Differential response of young and adult leaves to herbicide 2,4‐dichlorophenoxyacetic acid in pea plants: role of reactive oxygen species

Abstract

In this work the differential response of adult and young leaves from pea (Pisum sativum L.) plants to the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) (23 mm) applied by foliar spraying was investigated. The concentration of 2,4-D (23 mm) and the time of treatment (72 h) were previously optimized in order to visualize its toxic effects on pea plants. Under these conditions, the herbicide induced severe disturbances in mesophyll cells structure and proliferation of vascular tissue in young leaves and increased acyl-CoA oxidase (ACX), xanthine oxidase (XOD) and lipoxygenase (LOX) activities in young leaves, and only ACX and LOX in adult leaves. This situation produced reactive oxygen species (ROS) over-accumulation favoured by the absence of significant changes in the enzymatic antioxidants, giving rise to oxidative damages to proteins and membrane lipids. An increase of ethylene took place in both young and adult leaves and the induction of genes encoding the stress proteins, PRP4A and HSP 71,2, was observed mainly in young leaves. These results suggest that ROS overproduction is a key factor in the effect of high concentrations of 2,4-D, and ROS can trigger a differential response in young and adult leaves, either epinasty development in young leaves or senescence processes in adult tissues.

Effect of picloram herbicide on physiological responses of Eupatorium adenophorum Spreng

“…Plant cell can generate many reactive oxygen species (ROS) in response to stress conditions, such as heavy metal pollution, extreme temperature, drought, saline and herbicides (Pazmiño et al, 2011;Liu et al, 2012;Bhaskaran and Panneerselvam, 2013). If the ROS are not cleared promptly, plasma membranes can be attacked, causing lipid peroxidation and substantial leakage of electrolytes and small organic molecules, damaging the membrane system, causing disorder in various metabolic processes and damage to plant physiological processes (Semane et al, 2007).…”

Insights into the toxicity mechanism of and cell response to the herbicide 2,4-D in plants

“…8 The increase of ROS production induced by 2,4-D is a direct consequence of the activation of specific enzymes such as xanthine oxidoreductase (XOD) involved in ureide metabolism, acyl-CoA oxidase (ACX) involved in fatty acid β-oxidation and jasmonic acid biosynthesis, and lipoxygenase (LOX). 9 NADPH oxidases from the plasma membrane have been considered one of the main sources of ROS induced by auxinic compounds, although in pea plants this activity has been found not to change in response to 2,4-D. 9 ROS are also involved in 2,4-D-induced epinasty by promoting cell expansion and vasculartissue proliferation, 9,10 also acting as signal molecules to induce the cellular response against stress conditions. 6 In addition, these oxidants can participate in the onset of specific gene expression in response to 2,4-D, although the gene network involved in the cell response to 2,4-D governed by ROS has not yet been defined and thus is still under study (RomeroPuertas et al, unpublished results).…”

“…An overdose of 2,4-D as well as of IAA, activate de novo synthesis of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase, which is a key enzyme in ethylene biosynthesis. 13 However, the role of ET on 2,4-D toxicity is controversial and several authors have demonstrated that it does not participate in 2,4-D-dependent leaf epinasty, 9,14,15 although it can participate in the 2,4-Dinduced plant senescence. 8,9 Another consequence of ET overproduction is the formation of cyanide, an inhibitor of plant enzymes and proteins such as cytochrome-c oxidase, RuBisCo, nitrate/ nitrite reductase, catalase, and peroxidase.…”

“…13 However, the role of ET on 2,4-D toxicity is controversial and several authors have demonstrated that it does not participate in 2,4-D-dependent leaf epinasty, 9,14,15 although it can participate in the 2,4-Dinduced plant senescence. 8,9 Another consequence of ET overproduction is the formation of cyanide, an inhibitor of plant enzymes and proteins such as cytochrome-c oxidase, RuBisCo, nitrate/ nitrite reductase, catalase, and peroxidase. 13 As a response to the ET burst, the biosynthesis of abscisic acid (ABA) has been reported to be induced; through the overexpression of genes such as NCED1, which encodes a key regulatory enzyme of ABA biosynthesis.…”

“…16 ABA accumulation causes stomatal closure, which limits biomass production and can induce overproduction of reactive oxygen species (ROS), the main factor responsible for the oxidative damage and cell death. 9,10 Other hormones described to act during stress conditions such as jasmonic acid (JA) and salicylic acid (SA), can also be disturbed by 2,4-D, 17 although the mechanism has not been well established. Raghavan et al 18 have observed in Arabidopsis plants treated with 2,4-D an induction of OPR2, involved in jasmonic acid biosynthesis.…”