bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hydroxylation of fatty acids and alcohols by hepatic microsomal cytochrome P‐450 system from the Mongolian gerbil
Authors: Miura Yoshiro , Hisaki Harumi , Siems Werner , Oda Sen‐ichi 
Published: November 2006

AbstractThe liver microsomes of the Mongolian gerbilMeriones unguiculatus catalyzed the hydroxylation of various saturated fatty acids (C8−C18), alcohols (C12 and C16) and hydrocarbon (C12) to the corresponding ω‐ and (ω‐1)‐hydroxy derivatives. Lauric acid was hydroxylated most effectively among saturated fatty acids and the order of activity as hydroxylation substrates was C12>C14>C13>C16>C10>C18>C8. The specific activity of laurate hydroxylation (5.99 nmol/mg microsomal protein/min) in gerbil liver microsomes was higher than that observed in other species. 1‐Dodecanol was also hydroxylated very effectively (4.58 nmol/mg microsomal protein/min) by gerbil liver microsomes, but in general the hydroxylation rates for fatty alcohols were much lower than those for the corresponding acids. It was found from both inhibitor and cofactor studies that the enzyme catalyzing the hydroxylation of fatty acids and alcohols in the liver microsomes of the Mongolian gerbil was a typical cytochrome P‐450‐linked monooxygenase, and at least two different cytochrome P‐450 species were involved in the hydroxylation.
Properties of monoacylglycerol lipase in rabbit aorta
Authors: Hee‐Cheong Mariette , Severson David L. 
Published: November 2006

AbstractMonoacylglycerol lipase activity was characterized in a soluble preparation from rabbit aorta (intima‐media) obtained by combining a 100,000×g supernatant fraction with activity solubilized from the 100,000×g precipitate fraction by treatment with Triton X‐100. Rates of hydrolysis with 1‐monoolein and 2‐monoolein substrates were nearly identical. 1‐Monoolein was a competitive inhibitor (Ki 65 μM) of 2‐monoolein hydrolysis. 2‐Monoolein and 2‐monopalmitin were both hydrolyzed more rapidly than 2‐monoarachidonin. Lipase activity measured with a 2‐monoolein substrate was inhibited by the addition of oleate, NaF and CaCl2 to the assay. Preincubation of the lipase preparation with p‐bromophenacyl bromide resulted in a potent inhibition of lipase activity; this inhibition could be prevented by dithiothreitol.
The result of feeding palmitoyl glycerol on lymph and plasma lipids
Authors: Trumbo Paula , Sutherland‐Smith Margaret , Kitchell Barbara , Tove Samuel B. 
Published: November 2006

AbstractPalmitoyl glycerol is toxic when fed to mice, but the toxicity is alleviated by supplementing the toxic diet with 2–4% oleate or linoleate at the expense of sucrose. Lipid and fatty acid composition of lymph and plasma were studied in mice fed chow and palmitoyl glycerol diets to help explain the toxicity mechanism. When mice were fed chow, intestinal lymph contained a high proportion of saturated fatty acids; when they were given palmitoyl glycerol, the proportion approached 90% saturated fatty acids. The cholesteryl ester fraction was higher in lymph from mice fed a toxic diet than when the diet was fortified with supplemental safflower oil. However, there were no differences between diets in lipid composition of blood plasma. Similarly, except for plasma cholesterol esters, there were no differences in fatty acid composition between mice fed palmitoyl glycerol as the only fat or supplemented with a protective unsaturated fat. In the plasma, cholesteryl palmitate was elevated and cholesteryl oleate and cholesteryl linoleate were depressed when mice were given a toxic diet. Although a monoacylglycerol was toxic when fed, the percentages of monoacylglycerols in lymph or plasma were not materially elevated. The findings indicate that neither the total proportion of saturated fatty acids nor the amount of circulating monoacylglycerols was directly involved in the toxicity of palmitoyl glycerol.
Effect of cupric ions on serum and liver cholesterol metabolism
Authors: Tanaka Mitsuo , Iio Toshihiro , Tabata Toshikazu 
Published: November 2006

