BINDING OF ETHYL OLEATE TO LOW-DENSITY-LIPOPROTEIN, PHOSPHOLIPID-VESICLES, AND ALBUMIN - A C-13 NMR-STUDY

Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced org an damage. After ethanol ingestion in humans, FAEE circulate in blood, bound to lipoproteins and albumin. We have analyzed the binding of et hyl (1-C-13, 99%) oleate (EO) to small unilamellar phospholipid vesicl es (SUV), human low density lipoprotein (LDL), and bovine serum albumi n (BSA) by C-13-NMR spectroscopy. Binding of less than or equal to 25 mol% EO to SW yielded a single EO carbonyl peak (172.6-172.9 ppm) down field from that of EO oil (171.9 ppm). Thus, the carbonyl forms hydrog en bonds with water in the SUV aqueous interface. At 30 mol% EO in SW, a second EO carbonyl peak appeared, indicating a limit in FAEE solubi lity in SUV. Addition of EO to isolated human LDL yielded a peak at 17 1.9 ppm, suggesting that the EO exists in an unhydrated environment, m ost likely the core of the lipoprotein. This binding was also observed using high levels of EO added to human serum. The addition of EO diss olved in ethanol or as an oil to a solution of BSA yielded no visible EO peak, whereas addition of (1-C-13, 99%) oleic acid resulted in seve ral narrow peaks, demonstrating a much greater affinity of BSA for ole ic acid than for EO. Bidirectional transfer of EO between LDL and SUV was observed and was 85% complete within 30 min. There was no measurab le transfer of EO from LDL or SUV to albumin. The weak binding of EO t o albumin will result in increased transport of EO by lipoproteins as plasma levels of EO increase.