Abstract

The relative rates of degradation of the outer lipid bilayer of large multilamellar and small unilamellar bovine brain sphingomyelin/cholesterol ( 2:1; mol/mol) liposomes in the livers of Balb/c mice were compared. The rate of the release of entrapped In-111 ions from the aqueous reservoir of small unilamellar liposomes or from the outermost aqueous compartment of multilamellar liposomes was used to monitor the rate of degradation of the exterior lipid bilayer surface of these liposomes. The technique of gamma-ray perturbed angular correlation and a method for loading In-111 ions into the outermost aqueous compartment of liposomes were used in this investigation. It was found that in the liver the exterior lipid bilayer of large multilamellar liposomes was degraded more rapidly than the bilayer of small unilamellar liposomes in vivo. In contrast to the situation for small unilamellar liposomes, the degradative process for large multilamellar liposomes in the liver was not maintained under ischemic conditions. Our results suggest that multiple pathways operate in the degradation of liposomes in the liver. The rate of degradation of liposomes in the liver may depend on accessibility of liposomes to degradative sites.

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