AbstractCupric ions were administered subcutaneously to male Sprague‐Dawley rats at a single dose of 200 μmol/kg. At 24 hr after administration, a remarkable increase of total and free cholesterol was seen in the rat serum. Also, when lecithin‐cholesterol acyltransferase (LCAT) (E.C. 2.3.1.43) activity was expressed as the percentage of the total serum that free cholesterol esterified, the acyltransferase activity in rats treated with cupric ions showed a slight decrease while the triglyceride content in rat serum and liver decreased by 54% and 61%, respectively. However, the content of hepatic cholesterol in rats treated with cupric ions did not show such a marked change.On the other hand, acid cholesteryl ester hydrolase activity (Acid CEH) (E.C. 3.1.1.14) in liver lysosomes of rats treated with cupric ions showed a marked decrease with increasing cupric ion concentration both in vivo and in vitro. Furthermore, cupric ions caused a marked release of the lysosomal enzymes cathepsin D and β‐glucuronidase into the cytosolic fraction. The changes in acid cholesteryl ester hydrolase activity induced by cupric ions appear to be a direct effect of cupric ions on the enzyme. These results suggest that excessive cupric ion concentrations could cause various disorders in lipid metabolism.
Effects of ketoconazole on cholesterol synthesis and precursor concentrations in the rat liver
Authors: Strandberg Timo E. , Tilvis Reijo S. , Miettinen Tatu A. 
Published: November 2006

AbstractKetoconazole, an antimycotic agent, given to rats for a week as 0.05% food addition had no effect on the hepatic concentrations of free and esterified cholesterol or on the activity of acyl coenzyme A: cholesterol‐acyltransferase (ACAT). However, the levels of free methylated cholesterol precursors, especially lanosterols, less markedly Δ8,24 and Δ8‐dimethyl sterols and monomethyl sterols, were increased after only one day's treatment, while those of esterified methyl sterols were increased inconsistently, and those of free and esterified Δ8‐lathosterol, lathosterol and desmosterol were not affected at all. Cholestyramine treatment had no significant effect on ACAT in spite of a decrease in the hepatic content of esterified cholesterol and caused a marked increase in the free cholesterol precursor levels, especially in those of lathosterols. Cholestyramine given to ketoconazole‐treated rats increased the hepatic levels of Δ8 and Δ7‐lathosterols but not desmosterol or methylated cholesterol precursors. Ketoconazole increased and cholestyramine markedly decreased plantssterols, sitosterol and campesterol in the liver. In serum, the contents of both lanosterols and lathosterol were increased but that of cholesterol tended to be decreased by ketoconazole (−19%). The results indicate that ketoconazole impairs demethylation processes at C‐14 and to some extent at C‐4 in the rat liver, resulting in lowered serum cholesterol level.
Injection of tridocosahexaenoyl‐glycerol emulsion and fatty acid composition of blood cells
Authors: Hamazaki Tomohito , Urakaze Masaharu , Yano Saburo , Soda Yasuji , Miyamoto Akira , Kubota Kohji , Ibuki Fumio 
Published: November 2006

