bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neutral glycolipids of human and bovine milk
Authors: Newburg David S. , Chaturvedi Prasoon 
Published: November 2006

AbstractThe neutral glycolipids of milk, a small fraction of the total lipids, are of potential biological importance. The simultaneous quantitation of the simple (less than five sugars) glycosphingolipids of human milk samples was achieved by high‐pressure liquid chromatography. The samples, representing various stages of lactation, parity of the nursing child, and age of the mother, contained similar glycolipid patterns, but with varying individual glycolipid concentrations. The cerebrosides are major glycosphingolipids of human milk: the non‐hydroxylated fatty acid (NFA)‐containing species are present at 1.8 μM, and the hydroxylated and/or short‐chain fatty acid‐containing species (HFA) are present at 1.7 μM; NFA lactosylceramide is present at 931 nM. The cerebrosides appear to be primarily galactosylceramides (galactocerebrosides); glucosylceramides (glucocerebrosides) are a minor component. Globotriaosylceramide (Gb3) is found at 50 nM and 73 nM for the NFA and HFA species, respectively, while globoside (Gb4) is found at 45 nM and 46 nM for the NFA and HFA species. Bovine milk glycosphingolipids differ from those of human milk, with bovine milk containing mainly NFA glucosylceramide (8 μM) and NFA lactosylceramide (17 μM); bovine milk contains little Gb3 or Gb4.
Influence of dietary fats on butyrylcholinesterase and esterase‐1 (ES‐1) activity in plasma of rats
Authors: Van Lith H. A. , Herman S. , Zhang X. , Van Der Palen J. G. P. , Van Zutphen L. F. M. , Beynen A. C. 
Published: November 2006

AbstractWe studied the effects of dietary fats, especially fish oil, on the activities of esterase‐1 (ES‐1) and butyrylcholine‐sterase in the plasma of rats. The identification of nutritional determinants of these enzymes could provide clues as to their physiological function. Fish oil, when compared with corn oil, consistently caused increased activities of both enzymes. Plasma ES‐1 activity, but not butyrylcholinesterase activity, was increased after isocaloric replacement of carbohydrates by coconut fat. Dietary medium‐chain triglycerides, when compared with corn oil, produced decreased and increased activities of butyrylcholinesterase and ES‐1, respectively. Various plant fats, such as corn oil, linseed oil, coconut fat, palm oil, palm kernel oil, soybean oil and rapeseed oil, did not differentially influence butyrylcholinesterase activities. Plasma triglyceride concentrations were lowered by fish oil and increased by coconut fat and palm kernel oil. For individual rats in 5 out of 6 experiments, weak, negative correlation coefficients of the order of 0.3 were found between the changes in plasma butyrylcholinesterase activities and in plasma triglyceride concentrations.
Modulation of fatty acid incorporation and desaturation by trifluoperazine in fungi
Authors: Kamisaka Yasushi , Yokochi Toshihiro , Nakahara Toro , Suzuki Osamu 
Published: November 2006

AbstractThe effects of trifluoperazine (TFP) on [1‐14C]fatty acid incorporation into the lipids ofMortierella ramanniana var.angulispora were studied. TFP decreased [1‐14C]‐fatty acid incorporation into phosphatidylcholine, phosphatidylethanolamine and triacylglycerol, but greatly increased14C‐labeling in phosphatidic acid. These changes in [1‐14C]fatty acid incorporation induced by TFP were accompanied by a decrease in desaturation of some [1‐14C]fatty acids taken up by the fungal cells. When [1‐14C]lioleic acid (LA) was incubated with the fungal cells, total γ‐linolenic acid (GLA) formation from incorporated [1‐14C]LA decreased, but the14C‐labeled GLA conent in individual lipid classes was essentially unchanged. This suggests that the site of the TFP effect on GLA formation from [1‐14C]LA taken up from the medium is not the desaturase acting on LA linked to complex lipids. On the other hand, GLA formation from [1‐14C]oleic acid was much less susceptile to TFP, which suggests that in this fungus Δ6 desaturation to GLA has at least two different pathways with different degrees of susceptibility to TFP.
Dependence of the bilayer phase transition temperatures on the structural parameters of phosphatidylcholines
Authors: Huang C. , Li Shusen , Wang Zhao‐qing , Lin Hai‐nan 
Published: November 2006

