Cholesterol ester hydrolase in homogenates and lysosomal fractions of human aorta

Kothari, Himanshu V.; Bonner, Mary J.; Miller, Benjamin F.

doi:10.1016/0005-2760(70)90194-3

Cited by 59 publications

(12 citation statements)

References 15 publications

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“…1) (29). Cholesteryl esterase activity with a pH optimum in the neighborhood of neutrality, on the other hand, has been demonstrated by other researchers in the aorta of several animal species (2,6,12,(15)(16)(17)20). It seems liekly that differences in assay conditions account for the differences between our results and those of others.…”

Section: Insufficiency O F Ysosomal Acid Cholesteryl Esterasecontrasting

confidence: 45%

Lysosomal Acid Cholesteryl Esterase and Atherosclerosis in Cholesterol-Fed Rabbits

Takano

Imanaka

1978

Acta Histochem. Cytochem

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Section: Insufficiency O F Ysosomal Acid Cholesteryl Esterasecontrasting

confidence: 45%

Lysosomal Acid Cholesteryl Esterase and Atherosclerosis in Cholesterol-Fed Rabbits

Takano

Imanaka

1978

Acta Histochem. Cytochem

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“…Enzyme activity was expressed as nanomoles of cholesterol esterified/h/mg protein. Cholesterol ester hydrolase (CEH) activity was estimated by the method of Kothari et al [37] with slight modification by Kritchevsky and Kothari [38]. In this method, the free cholesterol liberated from cholesterol oleate was precipitated.…”

Section: Assay Of Lipid-metabolizing Enzymesmentioning

confidence: 99%

Effect of lupeol and lupeol linoleate on lipemic – hepatocellular aberrations in rats fed a high cholesterol diet

Sudhahar

Srinivasan

Varalakshmi³

2006

Molecular Nutrition Food Res

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Cholesterol feeding has been often used to study the etiology of hypercholesterolaemia-related metabolic disturbances. The aim of the present study is to investigate the effects of a pentacyclic triterpene, lupeol, and its ester derivative on hepatic abnormalities associated with hypercholesterolemic rats. Hypercholesterolaemia was induced in male Wistar rats by feeding them with a high cholesterol diet (HCD) containing normal rat chow supplemented with 4% cholesterol and 1% cholic acid, for 30 days. Lupeol and lupeol linoleate were supplemented (50 mg/kg body wt/day) during the last 15 days. Increased hepatic lipid profile along with abnormalities in lipid-metabolizing enzyme activities were seen in hypercholesterolemic rats. An apparent increase in the expression of Acyl-CoA cholesterol acyltransferase mRNA was seen in HCD fed rats. The activities of hepatic marker enzymes, which serve as indices of cellular injury, were altered in HCD fed rats. Treatment with triterpenes significantly modulated the abnormalities induced by hypercholesterolaemia. Also, an increased (P >0.001) faecal excretion of cholesterol and bile acids were observed in lupeol and lupeol linoleate group when compared with HCD fed group. Therefore, it can be concluded that triterpenes treatment afforded substantial protection against the anomalies, which are manifested during the early stage of hypercholesterolemic atherogenesis.

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“…The source of this activity within the smooth muscle cell is not clear; however, a reasonable site would be the lysosomes. Cholesterol esterase activity has been reported in aortic lysosomes (32,33), and this enzymatic activity may be reversible. The homogenization procedure used for our experiment may have disrupted aortic lysosomes, thereby causing the lysosomal enzymes to be present in the high-speed supernatant fraction.…”

Section: Effect Of Cpib and Tpia On Incorporation Of L-^c-oleate Intomentioning

confidence: 99%

Cholesteryl Ester Synthesis in Normal and Atherosclerotic Aortas of Rabbits and Rhesus Monkeys

Brecher

Chobanian

1974

Circulation Research

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The formation of cholesteryl ester in aortic tissue was studied using subcellular fractions from normal and atherosclerotic rabbit and rhesus monkey aortas. The properties of two enzyme systems capable of esterifying l-M C-oleic acid into cholesteryl ester in vitro were Investigated, and increased activity was demonstrated for both systems as a result of cholesterol feeding. Microsomal preparations were used to study the ATP, CoA-dependent esterification which involves two enzymes, fatty acyl CoA synthetase and fatty acyl CoA:cholesterol acyltransferase. The properties of both enzymes were investigated, and an increase of about fourfold in activity of the acryltransfrease was demonstrated in aortic microsomes as a result of cholesterol feeding for 3-6 months. Esterification of oleic acid into cholesteryl ester by aortic high-speed supernatant fractions at an acidic pH was also observed; the enzyme system involved did not require cofactors, and its activity greatly increased as a result of cholesterol feeding. Similar increases in the activity of both esterifying enzyme systems were found when normal and atherosclerotic rhesus monkey aortic fractions were compared. p-Chlorophenoxyisobutyrate (CPIB) and 2-methyl-2-[p-(l, 2, 3, 4-tetrahydro-l-naphthyl)-phenoxy]propionic acid (TPIA) produced inhibition of both cholesterol-esterifying enzyme systems. TPIA was a more effective inhibitor than CPIB on both enzyme systems by at least an order of magnitude. These studies suggest that increased intracellular synthesis of cholesteryl ester by aortic tissue may contribute to its accumulation in atherosclerosis.

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Cholesterol ester hydrolase in homogenates and lysosomal fractions of human aorta

Cited by 59 publications

References 15 publications

Lysosomal Acid Cholesteryl Esterase and Atherosclerosis in Cholesterol-Fed Rabbits

Lysosomal Acid Cholesteryl Esterase and Atherosclerosis in Cholesterol-Fed Rabbits

Effect of lupeol and lupeol linoleate on lipemic – hepatocellular aberrations in rats fed a high cholesterol diet

Cholesteryl Ester Synthesis in Normal and Atherosclerotic Aortas of Rabbits and Rhesus Monkeys

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