AbstractAn injectable emulsion of docosahexaenoic acid (DHA) was prepared. One hundred ml of the emulsion contained 3 g of 93%‐pure 1,2,3‐tridocosahexaenoylglycerol (DHA‐TG), 1.2 g of 93%‐pure 2‐docosahexaenoyl‐phosphatidylcholine as an emulsifier and 2.5 g of glycerol. Thirty ml of the emulsion of DHA‐TG was injected into three rabbits on days 1 and 4 of the study. Blood was taken on day 0, on day 4 just before the second injection and on day 7. The percentage of DHA in the total phospholipid fraction of platelets increased from 0.46% (day 0) to 1.88% (day 4, p<0.05) and 3.66% (day 7; p<0.02 vs day 0). The percentage of eicosapentaenoic acid (EPA) increased from 0.46% (day 0) to 1.03% (day 4, p<0.02) and 1.63% (day 7: p<0.05 vs day 0). The percentage of arachidonic acid (AA) decreased from 9.45% (day 0) to 4.31% (day 4, p<0.05) and 6.68% (day 7; p<0.02 vs day 0). The percentage of DHA in the total phospholipid fraction of erythrocyte membranes increased from 0.23% (day 0) to 0.91% (day 4, p<0.05) and 1.52% (day 7; p<0.005 vs day 0); that of EPA increased from 0.21% (day 0) to 0.34% (day 4, p<0.005%) and 0.52% (day 7, p<0.01 vs day 0); that of AA was unchanged. Blood lipids were the same before and after the two injections of the emulsion, except that free fatty acids decreased markedly from 0.32 to 0.06 mEq/1 (p<0.02). On day 8, free AA (2 mg/kg) was injected into ear veins of the three treated rabbits and of four control rabbits (not treated with DHA‐TG). All the control rabbits died a few minutes after the AA injection, but none of the DHA‐treated rabbits died after AA injection (p<0.01). An emulsion of DHA‐TG may be useful for patients having immediate risk of thrombosis or for those who need DHA but cannot take it orally.
Effects of dietary primrose oil on mammary tumorigenesis induced by 7,12‐dimethylbenz(a) anthracene
Authors: Abou El‐Ela Soad H. , Prasse Keith W. , Carroll Richard , Bunce Opal R. 
Published: November 2006

AbstractThe mammary tumor‐promoting effect of a high‐fat diet containing 20% evening primrose oil (PO) was compared to that of a 20% corn oil (CO) diet. Mammary tumors were induced in female Sprague‐Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12‐dimethylbenz(a)anthracene (DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and 73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for PO‐fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27% for PO‐ and 63% for CO‐dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed significant increases in 18∶3 and 20∶4 fatty acids and significant decreases in 16∶0 and 18∶1 compared to animals fed a 20% CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high‐fat diet could be depressed by feeding a source of γ‐linolenic acid (GLA).
Short‐Term changes in hepatic HMG‐CoA reductase in rats fed diets containing cholesterol or oat bran
Authors: Kelley Micheal J. , Story Jon A. 
Published: November 2006

AbstractIn vivo regulation of hepatic HMG‐CoA reductase (HMGR) (mevalonate: NADP+ oxidoreductase [acylating CoA]; EC 1.1.1.34] by phosphorylation/dephosphorylation has not been demonstrated. Rats were meal‐fed semipurified diets; effects of inclusion of cholesterol (2%) or oat bran (15%) in a single meal on expressed (phosphorylated) and total (dephosphorylated) activities of HMGR were measured from 15 min to 4 hr after presentation of the meal. Expressed activity was not significantly altered in response to the control diet during the time periods examined, while total HMGR activity declined by 15 min and increased through 4 hr to an activity about 1.5 times control levels. Addition of cholesterol resulted in little change in expressed activity but a greater and more sustained reduction in total activity. Oat bran caused reductions in both total and expressed activities, which were maintained through 4 hr. Total HMGR activity was best correlated with apparent demand for cholesterol synthesis.
Relationship between translocation of long‐chain acyl‐CoA hydrolase, phosphatidate phosphohydrolase and CTP:Phosphocholine cytidylyltransferase and the synthesis of triglycerides and phosphatidylcholine in rat liver
Authors: Asiedu Daniel , Skorve Jon , Demoz Abraham , Willumsen Nina , Berge Rolf K. 
Published: November 2006