AbstractMost saturated diacyl phosphatidylcholines C(X):C(Y)PC (saturated 1,2‐diacyl‐sn‐glycero‐3‐phosphocholine with X carbons in thesn‐1 acyl chain and Y carbons in thesn‐2 acyl chain), in excess water, can self‐assemble into lamellae which, upon heating, may undergo multiple thermotropic phase transitions at well‐defined, discrete temperatures. The transition temperature corresponding to the main or the gel to liquid‐crystalline phase transition (Tm) is known for many bilayers of fully hydrated phosphatidylcholines. In this study, we have analyzed the Tm values of 44 molecular species of phosphatidylcholines in terms of their structural and packing characteristics in the gel‐state bilayer. Two general equations are thus derived: Tm=162.26−3651.71 (1/N)−88.42 (ΔC/N) for C(X):C(Y)PC with X≥Y, and Tm=157.68−3525.44 (1/N)−93.28 (ΔC/N) for C(X):C(Y)PC with X<Y. Here, N is the minimal hydrophobic thickness of the dimeric C(X):C(Y)PC in the gel‐state bilayer and ΔC is the effective chain length difference between thesn‐1 andsn‐2 acyl chains for the monomeric C(X):C(Y)PC in the gel‐state bilayer. The advantage of these two equations in predicting the Tm values for phosphatidylcholines with ΔC/CL values in the range of 0.07 to 0.40 is their simplicity. A figure containing a total of 173 calculated Tm values is also presented.
Effect of cell density on cytotoxicity of ether lipid analogues in variants of B16 murine melanoma
Authors: Lligona Trulla Luis , Magistrelli Armondo , Salmona Mario , Teresa Tacconi Maria 
Published: November 2006

AbstractEther lipids are defined here as analogues of naturally occurring lysophosphatidylcholines with cytotoxic activity against neoplastic cells. The activity of 1‐O‐octadecyl‐2‐O‐methyl‐rac‐glycero‐3‐phosphocholine (ET18OMe) and 3‐hexadecylmercapto‐2‐methoxymethyl‐propyl‐1‐phosphocholine (Ilmofosine®) (BM 41.440) was tested in variants of B16 murine melanoma, grown in adhesion cultures (B16F1 with low metastatic potential; B16F10 and B16BL6 with high metastatic potential). Cytotoxicity was evaluated by counting the cells that survived after 24h of drug exposure. Cholesterol, sphingomyelin, total phospholipid and phosphatidylcholine levels were determined. After 24 h of drug exposure, cultures of the B16BL6 variant contained a larger number of cells, especially when high drug concentrations (100–250 μM) were used, than cultures of the B16F1 and B16F10 variants. The sensitivity of ET18OMe of the three variants was evaluated at different cell densities (at each density the dose was equalized per number of cells/well; 0.1 μmol/106 cells/well). In B16F1 and B16F10 cultures the dose‐response curve was not affected by the number of cells/well, while in B16BL6 no more than 20% of the cells were killed at all cell densities measured. A linear relationship was noted between cell density and cholesterol/phospholipid and sphingomyelin/phosphatidylcholine ratios in the resistant variant B16BL6, confirming that lipid composition modulates the cytotoxic activity of ether lipids.
Modulation of phorbol ester‐associated events in epidermal cells by linoleate and arachidonate
Authors: Belury Martha A. , Locniskar Mary , Fischer Susan M. 
Published: November 2006

