Intrahepatic distribution of small unilamellar liposomes as a function of liposomal lipid composition

Spanjer, Hh; Vangalen, M; Roerdink, Fh; Regts, Joke; Scherphof, Gl

doi:10.1016/0005-2736(86)90262-2

Cited by 85 publications

(34 citation statements)

References 14 publications

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“…To the best of our knowledge no reports in the literature have described significant uptake of liposomes of any composition by endothelial cells in vivo. We and others have repeatedly found and reported the actual lack of involvement of liver endothelial cells in clearance of liposomes from the blood (21).…”

Section: Discussionmentioning

confidence: 86%

Massive targeting of liposomes, surface-modified with anionized albumins, to hepatic endothelial cells

Kamps¹,

Morselt²,

Meijer³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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118

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Human serum albumin (HSA) derivatized with cis-aconitic anhydride was covalently coupled to liposomes with a size of approximately 100 nm [polyaconitylated HSA (Aco-HSA) liposomes]. Within 30 min after injection into a rat, Aco-HSA liposomes were completely cleared from the blood and almost exclusively taken up by the liver, whereas in control liposomes 80% was still present in the blood at that time. Endothelial cells were shown to account for almost two-thirds of the hepatic uptake of the Aco-HSA liposomes, the remainder being recovered mainly in the liver macrophages

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Section: Discussionmentioning

confidence: 86%

Massive targeting of liposomes, surface-modified with anionized albumins, to hepatic endothelial cells

Kamps¹,

Morselt²,

Meijer³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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118

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“…In addition, intravenously injected [3H]cholesteryl oleate-labeled liposomes (small unilamellar vesicles) were used as a tool to introduce labeled cholesteryl oleate into the liver. These small liposomes are known to be preferentially taken up by hepatocytes (15)(16)(17). After intralysosomal hydrolysis, the labeled cholesterol becomes available to the cell and can be used for bile acid synthesis ( 16,17).…”

Section: Introductionmentioning

confidence: 99%

Dietary fish oil-induced changes in intrahepatic cholesterol transport and bile acid synthesis in rats.

Smit¹,

Temmerman²,

Wolters³

et al. 1991

J. Clin. Invest.

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Hepatic cholesterol metabolism was studied in rats fed purified diets supplemented (9% wt/wt) with either fish oil (FO) (n-3 fatty acids) or corn oil (CO) (n-6 fatty acids) for 4 wk. Rats were equipped with permanent catheters in heart, bile duct, and duodenum to allow studies under normal feeding conditions. [3H, cholesteryl oleate-labeled small unilamellar liposomes, which are rapidly endocytosed by hepatocytes, were intravenously injected to label intrahepatic cholesterol pools, and plasma and bile were collected. FO as compared to CO induced a lowering of plasma cholesterol levels by 38% and oftriglyceride levels by 69%. This reduction in plasma lipids in FO rats was accompanied by: (a) an increased bile acid pool size (28%); (b) a fourfold increase in the ratio cholic acid/chenodeoxycholic acid in bile; (c) increased biliary excretion of cholesterol (51%) (d) accelerated excretion of endocytosed free cholesterol into bile; (e) accelerated incorporation ofendocytosed cholesterol in bile acids; (f) a significant increase in the bile acid-independent fraction of bile flow, and (g) a threefold increase in hepatic alkaline phosphatase activity. The results show that FO induces changes in transport and metabolic pathways of cholesterol in the rat liver, which result in a more rapid disposition of plasmaderived cholesterol into the bile. (J. Clin. Invest. 1991. 88:943-951.)

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“…We observed that the radioactivity recovered in the liver as well as in the spleen reaches a maximum between 6 and 12 hr after injection of the SUVs, and within 1 hr for the MLVs. The subsequent decrease in radioactivity reflects an organ redistribution of the label as indicated by the accumulation of radioactivity in the kidneys and at later time points in the urine.…”

Section: Discussionmentioning

confidence: 74%

“…Although small unilamellar vesicles (SUVs) of appropriate lipid compositions may be taken up by nonphagocytic cells, such as hepatocytes (6), the major mechanism of removal of liposomes from the bloodstream involves endocytosis by the mononuclear phagocyte system, especially for large liposomes (7)(8)(9). This has led to the recognition that liposomes not only may be considered as a direct drug-delivery system to diseased target cells but also as a vehicle for the creation of intracellular drug depots; thus, in cells other than the ultimate target cells, a sustained release of drug may be effectuated concomitant with degradation of the drugcontaining liposomes (10,11).…”

mentioning

confidence: 99%

In vivo stability of ester- and ether-linked phospholipid-containing liposomes as measured by perturbed angular correlation spectroscopy.

Derksen

Baldeschwieler²,

Scherphof³

1988

Proc. Natl. Acad. Sci. U.S.A.

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To evaluate liposome formulations for use as intracellular sustained-release drug depots, we have compared the uptake and degradation in rat liver and spleen of liposomes of various compositions, containing as their bulk phospholipid an ether-linked phospholipid or one of several ester-linked phospholipids, by perturbed angular correlation spectroscopy. Multilamellar and small unilamellar vesicles (MLVs and SUVs), composed of egg phosphatidylcholine, sphingomyelin, distearoyl phosphatidylcholine (DSPC), dipalmitoyl phosphatidylcholine (DPPC) or its analog dihexadecylglycerophosphorylcholine (DHPC), and cholesterol plus phosphatidylserine, and containing "'In complexed to nitrilotriacetic acid, were injected intravenously in rats. Recovery of "'In-labeled liposomes in blood, liver, and spleen was assessed at specific time points after injection and the percentage of liposomes still intact in liver and spleen was determined by measurement of the time-integrated angular perturbation factor [G22(o)] of the "'In label. We found that MLVs but not SUVs, having DHPC as their bulk phospholipid, showed an increased resistance against lysosomal degradation as compared to other phospholipid-containing liposomes. The use of diacyl phospholipids with a high gel/liquid-crystalline phase-transition temperature, such as DPPC and DSPC, also retarded degradation of MLV, but not of SUV in the dose range tested, while the rate of uptake of these liposomes by the liver was lower.

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Intrahepatic distribution of small unilamellar liposomes as a function of liposomal lipid composition

Cited by 85 publications

References 14 publications

Massive targeting of liposomes, surface-modified with anionized albumins, to hepatic endothelial cells

Massive targeting of liposomes, surface-modified with anionized albumins, to hepatic endothelial cells

Dietary fish oil-induced changes in intrahepatic cholesterol transport and bile acid synthesis in rats.

In vivo stability of ester- and ether-linked phospholipid-containing liposomes as measured by perturbed angular correlation spectroscopy.

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