AbstractTranslocation of long‐chain acyl‐coenzyme A hydrolase from the microsomal fraction to the cytosolic fraction was promoted in cell‐free extracts of rat liver by palmitic acid, oleic acid, tetradecylthioacetic acid, and tetradecylthiopropionic acid, and by their CoA esters. The CoA esters were more effective than the non‐esterified acids in the translocation of the enzyme. Treatment of normolipidemic rats with sulfur‐substituted non‐β‐oxidizable fatty acid analogues resulted in a transitory increase in hepatic concentration of long‐chain acyl‐CoA. Longer feeding times almost normalized the hepatic long‐chain acyl‐CoA content. Microsomal long‐chain acyl‐CoA hydrolase activity was inhibited, whereas the activity of the cytosolic form was stimulated. The rise in enzyme activity coincided with a reduction in liver content of triglyceride and an increase in hepatic phospholipid content. The results suggest that the activity of long‐chain acyl‐CoA hydrolase in the cytosol may control the amount of acyl‐CoA thioesters in the liver. Esterified and non‐esterified fatty acids causedin vitro translocation of phosphatidate phosphohydrolase and cytidine 5′‐triphosphate (CTP):phosphocholine cytidylyltransferase from the cytosolic fraction to the microsomal fraction. However, the translocation of these two enzyme systems was not obtainedin vivo. The activity of phosphatidate phosphohydrolase decreased in microsomal and cytosolic fractions while the activity of cytidylyltransferase in these fractions increased. The activities of soluble phosphatidate phosphohydrolase and long‐chain acyl‐CoA hydrolase appeared to be inversely correlated. The results imply that in cytoplasm, long‐chain acyl‐CoA hydrolase may compete with the biosynthetic enzymes for the acyl‐CoA substrate, thus influencing the rate of lipid synthesis. The reduced hepatic triglyceride content observed in tetradecylthioacetic acid‐treated rats is probably due to reduced triglyceride synthesis, which is mediated by an inhibition of phosphatidate phosphohydrolase accompanied with translocation and stimulation of long‐chain acyl‐CoA hydrolase. Development of fatty liver as an effect of tetradecylthiopropionic acid is probably due to accelerated triglyceride biosynthesis, which is mediated by a stimulation of phosphatidate phosphohydrolase and a decrease in cytosolic palmitoyl‐CoA hydrolase activity.
Transfer of liposomes containing dolichol into isolated hepatocytes
Authors: Tollbom Örjan , Chojnacki Tadeusz , Dallner Gustav 
Published: November 2006

AbstractIsolated rat hepatocytes were preincubated with egg lecithin liposomes containing [3H]dolichol and [3H]‐dolichyl ester, and the intracellular levels and distributions of these lipids were subsequently determined after incubation in a liposome‐free medium. [3H]Dolichol was recovered initially mainly in microsomes, and no increase with time in the low level of this compound in the mitochondrial/lysosomal fraction could be observed. A small portion of the labeled dolichol was esterified in the endoplasmic reticulum and transferred to the lysosomecontaining fraction. [3H]Dolichyl linoleate was initially localized in microsomes and supernatant, but later accumulated in the mitochondria/lysosomes. Dolichyl linoleate was found in the membrane of microsomes, in the membrane and lumen of lysosomes, and in the soluble cytoplasm. Exogenous dolichol recovered in microsomes was not phosphorylated to any significant extent. Liposomal phosphatidylcholine also showed preferential accumulation in microsomes after incubation with hepatocytes. These results indicate that exogenous or endogenously formed dolichyl esters are transferred from the endoplasmic reticulum to lysosomes, probably through the cytoplasm. It appears that fatty acids play a role in targeting these lipids to their intracellular locations.
The dual effect of oxidation on lipid bilayer structure
Authors: Borchman Douglas , Lamba Om P , Salmassi Samira , Lou Marjorie , Cecilia Yappert M. 
Published: November 2006

