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Cholesterol Transfer From Normal and Atherogenic Low Density Lipoproteins to Mycoplasma Membranes

Cholesterol Transfer From Normal and Atherogenic Low Density Lipoproteins to Mycoplasma Membranes The purpose of this study was to determine whether the free cholesterol of hypercholesterolemlc low density llpoproteln from cholesterol-fed nonhuman primates has a greater potential for surface transfer to cell membranes than does the free cholesterol of normal low density llpoproteln. The low density lipoproteins were isolated from normal and hypercholesterolemic rhesus and cynomolgus monkeys, incubated with membranes from Acholeplama laldlawll, a mycoplasma species devoid of cholesterol in its membranes, and the mass transfer of free cholesterol determined by measuring membrane cholesterol content. Since these membranes neither synthesize nor esterlfy cholesterol, nor degrade the protein or cholesteryl ester moieties of low density lipoproteln, they are an Ideal model with which to study differences in the cholesterol transfer potential of low density llpoprotein Independent of the uptake of the intact low density llpoprotein particle. When added at an equivalent particle concentration, there was greater enrichment of membranes with free cholesterol from hypercholesterolemic low density llpoprotein. Hypercholesterolemic low density lipoproteln, however, contains more cholesterol per particle than normal low density llpoprotein; yet calculations on the basis of equivalent free cholesterol content showed no difference In either the rate or extent of free cholesterol transfer from normal or hypercholesterolemic low density llpoprotein. This was true for the transfer of at least 90% of the free cholesterol from both llpoprotelns. These studies Indicate that, even though there are marked differences In the cholesterol composition of normal and hypercholesterolemic low density llpoprotelns, this does not result In a greater chemical potential for surface transfer of free cholesterol. Consequently, if a difference In the surface transfer of free cholesterol Is responsible for the enhanced ability of hypercholesterolemic low density llpoproteln to promote cellular cholesterol accumulation and, perhaps, also atherosclerosis, It must be the result of differences In the interaction of the hypercholesterolemic low density llpoproteln with the more complicated mammalian cell membranes, rather than differences In the chemical potential for cholesterol transfer. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Cholesterol Transfer From Normal and Atherogenic Low Density Lipoproteins to Mycoplasma Membranes

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Copyright
© 1981 by American Heart Association, Inc.
ISSN
1079-5642

Abstract

The purpose of this study was to determine whether the free cholesterol of hypercholesterolemlc low density llpoproteln from cholesterol-fed nonhuman primates has a greater potential for surface transfer to cell membranes than does the free cholesterol of normal low density llpoproteln. The low density lipoproteins were isolated from normal and hypercholesterolemic rhesus and cynomolgus monkeys, incubated with membranes from Acholeplama laldlawll, a mycoplasma species devoid of cholesterol in its membranes, and the mass transfer of free cholesterol determined by measuring membrane cholesterol content. Since these membranes neither synthesize nor esterlfy cholesterol, nor degrade the protein or cholesteryl ester moieties of low density lipoproteln, they are an Ideal model with which to study differences in the cholesterol transfer potential of low density llpoprotein Independent of the uptake of the intact low density llpoprotein particle. When added at an equivalent particle concentration, there was greater enrichment of membranes with free cholesterol from hypercholesterolemic low density llpoprotein. Hypercholesterolemic low density lipoproteln, however, contains more cholesterol per particle than normal low density llpoprotein; yet calculations on the basis of equivalent free cholesterol content showed no difference In either the rate or extent of free cholesterol transfer from normal or hypercholesterolemic low density llpoprotein. This was true for the transfer of at least 90% of the free cholesterol from both llpoprotelns. These studies Indicate that, even though there are marked differences In the cholesterol composition of normal and hypercholesterolemic low density llpoprotelns, this does not result In a greater chemical potential for surface transfer of free cholesterol. Consequently, if a difference In the surface transfer of free cholesterol Is responsible for the enhanced ability of hypercholesterolemic low density llpoproteln to promote cellular cholesterol accumulation and, perhaps, also atherosclerosis, It must be the result of differences In the interaction of the hypercholesterolemic low density llpoproteln with the more complicated mammalian cell membranes, rather than differences In the chemical potential for cholesterol transfer.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Mar 1, 1981

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