Lipid peroxidation-derived reactive carbonyl species (RCS): Their interaction with ROS and cellular redox during environmental stresses

It is well known that environmental stress conditions enhance the production of reactive oxygen species (ROS), which have dual roles with damaging effects to biomolecules and with signaling roles. When enzymatic or non enzymatic antioxidant defense of the cell is overwhelmed with excess production of ROS, it results in disruption of lipids via oxidation, which causes production of highly reactive lipid peroxidation-derived molecules such as 4-hydroxy-2-nonenal, 4-hydroxy-2-hexenal, malondialdehyde and acrolein. These unstable molecules are named as reactive carbonyl species (RCS) and high concentrations of RCS can cause irreversible damage in plant cells, which ultimately leads to cell death. Although there is a vast amount of studies on the nature of RCS in animals, studies in plants are limited, which mostly investigate their detoxification mechanisms and their damaging effects. Recently, just like ROS, signal roles are being postulated for RCS. In this review, the ROS and RCS production mechanisms and sites in plant cells are introduced and the RCS detoxification mechanisms including aldehyde dehydrogenases, aldo/keto reductases, 2-alkenal reductases and glutathione transferases are described. Moreover, besides their damaging effects, evidence related to signal roles of RCS are discussed. Also, the interaction between ROS and RCS metabolism is evaluated via RCS antioxidant defense interaction.