AbstractSphingomyelin membranes were prepared with different levels of oxidative damage caused bytert‐butyl hydroperoxide (TBH). Temperature‐induced changes in membrane hydrocarbon chain packing (phase transitions) were monitored using infrared spectroscopy. Lipid phase transition characteristics were evaluated from thermodynamic parameters fitted to the experimental transition curve data. At temperatures below the lipid phase transition Tc, hydrocarbon chains pack in an ordered state whereas above the Tcthe hydrocarbonchains pack in a disordered state. Compared to the non‐oxidized control, the packing of the hydrocarbon chains of mildly oxidized sphingomyelin (<10 nmol TBH/mg lipid) was no different at all temperatures below the Tc, and was more ordered above the Tc. The hydrocarbon chains of strongly oxidized sphingomyelin (>10nmol TBH/mg lipid) were more disordered at temperatures above and below the Tccompared to the control samples. These results suggest that lipid oxidation has a dual effect on lipid order. A more ordered or disordered state may result depending on the degree of oxidation and the state of lipid order prior to oxidation. These results could be important for explaining the structural changes in oxidized membranes high in sphingomyelin such as those found in the ocular lens and liver plasma membranes.
Decreased lecithin: Cholesterol acyltransferase activity in the plasma of hypercholesterolemic pigs
Authors: Lacko Andras G. , Lee S‐M. , Mirshahi Iraj , Hasler‐Rapacz Judith , Kudchodkar Bhalchandra J. 
Published: November 2006

AbstractLecithincholesterol acyltransferase (LCAT) activity levels were determined, as function of plasma total cholesterol (TC) in 13 normocholesterolemic (TC<85 mg/dL) and in 28 hypercholesterolemic (TC>98 mg/dL) pigs. The normocholesterolemic group consisted of pigs that carried apo‐B allelic genes other thanLpb5 and orLpb8. The hypercholesterolemic group consisted ofLpb5/x andLpb5/8 heterozygous andLpb5/5 homozygous animals. The data reported in this study show that the LCAT activity in the plasma of hypercholesterolemic (HC) pigs (79±43 units) was significantly lower (p<0.0005) compared to the normocholesterolemic controls (175±45 units). Furthermore, LCAT activity was positively correlated with TC in the normocholesterolemic group (r=+0.54; p<0.05), whereas it was negatively correlated with TC in the hypercholesterolemic group (r=−0.73; p<0.001). Additional data obtained from incubation experiments suggest that the lower LCAT activity in hypercholesterolemic pigs may be due, at least in part, to inhibition of LCAT activity by components found in the lipoprotein‐deficient fractions of the plasma of hypercholesterolemic pigs.
Oxysterols in cultured bovine aortic smoth muscle cells and in the monocyte‐like cell line U937
Authors: Pie Jae Eun , Seillan Christine 
Published: November 2006

AbstractOxysterols in cultured bovine aortic smooth muscle cells and in the monocyte‐like cell line U937 were analyzed by gas‐liquid chromatography. The following products were detected: 7α‐ and 7β‐hydroxycholesterol, 7‐ketocholesterol, cholesterol‐α‐epoxide, cholesterol‐β‐epoxide, cholestanetriol, and 20‐ and 25‐hydroxycholesterol. The proportions of oxidized cholesterol varied from 1 to 3% of total cholesterol. The concentrations of oxysterols were lower when the smooth muscle cells were maintained in a vitamin E‐enriched medium, and were higher in U937 cells when the cells were activated with phorbol myristate acetate. The cell oxysterol content appears to be regulated by factors that inhibit or enhanced free radical generation. The concentrations of oxysterols found in cells may serve as an indicator of the extent of lipid peroxidation.
Phospholipids inTrypanosoma cruzi: Phosphoinositide composition and turnover
Authors: Racagni G. , Garcia de Lema M. , Domenech C. E. , Machado de Domenech E. E. 
Published: November 2006

