Echinochloa crusgalli var. Mitis metabolism as resistance mechanism to imazapyr and imazapic

Abstract

Selection pressure caused by continuous use of imazapyr and imazapic herbicides in rice fields without crop rotation, has selected for resistant biotypes of Echinochloa crusgalli var. mitis. To know the mechanism of resistance involved becomes important in order to define effective management strategies. Therefore, the objective of this work was to verify if enhanced metabolism of herbicide is responsible for imazapyr and imazapic resistance in Echinochloa crusgalli var. mitis biotypes from Rio Grande (ECH38 resistant and ECH44 susceptible), Pelotas (ECH1 resistant and ECH14 susceptible) and Arroio Grande (ECH27 resistant) in the state of Rio Grande do Sul. For this purpose, forty-nine biotypes were collected from the southern region of the state in areas with barnyard grass control difficulties with ALS inhibitor herbicides. The treatments of study consisted of application of malathion (1000 g a.i. ha-1) and piperonyl butoxide (525 g a.i. ha-1), inhibitors of the cytochrome P450 mono-oxygenase enzymes and after 60 minutes, preceding herbicide application (73.5 + 24.5 g a.e. ha-1. Visual control evaluations were taken at 14 and 28 days after treatments (DAT) and shoot dry mass (SDM) determination at 28 DAT. The results indicate that the application of inhibitors does not alter the control response of the ECH38, but shows a significant increase in phytotoxicity in 28 DAT, with values of 78% for the ECH1. The use of Malathion associated with the herbicide provided a reduction in the SDM of 1.34 g.plant-1 in relation to the isolated application of herbicide and for piperonyl butoxide (PBO) of 1.28 g.plant-1 for the resistant biotype from Pelotas. For ECH27, the SDM reduction was lower than the values of 0.87 g.plant-1 for Malathion and 1.04 g.plant-1 for PBO. The resistance mechanism to imazapyr + imazapic herbicide in Pelotas and Arroio Grande biotypes is related to increased metabolism of the herbicide, and it cannot be stated that this mechanism is involved in the resistance of the ECH38 biotype.