Reactive carbonyl species: their production from lipid peroxides, action in environmental stress, and the detoxification mechanism.

Accumulation of lipid peroxide-derived aldehydes and ketones is a ubiquitous event in oxidative stress. The toxicity of these carbonyls, especially the α,β-unsaturated carbonyls (reactive carbonyls; RCS), in environmental-stressed plants has been demonstrated by several independent research groups, on the basis of the results that overexpression of different carbonyl-detoxifying enzymes commonly improved tolerance of the transgenic plants against environmental stresses. A positive correlation between the level of carbonyls and the stress-induced damage in these plants proves the cause-effect relationship between carbonyls and the cell injury. Comprehensive analysis of carbonyls has revealed that dozens of distinct RCS including highly toxic acrolein and 4-hydroxy-2-nonenal are contained at nmol/g fresh weight levels in the tissues of non-stressed plants. Stress treatments of plants increase the levels of these RCS, likely reaching a sub-mM order, but in the transgenic plants overproducing RCS-detoxifying enzymes, their increase is significantly suppressed. Immunological analyses have demonstrated that in non-stressed cells several proteins are modified by RCS and the extent of modification is increased on stresses. In heat-stressed leaves, the inactivation of the oxygen-evolving complex was associated with selective modification of OEC33 protein and photosystem II core proteins. RCS consume glutathione and inactivate various enzymes in chloroplasts and mitochondria, thereby accelerating oxidative stress status. Thus RCS, formed downstream of reactive oxygen species (ROS), act in a way biochemically distinct from that of ROS and play critical roles in the plant responses to oxidative stress.