Intestinal and Hepatic Uptake of Dietary Peroxidized Lipids and Their Decomposition Products, and Their Subsequent Effects on Apolipoprotein A1 and Paraoxonase1.

Xueting Jiang,Sampath Parthasarathy,Dmitry Litvinov,Pragney Deme,Rajat Gupta,Kathryn Burge,Chandrakala Aluganti Narasimhulu

doi:10.3390/antiox10081258

Xueting Jiang, Sampath Parthasarathy + Show 5 more

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https://doi.org/10.3390/antiox10081258

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Abstract

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.

Highlights

IntroductionEpidemiological evidence has suggested a relationship between high-fat diets, especially diets high in saturated fat [1], and the incidence of coronary artery disease (CAD) [2,3,4]
Sesame oil generated far fewer peroxides, compared to canola oil, despite higher levels of polyunsaturated fatty acid (PUFA) found in the former
A Thiobarbituric Acid Reactive Substances (TBARS) assay was performed to measure the presence of MDA (Figure S1B), a peroxidation product of both arachidonic acid and linoleic acid (LA) [57]

Summary

Introduction

Epidemiological evidence has suggested a relationship between high-fat diets, especially diets high in saturated fat [1], and the incidence of coronary artery disease (CAD) [2,3,4]. The Western diet is rich in fats and contains high levels of peroxidized fats [5,6,7]. Deep-fried foods, and the culinary oils in which they are cooked, contain high levels of potentially harmful peroxidized lipids and their decomposition products [6]. The pathophysiological effects of these lipids have been documented extensively in CAD [12,13,14,16,17] and cancer [15], in addition to other contexts [18,19,20]

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