Lipid peroxidation (LPO), is induced by a variety of abiotic stresses. Although LPO is involved in diverse signaling processes, and precedes programmed cell death.

Singlet oxygen was identified as the major cause of lipid oxidation under basal conditions, while a 13-lipoxygenase (LOX2) and free radical catalyzed lipid oxidation substantially contribute to the increase upon stress.

Stress also induced an accumulation of fragmented lipids. Fragmentation mechanism is responsible for the formation of the essential biotin precursor of Dicarboxilic acids, which was a prime signal.

Lipid perox

idation (LPO), triggered by lipoxygenases (LOX) and reactive oxygen species (ROS), is a hallmark of plant stress responses. Typically, LOX oxidize free fatty acids in the cytosol or chloroplasts, thereby initiating several oxylipin pathways. Among the ROS typically produced in plant stress responses, only singlet oxygen and free radicals are sufficiently reactive to oxidize polyunsaturated fatty acids directly.

These short-lived ROS produced in different cellular compartments, including plasma membrane, plastids, mitochondria, peroxisomes, endoplasmic reticulum, and cytosol, are thought to oxidize predominantly glycerolipids close to the site of ROS production.

LOXs and ROS have also been implicated in the formation of fragmented fatty acids in plants and animals. The enzymatic fragmentation pathway FIG 1 , which has been described in plants only, involves LOX and hydroperoxide lyases (HPL) acting on free fatty acids (Matsui et al., 2006). Finally, oxo-fatty acids can be oxidized by aldehyde dehydrogenase.

It has been proposed that nonenzymatic LPO protects plants from oxidative stress by scavenging ROS. Hence, LPO produces plastid lipid signals in the early stages of oxidative stress associated with stress. However, massive LPO, exceeding a certain threshold level of oxidized lipids, may contribute to the execution of cell death.

Among these free oxylipins with reported or proposed signaling functions are Dicarboxilic acids. Free dicarboxylic as a phloem-mobile signal of stress. Then dicarboxilic acids and derivates acting in the reversing of the stress process. 


FIG 1.-. Fatty acid fragmentation pathways.

A.- Enzymatic oxidative fragmentation of 18:3 via 9-LOX, 9-HPL, and aldehyde dehydrogenase (ADH), yielding ONA, nonadienal (NDE). Gray bars represent the carbohydrogen backbone of fatty acids.

B.- Radical-catalyzed oxidative fragmentation of esterified 18:2 in glycerolipids via the dimer pathway, yielding oxidized glycerolipids (GL), ONA, and hydroperoxynonenal (HPNE) in animals (Schneider et al., 2008).

C.- Structures of predicted carboxylic acidic fragments generated through the dimer pathway from different plant polyunsaturated fatty acids: ONA, OHA, and PIM.