AbstractTo elucidate the events elicited by the skin tumor promotor 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), which are modulated by linoleic acid (LA) and arachidonic acid (AA), the activity of these fatty acids in cultured mouse epidermal cells was compared. Approximately 94% of either exogenous radiolabelled fatty acid was incorporated into the total phospholipid pool over 15 h. The relative distribution among the phospholipid classes differed, however, such that approximately 70% of phospholipid‐associated [14C]‐LA was found in phosphatidylcholine, compared to approximately 30% for [14C]AA. Phosphatidylethanolamine and phosphatidylinositol/phosphatidylserine contained 17 and 13% of the phospholipid [14C]LA, and 34 and 30% of [14C]AA, respectively. Prostaglandin (PG) E2 production was low but similar in unstimulated cultures prelabelled with either [14C]LA or [14C]AA. However, in cultures treated with TPA (1.6 μM), [14C]AA‐prelabelling resulted in approximately three times the amount of [14C]PGE2 compared with cultures prelabelled with [14C]LA. Cultured cells were found to contain significant δ6 desaturase activity, which may enable conversion of LA to AA, and thus may account for the observed PGE2 production from [14C]LA treated cells. AA‐Supplemented (1.6 μM) cultures supported approximately twice the induction of ornithine decarboxylase activity by TPA compared with cultures treated with 1.8 μM LA. Activation of partially purified protein kinase C was similar for either fatty acid tested over a 10–300 μM dose range. Overall, the results suggest that LA does not have the same biological activity as AA with regard to several TPA‐associated events known to be important in skin tumor promotion. This reduced biological activity of LA may be partly responsible for the known inhibition of mouse skin tumor promotion by high dietary levels of LA [Leyton, J., Lee, M.L., Locniskar, M.F., Belury, M.A., Slaga, T.J., Bechtel, D., and Fischer, S.M. (1991)Cancer Res. 51, 907–915].
Compounds biologically similar to platelet activating factor are present in stored blood components
Authors: Silliman Christopher C. , Johnson Chris A. , Clay Keith L. , Thurman Gail W. , Ambruso Daniel R. 
Published: November 2006

AbstractAgents which prime the neutrophil NADPH oxidase develop during routine storae of whole blood and packed red blood cells. This plasma priming activity can be inhibited by bepafant (WEB 2170), a specific platelet activating factor (PAF) receptor antagonist. Quantitation of the priming agent(s), by a commercially available radioimmunoassay for PAF, reproducibly demonstrated high levels of PAF activity. However, analysis of these plasma samples from stored blood components by gas chromatography/mass spectroscopy did not reveal any 1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine. We conclude that the polyclonal antibody to PAF used in these studies may have recognized different epitopes of a family of heterogeneous, biologically active lipids that manifest their effects through the PFA receptor.
Involvement of vitamin E and protein thiols in the inhibition of microsomal lipid peroxidation by glutathione
Authors: Palamanda Jairam R. , Kehrer James P. 
Published: November 2006

