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Journal of Lipid Research, Vol 37, 1449-1458, Copyright © 1996 by Lipid Research, Inc.
DA Bird, M Laposata and JA Hamilton
Fatty acid ethyl esters (FAEE), esterification products of ethanol and
fatty acids, have been implicated as mediators of ethanol-induced organ
damage. After ethanol ingestion in humans, FAEE circulate in blood, bound
to lipoproteins and albumin. We have analyzed the binding of ethyl (1-13C,
99%) oleate (EO) to small unilamellar phospholipid vesicles (SUV), human
low density lipoprotein (LDL), and bovine serum albumin (BSA) by 13C-NMR
spectroscopy. Binding of < or = 25 mol% EO to SUV yielded a single EO
carbonyl peak (172.6-172.9 ppm) downfield from that of EO oil (171.9 ppm).
Thus, the carbonyl forms hydrogen bonds with water in the SUV aqueous
interface. At 30 mol% EO in SUV, a second EO carbonyl peak appeared,
indicating a limit in FAEE solubility in SUV. Addition of EO to isolated
human LDL yielded a peak at 171.9 ppm, suggesting that the EO exists in an
unhydrated environment, most likely the core of the lipoprotein. This
binding was also observed using high levels of EO added to human serum. The
addition of EO dissolved in ethanol or as an oil to a solution of BSA
yielded no visible EO peak, whereas addition of (1-13C, 99%) oleic acid
resulted in several narrow peaks, demonstrating a much greater affinity of
BSA for oleic acid than for EO. Bidirectional transfer of EO between LDL
and SUV was observed and was 85% complete within 30 min. There was no
measurable transfer of EO from LDL or SUV to albumin. The weak binding of
EO to albumin will result in increased transport of EO by lipoproteins as
plasma levels of EO increase.
ARTICLES
Binding of ethyl oleate to low density lipoprotein, phospholipid vesicles, and albumin: a 13C NMR study
Department of Pathology, Massachusetts General Hospital, Boston, USA.
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