Accumulation of reactive carbonyl species in roots as the primary cause of salt stress‐induced growth retardation of Arabidopsis thaliana

Abstract

AbstractSalt stress on plants induces an increase in reactive oxygen species (ROS), which then leads to the formation of reactive carbonyl species (RCS) such as acrolein and 4‐hydroxy‐(E)‐2‐nonenal (HNE), potent cytotoxins generated from lipid peroxides. We recently showed that salt‐stress treatment of Arabidopsis thaliana plants increased RCS levels, and exogenously added RCS‐scavenging chemicals alleviated the stress symptoms, indicating that RCS were responsible for the tissue damage in salt‐stressed plants. To obtain deeper insights into the role of RCS in stressed plants, we here analyzed changes in the levels of various RCS in the roots and shoots of A. thaliana. NaCl (90 mM) addition to the culture medium as a salt‐stress treatment caused growth inhibition and leaf chlorosis. Carbonyl analysis using HPLC revealed that the stress treatment induced a 2‐fold increase in the root levels of RCS, including acrolein, HNE and 4‐hydroxy‐(E)‐2‐hexenal (HHE). In the shoots, basal levels and stress‐induced increases of the RCS were lower than in roots. In the transgenic A. thaliana plants that overexpress the RCS‐scavenging enzyme 2‐alkenal reductase (AER) cDNA under the β‐estradiol (β‐ED)‐responsive promoter, salt stress induced less damage than in the wild‐type under β‐ED supplementation. The AER overexpression suppressed the stress‐induced increases in HNE, acrolein, HHE and (E)‐2‐hexenal in roots and in HNE in leaves, but not the ROS increase. These results suggest that the RCS increase in roots was the primary cause of salt‐induced damages. Enhancing RCS‐scavenging abilities, such as by AER overexpression, could be a new strategy to confer salt‐stress tolerance to plants.