AbstractIron‐ascorbate stimulated lipid peroxidation in rat liver microsomes can be inhibited by glutathione (GSH). The role of protein thiols and vitamin E in this process was studied in liver microsomes isolated from rats fed diets either sufficient or deficient in vitamin E and incubated at 37°C unde 100% O2. Lipid peroxidation was induced by adding 400 μM adenosine 5′‐triphosphate, 2.5 to 20 μM FeCl3, and 450 μM ascorbic acid. One mL of the incubation mixture was removed at defined intervals for the measurement of thiobarbituric acid reactive substances (TBARS), protein thiols and vitamin E. In vitamin E sufficient microsomes, the addition of GSH enhanced the lag time prior to the onset of maximal TBARS accumulation and inhibited the loss of vitamin E. Treatment of these microsomes with the protein thiol oxidant diamide resulted in a 56% loss of protein thiols, but did not significantly change vitamin E levels. However, diamide treatment abolished the GSH‐mediated protection against TBARS formation and loss of vitamin E during ascorbate‐induced peroxidation. Liver microsomes isolated from rats fed a vitamin E deficient diet contained 40‐fold less vitamin E and generated levels of TBARS similar to vitamin E sufficient microsomes at a 4‐fold lower concentration of iron. GSH did not affect the lag time prior to the onset of maximal TBARS formation in vitamin E deficient microsomes although total TBARS accumulation was inhibited. Similar to what was previously found in vitamin E sufficient microsomes [Palamanda and Kehrer, (1992)Arch. Biochem. Biophys. 293, 103–109], GSH prevented the loss of protein thiols in vitamin E deficient microsomes. However, GSH did not protect efficiently against the loss of residual vitamin E in deficient microsomes. These data provide support for the concept that GSH protects against microsomal lipid peroxidation by maintaining protein thiols, and consequently vitamin E, in the reduced state. The lack of protection in vitamin E deficient microsomes may be related to the inability of such low levels of vitamin E to inhibit peroxidation.
Effect of varying proportions of dietary menhaden and corn oil on experimental rat mammary tumor promotion
Authors: Cohen Leonard A. , Chen‐Backlund Jye‐Yu , Sepkovic Daniel W. , Sugie Shigeyuki 
Published: November 2006

AbstractDose‐related effects of long‐chain highly unsaturated n−3 fatty acids on the development ofN‐nitrosomethylurea (NMU)‐induced rat mammary tumors were assessed in female F344 rats. Four test groups (36 rats/group) were fed the following high‐fat (HF) diets (23% fat, w/w): Group 1, 18% menhaden oil (MO) and 5% corn oil (CO); Group 2, 11% MO and 11.8% CO; Group 3,5% MO and 18% CO; Group 4, CO alone. A fifth group, serving as an internal control, was fed a low‐fat diet containing 5% CO alone. Experimental diets were begun after initiation with NMU, and the experiment was terminated 31 wk later. Total tumor numbers in the five groups were 28, 16, 32, 26 and 11, respectively, indicating that the promotion phase of NMU‐induced carcinogenesis was significantly suppressed only when equal parts of CO and MO (Group 2) were fed or when CO alone was fed at 5% (w/w). At high (Group 1) or low (Group 3) levels of MO, tumor numbers were indistinguishable from the HF CO group (Group 4). The same pattern was observed when assessed in terms of cumulative tumor incidence and multiplicity. However, when expressed in terms of final tumor incidence, dietary MO did not suppress tumor promotion in a statistically significant fashion at any concentration. Animals fed MO gained weight at the same rate as those fed CO, indicating that the presence of MO in the diet did not result in food avoidance behavior. Measurement of total serum cholesterol indicated an inverse trend with respect to the MO content of the diet. Analysis of serum fatty acid profiles indicated that the proportion of n−3 and n−6 polyun‐saturated fatty acids (PUFA) in the serum reflected that of the diet. These results support the hypothesis that the relative proportions of dietary n−3/n−6 fatty acids play an important role in the suppression of experimental mammary tumorigenesis and suggest that changes in circulating cholesterol or n−3 PUFA levels, induced by dietary MO, are not directly related to tumor development.
Pollen sterols from three species of sonoran cacti
Authors: Lusby W. R. , Buchmann S. L. , Feldlaufer M. F. 
Published: November 2006

AbstractCactus bees are important pollinators that contribute to the long‐term stability of arid regions in the United States. Since all insects are dependent upon a dietary source of sterol for normal growth, development and reproduction, a study was undertaken to determine neutral sterols available to cactus bees. The total neutral sterol composition of hand‐collected pollen was determined for three species of Sonoran cacti by gas‐liquid chromatography and mass spectrometry. 24‐Methylenecholesterol was the predominant pollen sterol in Engelmann's prickly pear,Opuntia phaeacantha, cholla,O. versicolor, and cardon,Pachycereus pringlei. Two pentacyclic triterpene alcohols, lupeol and moretenol, were also isolated. Since no cholesterol was detected in any of the pollen samples, cactus bees would have to utilize the 24‐alkyl sterols unchanged or convert these sterols to cholesterolvia dealkylation.
Garlic supplementation and lipoprotein oxidation susceptibility
Authors: Phelps Stacy , Harris William S. 
Published: November 2006

