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C. Müller, B. Friedrichs, K. Wingler, R. Brigelius-Flohé
Perturbation of Lipid Metabolism by Linoleic Acid Hydroperoxide in CaCo-2 Cells
Dietary hydroperoxides are being discussed as potential health hazards contributing to oxidative stressrelated diseases. However, how foodborn hydroperoxides could exert systemic effects remains elusive in view of the limited chances to be absorbed. Therefore, the metabolic fate of 13-HPODE (13-hydroperoxy octadecadienoic acid), 13-HODE (13-hydroxy octadecadienoic acid) and linoleic acid (LA) was investigated in a CaCo-2 cell monolayer as a model of the intestinal epithelium. [1-14C]-13-HPODE, up to a noncytotoxic concentration of 100 M, did not cross the CaCo-2 cell monolayer unreduced if applied to the luminal side. The [1-14C]HPODEderived radioactivity was preferentially recovered from intracellular and released diacylglycerols (DG), phospholipids (PL) and cholesterol esterified with oxidized fatty acids (oxCE). A similar distribution pattern was obtained with 13- HODE. In contrast, LA is preferentially incorporated into triacylglycerols (TG), cholesteryl esters (CE) and PL (but mainly released as TG). 13-HPODE dosedependently decreased the incorporation of LA into released TG, while LA accumulated in cellular and released DGs, effects similarily exerted by 13-HODE. We concluded that foodborn hydroperoxy fatty acids are instantly reduced by the gastrointestinal glutathione peroxidase, which was previously shown to persist in selenium deficiency. Accordingly, modulation of the glutathione peroxidases by selenium deprivation/repletion did not modify the disturbance of the lipid metabolism by 13-HPODE. Thus, hydroperoxy fatty acids disturb intestinal lipid metabolism by being esterified as hydroxy fatty acids into complex lipids, and may render lipoproteins synthesized thereof susceptible to further oxidative modifications.
Biological Chemistry, Walter de Gruyter
Print ISSN: 1431-6730
Volume: 383, 04/2002
Pages: 637 - 648