Reactive oxygen species (ROS) are critical factors that cause damage in salt-stressed plants, but their mechanisms of action in living cells are largely unknown. We investigated the roles of reactive carbonyl species (RCS), i.e., the lipid peroxide-derived α,β-unsaturated aldehydes and ketones, in plant growth retardation under salt stress. When Arabidopsis thaliana Col-0 seeds were exposed to 100 mM NaCl, germination was delayed and the levels of ROS, RCS, and protein carbonylation in the seedlings were increased. Adding the histidine-containing dipeptides carnosine, N-acetylcarnosine, and anserine, which are reported RCS scavengers, restored the germination speed and suppressed the increases in RCS and protein carbonylation but did not affect the ROS level. Increases in the levels of the RCS acrolein, crotonaldehyde, (E)-2-pentenal, and 4-hydroxy-(E)-2-nonenal were positively correlated with the delay of germination and growth inhibition. These RCS, generated downstream of ROS, are thus primarily responsible for the salt-stress symptoms of plants.
Keywords: 4-hydroxy-(E)-2-nonenal; acrolein; carnosine; protein carbonylation; reactive carbonyl species; reactive oxygen species; salt stress.