AbstractThe polyphosphoinositides fromTrypanosoma cruzi were isolated by preparative thin‐layer chromatography (TLC) and identified. When myo‐[3H]inositol was present in the culture medium for five days, analyses showed the presence of phosphatidylinositol (PI), lysophosphatidylinositol (lysoPI), phosphatidylinositol 4‐phosphate (PIP) and phosphatidylinositol 4,5‐bisphosphate (PIP2). Short‐term incubation with32Pi led to higher percentages of incorporation into phosphatidylethanolamine (PE), lysophosphatidylethanolamine (lysoPE) and PI compared to the other glycerophospholipids. The phosphoinositides (PI, PIP and PIP2) contained a larger proportion of unsaturated than saturated fatty acids. High proportions of 18∶2 were found in the three phosphoinositides analyzed, whereas the major saturated fatty acid was 18∶0. Watersoluble inositol phosphates (IP, IP2 and IP3) were also identified.
Chemiluminescence detection of 8a‐hydroperoxy‐tocopherone in photooxidized α‐tocopherol
Authors: Miyazawa Teruo , Yamashita Toyonobu , Fujimoto Kenshiro 
Published: November 2006

AbstractPhotosensitized oxidation products of α‐tocopherol were analyzed by reversed phase high‐performance liquid chromatography (CL‐HPLC) in combination with chemiluminescence detection, to measure hydroperoxide derivatives. An intense peak was observed on the chemiluminescence chromatogram, corresponding to 8a‐hydroperoxy‐α‐tocopherone (α‐tocopherol hydroperoxide), the identity of which was confirmed by1H nuclear magnetic resonance and mass spectrometry. Observed peak intensities correlated with the peroxide value of oxidized α‐tocopherol. As little as 50 pmol of 8a‐hydroperoxy‐α‐tocopherone was detectable. The CL‐HPLC method, which is specific for the detection of hydroperoxides, should prove useful in studies on tocopherol oxidation in foods and biological systems.
α‐Helical requirements for free apolipoproteins to generate HDL and to induce cellular lipid efflux
Authors: Hara Hitoshi , Hara Hiroko , Komaba Akira , Yokoyama Shinji 
Published: November 2006

AbstractThe structural requirement has been studied for apolipoproteins in their free form to interact with cells, to generate high density lipoprotein (HDL), and to cause cellular lipid efflux (J. Biol. Chem. 266, 3080–3086, 1991). It is shown that human apolipoprotein (apo) A‐IV and apolipophorin III ofManduca sexta cause cholesterol efflux from cholesterol‐loaded mouse peritoneal macrophages and reduce intracellularly accumulated cholesteryl ester as a results of forming HDL‐like particles with cellular lipids, as do apoA‐I, A‐II and E. On the other hand, similar to apoC‐III, reduced‐and‐carboxymethylated human apoA‐II had no such effect. Thus, apolipoproteins seem to require at least four amphiphilic helical segments per molecule to express this function.
Inhibition of myocardial lipoprotein lipase by U‐57,908 (RHC 80267)
Authors: Carroll Rogayah , Severson David L. 
Published: November 2006

AbstractU‐57,908 (RHC 80267) was shown to inhibit lipoprotein lipase (LPL) activity in cardiac myocytes from rat hearts; the concentrations required for inhibition to 50% of control activity were 1.1 μM and 2.5 μM for myocyte homogenates and a post‐heparin medium preparation, respectively. The inhibition of LPL activity by U‐57,908 was not changed when the concentration of the triolein substrate and apolipoprotein CII activator in the assay was reduced. The availability of U‐57,908 as a potent and selective LPL inhibitor may provide a useful experimental approach in studies on lipoprotein metabolism.
Glycolipids of a human glioma cell line bearing receptors for platelet‐derived growth factor (PDGF)
Authors: Yates Allan J. , Agudelo Javier D. , Sung Ching‐Ching 
Published: November 2006

AbstractGlycolipids of U‐1242 MG were characterized because results of previous studies showed that exogenous gangliosides, especially GM3, inhibit PDGF‐stimulated growth of this human glioma cell line. GM3 and GM2 are the major gangliosides; both separate as doublets with thin‐layer chromatography. The major neutral glycolipid is glucocerebroside with nonhydroxy fatty acids, but paragloboside, ceramide dihexoside, globoside, and asialoGM2 (GA2) are also present. The coexistence in U‐1242 MG of these gangliosides and the PDGF receptor, whose mitogenic signal is modulated by GM3 in these cells, suggests a possible functional relationship among them with respect to growth regulation.