AbstractInterventions which make serum lipoproteins less susceptible to oxidation may be antiatherogenic. The antioxidant properties of garlic which have been demonstratedin vitro led us to investigate the effects of garlic supplements on lipoprotein oxidation susceptibility in humans. Ten healthy volunteers were given 600 mg/d of garlic powder (6 tablets of Kwai®) for two weeks in a placebo‐controlled, randomized, double‐blind crossover trial. We found that although serum lipid and lipoprotein levels were not lowered in this short time period, theex vivo susceptibility of apolipoprotein B‐containing lipoproteins to oxidation was significantly decreased (−34%). Because garlic has been reported to beneficially affect serum lipid levels, platelet function, fibrinolysis and blood pressure, this additional effect of retarding lipoprotein oxidation may contribute to the potential antiatherosclerotic effect of garlic.
Transient activation of 1‐O‐alkyl‐sn‐glycero‐3‐phosphocholine: Acetyl‐CoA acetyltransferase during the incubation of macrophages
Authors: Sugiura Takayuki , Fukuda Teruo , Cheng Neng‐neng , Waku Keizo 
Published: November 2006

AbstractThe activity of the platelet‐activating factor (PAF)‐synthesizing enzyme, 1‐O‐alkyl‐sn‐glycero‐3‐phosphocholine (lysoPAF):acetyl‐CoA acetyltransferase (EC 2.3.1.67) in alveolar macrophage lysate was found to be elevated after warming the cells to 37°C. Such an increase in enzyme activity was detectable only when intact cells were warmed. The stimulation was transient, reaching a peak at 2 min, and then gradually decreased to the control level. We could not find increased PAF formation in warmed cells which had increased acetyltransferase activity, even though substantial amounts of lysoPAF were shown to be present within cells. In contrast, considerable amounts of PAF were formed after treatments of the cells with exogenous lysoPAF. These results suggest that the activation of acetyltransferase is not sufficient to induce PAF formation and that the increased availability of substrates, especially lysoPAF, in the cells is indispensable for triggering PAF biosynthesis in this type of cells.
Effects of an eicosapentaenoic and docosahexaenoic acid concentrate on a human lung carcinoma grown in nude mice
Authors: de Bravo M. G. , de Antueno R. J. , Toledo J. , De Tomás M. E. , Mercuri O. F. , Quintans C. 
Published: November 2006

AbstractThe effects of the n−3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on the growth of a human lung mucoepidermoid carcinoma (HLMC) in athymic mice were studied. The mice were divided into three groups which were given either a control chow diet (C), a chow diet supplemented with EPA/DHA (P) (25 or 50 mg of free n−3 fatty acids/g of pellet/day), or chow diet supplemented with palmitic acid (S) (isocaloric with P). Two independent experimental schedules were followed: i) host mice bearing either tumors that were allowed to reach 4000 mm3, or only 35 mm3, were fed C, P or S for 21 or 41 days; ii) animals were fed C, P and S for 9 days before tumor implant and were maintained on these diets throughout tumor growth. Food consumption, mouse weight and liver/body weight ratio showed no significant differences between supplemented diets and chow. Tumor growth was markedly inhibited (45%) in both experiments by the EPA/DHA supplemented diet. In Experiment 2, only 60% of mice fed diet P had tumors. The fatty acid composition of neutral and polar lipids of host liver and tumor reflected the dietary intake of n−3 fatty acids; the content of arachidonic acid was reduced by 50%, and EPA/DHA was increased 3‐to 5‐fold. Tumor prostaglandin E2 levels were reduced 7.4‐fold in the P group. The reduced PGE2 content may be a factor in tumor growth inhibition.
Fatty acid composition of subcellular particles from sheep platelets and topological distribution of phosphatidylethanolamine fatty acids in the plasma membrane
Authors: Sánchez‐Yagüe J. , Cabezas J. A. , Llanillo M. 
Published: November 2006

