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Abstract
Exposure of Arabidopsis thaliana young and mature leaves to the herbicide paraquat (Pq) resulted in a localized increase of hydrogen peroxide (H2O2) in the leaf veins and the neighboring mesophyll cells, but this increase was not similar in the two leaf types. Increased H2O2 production was concomitant with closed reaction centers (qP). Thirty min after Pq exposure despite the induction of the photoprotective mechanism of non-photochemical quenching (NPQ) in mature leaves, H2O2 production was lower in young leaves mainly due to the higher increase activity of ascorbate peroxidase (APX). Later, 60 min after Pq exposure, the total antioxidant capacity of young leaves was not sufficient to scavenge the excess reactive oxygen species (ROS) that were formed, and thus, a higher H2O2 accumulation in young leaves occurred. The energy allocation of absorbed light in photosystem II (PSII) suggests the existence of a differential photoprotective regulatory mechanism in the two leaf types to the time-course Pq exposure accompanied by differential antioxidant protection mechanisms. It is concluded that tolerance to Pq-induced oxidative stress is related to the redox state of quinone A (QA).
Highlights
In plants, most environmental stresses provoke oxidative damage due to excessive accumulation of reactive oxygen species (ROS), such as superoxide anions (O2·−), hydrogen peroxide (H2O2), hydroxyl radical (OH·), and singlet oxygen (1O2) [1]
Four hours after Pq treatment, non-photochemical quenching (NPQ) decreased by 13% (p < 0.05) and 22% (p < 0.005) in mature and young leaves respectively, compared to 60 min after Pq treatment, resulting to an increase of 143% (p < 0.0001)
The electron transport rate (ETR) in both leaf types reduced after exposure to Pq (Figure 1B)
Summary
Most environmental stresses provoke oxidative damage due to excessive accumulation of reactive oxygen species (ROS), such as superoxide anions (O2·−), hydrogen peroxide (H2O2), hydroxyl radical (OH·), and singlet oxygen (1O2) [1]. Chloroplasts are the main targets of ROS-linked damage during various environmental stresses that may lead to leaf senescence and to cell death [2,3,4]. Excess intracellular ROS reacts with a large variety of biomolecules and causes irreversible cellular damage leading to programmed cell death [5]. In plants under oxidative stress conditions, over-accumulation of ROS is followed by the induction of different genes involved in detoxification stress response and defense [7]
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