Both pro- and antiatherosclerotic effects have been ascribed to dietary peroxidized
lipids.
Confusion on the role of peroxidized
lipids in atherosclerotic
cardiovascular disease is punctuated by a lack of understanding regarding the metabolic fate and potential physiological effects of dietary peroxidized
lipids and their decomposition products. This study sought to determine the metabolic fate and physiological ramifications of 13-hydroperoxyoctadecadienoic
acid (13-HPODE) and
13-HODE (13-hydroxyoctadecadienoic acid) supplementation in intestinal and hepatic cell lines, as well as any effects resulting from
13-HPODE or
13-HODE degradation products. In the presence of Caco-2 cells,
13-HPODE was rapidly reduced to
13-HODE. Upon entering the cell,
13-HODE appears to undergo decomposition, followed by esterification. Moreover,
13-HPODE undergoes autodecomposition to produce
aldehydes such as
9-oxononanoic acid (9-ONA). Results indicate that 9-ONA was oxidized to
azelaic acid (AzA) rapidly in cell
culture media, but AzA was poorly absorbed by intestinal cells and remained detectable in cell
culture media for up to 18 h. An increased
apolipoprotein A1 (ApoA1) secretion was observed in Caco-2 cells in the presence of
13-HPODE, 9-ONA, and AzA, whereas such induction was not observed in HepG2 cells. However,
13-HPODE treatments suppressed
paraoxonase 1 (PON1) activity, suggesting the induction of ApoA1 secretion by
13-HPODE may not represent functional
high-density lipoprotein (HDL) capable of reducing oxidative stress. Alternatively, AzA induced both ApoA1 secretion and PON1 activity while suppressing
ApoB secretion in differentiated Caco-2 cells but not in HepG2. These results suggest oxidation of 9-ONA to AzA might be an important phenomenon, resulting in the accumulation of potentially beneficial dietary peroxidized
lipid-derived
aldehydes.