AbstractThe fatty acid composition of individual phospholipids in subcellular fractions of sheep platelets and the asymmetrical distribution of phosphatidylethanolamine (PE) fatty acyl chains across the plasma membrane were examined. The main fatty acids of total lipid extracts were oleic (18∶1; 32–41%), linoleic (18∶2, 10–17%), stearic (18∶0; 13–15%), palmitic (16∶0; 11–15%) and arachidonic (20∶4; 8–12%) acids, with a saturated/unsaturated ratio of about 0.4. Each phospholipid class had a distinct fatty acid pattern. Sphingomyelin (SM) showed the highest degree of saturation (50%), with large proportions of behenic (22∶0), 18∶0 and 16∶0 acids. The main fatty acid in PE, phosphatidylserine (PS) and phosphatidylcholine (PC) was 18∶1n−9. Our findings suggest that fatty acids are asymmetrically distributed between thecholineversus the non‐choline phospholipids, and also between plasma membranes and intracellular membranes. The transbilayer distribution of PE fatty acids in plasma membranes from non‐stimulated sheep platelets was investigated using trinitrobenzenesulfonic acid (TNBS). A significant degree of asymmetry was found, which is a new observation in a non‐polar cell. The PE molecules from the inner monolayer contained higher amounts of 18∶2 and significantly less 18∶1 and 20∶5 than those found in the outer monolayer, although no major differences were detected in the transbilayer distribution of total unsaturatedversus saturated PE acyl chains.
Effect of ethanol on low density lipoprotein and platelet composition
Authors: Hojnacki Jerome L. , Cluette‐Brown Joanne E. , Deschenes Randall N. , Mulligan John J. , Osmolski Thaddeus V. , Rencricca Nicholas J. , Barboriak Joseph J. , Jakubowski Joseph A. 
Published: November 2006

AbstractThe present study was designed to investigate the effect of ethanol (EtOH) dose on low density lipoprotein (LDL) and platelet composition. Male squirrel monkeys were divided into three groups designated Control, Low, and High EtOH, and fed isocaloric liquid diets containing 0%, 12%, and 24% of calories as EtOH, respectively. After four months of treatment, monkeys fed the 12% alcohol dose had LDL and platelet cholesterol concentrations similar to Controls. By contrast, platelet membranes from High EtOH animals contained significantly more cholesterol which was associated with higher levels of plasma LDL cholesterol and apolipoprotein B. Blood platelet count, size, and mass were similar for all groups and circulating platelet aggregates were absent in the two alcohol cohorts. Despite elevations in platelet cholesterol mass and thromboxane A2 (TXA2) precursor, phospholipid arachidonate, platelet responsiveness, measured as thromboxane formed in response to a collagen challengein vitro, and the cholesterol/phospholipid molar ration, were not significantly altered by high dose alcohol. Normal platelet activity in High EtOH monkeys may have resulted from a significant increase in the platelet phospholipid polyunsaturated/saturated fatty acid ratio and a non‐significant increase in platelet phospholipid mass, both of which would have a fluidizing effect on platelet membranes. Our data indicate that low EtOH intake has no effect on platelet composition and function while unfavorable platelet cholesterol enrichment following consumption of high dose ethanol may arise from elevations in plasma LDL. Potentially thrombogenic (TXA2 formation, platelet aggregate formation) consequences of increased platelet cholesterol in squirrel monkeys fed high levels of alcohol may be averted by compensatory physicochemical changes in platelet membrane lipid composition although persistent elevations in circulating LDL may contribute to increased risk of cardiovascular disease.