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Probucol inhibits oxidative modification of low density lipoprotein.
The findings suggest the hypothetical but intriguing possibility that probucol, in addition to its recognized effects on plasma LDL levels, may inhibit atherogenesis by limiting oxidative LDL modification and thus foam cell formation and/or EC injury. Expand
A nonendocytotic mechanism for the selective uptake of high density lipoprotein-associated cholesterol esters.
Not only receptor recycling, but endocytosis as well, appears not to be involved in selective uptake, which represents a net uptake of cholesterol esters and not an isotope exchange, as shown by mass flux studies in adrenal cells. Expand
A radioiodinated, intracellularly trapped ligand for determining the sites of plasma protein degradation in vivo.
A simple double-label method was devised to provide a correction for intact protein in trapped plasma, the extravascular spaces, and within cells, and by using this method it becomes unnecessary to fractionate tissue samples. Expand
Dissociation of tissue uptake of cholesterol ester from that of apoprotein A-I of rat plasma high density lipoprotein: selective delivery of cholesterol ester to liver, adrenal, and gonad.
Whereas uptake of low density lipoprotein appears to involve endocytosis of intact particles, uptake of HDL in at least some rat tissues involves additional, more complex, transfer mechanisms, the results reflect direct uptake from HDL itself. Expand
Methods for assessment of tissue sites of lipoprotein degradation.
This chapter describes various methods for assessments of tissues sites of lipoproteins degradation, and the tyramine-cellobiose technique, developed to provide a higher specific activity label. Expand
Uptake of high-density lipoprotein-associated apoprotein A-I and cholesterol esters by 16 tissues of the rat in vivo and by adrenal cells and hepatocytes in vitro.
The uptake of high-density lipoprotein (HDL)-associated apolipoprotein A-I and cholesterol esters was estimated in 16 tissues of the rat using rat HDL doubly labeled with nondegradable tracers;Expand
Tissue sites of degradation of apoprotein A-I in the rat.
It is postulated that the high activity of kidney was not due to uptake of intact HDL particles, but rather, due to glomerular filtration and tubular reabsorption of free apo-A-I, the most active organ of catabolism/g of wet weight. Expand
Receptor-dependent and receptor-independent degradation of low density lipoprotein in normal rabbits and in receptor-deficient mutant rabbits.
Low density lipoprotein (LDL) catabolism was studied using WHHL rabbits, an inbred strain deficient in LDL receptor activity and, thus, an animal model for homozygous familial hypercholesterolemia, and there was no evidence that the increased degradation occurred in any special subset of "scavenger" cells. Expand
Measurement in vivo of irreversible degradation of low density lipoprotein in the rabbit aorta. Predominance of intimal degradation.
The development of a highly sensitive method for assessing, tissue by tissue, the rates of irreversible protein degradation in vivo has allowed us to quantify low density lipoprotein degradation inExpand
Cholesterol esterase in rat adipose tissue and its activation by cyclic adenosine 3':5'-monophosphate-dependent protein kinase.
A high level of cholesterol esterase activity, comparable to that of hormone-sensitive triglyceridase, has been demonstrated in rad adipose tissue and its relationship to hormone- sensitive triglyceride lipase, with which it extensively co-fractionates, and its possible involvement in fat mobilization remain to be determined. Expand