 biotypes is net due to reduced target site affinity for herbicides. There was no difference in the absorption and translocation of [C-14]chlorotoluron in the resistant and susceptible biotypes. Fast fluorescence induction curves showed that substituted ureas inhibited whole-leaf photosynthesis in all biotypes, The R-1 and R-3 biotypes later recovered fluorescence activity at a slightly slower rate in the R-1 biotype than in the R-3 biotype. The R-3 population was also tolerant to benzthiazuron, buturon, fenuron, methabenzthiazuron, metobromuron, metoxuron, and monolinuron, with tolerance at a lower level to chloroxuron, diuron, and linuron. This biotype was susceptible to chlorobromuron. The R-1 biotype was tolerant to benzthiazuron and metoxuron and was less tolerant to buturon, fenuron, methabenzthiazuron, and metobromuron, while this biotype was susceptible to chlorobromuron. chloroxuron, diuron, linuron, and monolinuron. L. rigidum biotypes produced the same pattern of metabolites, but the R-1 and R-3 resistant biotypes detoxified the chlorotoluron to conjugated chlorotoluron at a higher rare than the R-2 and S susceptible biotypes. In all biotypes treated with 1-aminobenzotriazole, a cytochrome P450 inhibitor. N-dealkylation was not affected. while ring methyl hydroxylation was strongly inhibited. These data suggested that the resistance mechanism in both biotypes is due to chlorotoluron metabolism via alkyl oxidation, and this is greater in R-3 than R-1. The cytochrome P450 enzyme could be involved in this oxidation reaction, (C) 1997 Academic Press.