Fluazifop-P-butyl induced ROS generation with IAA (indole-3-acetic acid) oxidation in Acanthospermum hispidum D.C.

Abstract

Acanthospermum hispidum D.C. was particularly susceptible to fluazifop-P-butyl, an aryloxyphenoxypropionate herbicide, and the primary action site for the herbicide was shoot apical meristem, which is also the main site of indole-3-acetic acid (IAA) biosynthesis and action. Membrane lipid peroxidation caused by increasing levels of reactive oxygen species (ROS) was considered as an action mechanism of fluazifop-P-butyl in A. hispidum. To further clarify the ROS inducing mechanism of fluazifop-P-butyl in the plant, the interactions between fluazifop-P-butyl and auxin compounds IAA or 2,4-dichlorophenoxyacetic acid (2,4-D) were studied. Haloxyfop-P-methyl, an AOPP herbicide which is inactive on A. hispidum, was used for comparison. The results showed that the growth inhibition and malondialdehyde or H2O2 increases induced by fluazifop-P-butyl on A. hispidum were reversed by IAA or 2,4-D. The IAA content was decreased but the contents of three IAA oxidation metabolites, indole-3-methanol, indole-3-aldehyde and indole-3-carboxylic acid were increased by fluazifop-P-butyl in A. hispidum, but not by haloxyfop-P-methyl. The growth of A. hispidum was not inhibited by three IAA oxidative compounds. Moreover, the activities of IAA oxidase and peroxidase were increased by fluazifop-P-butyl but not by haloxyfop-P-methyl, and the increase was reversed by IAA or 2,4-D. We suggest that there is an antagonistic effect between fluazifop-P-butyl and IAA or 2,4-D, and the IAA oxidation may be involved in the action mechanism of fluazifop-P-butyl in A. hispidum.