bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synthesis of deuterated cyclopropene fatty esters structurally related to palmitic and myristic acids
Authors: Gosalbo Laura , Barrot Mireia , Fabriás Gemma , Arsequell Gemma , Camps Francisco 
Published: November 2006

AbstractTo develop a synthesis of tritiated cyclopropene fatty acids (CPFA), compounds that should prove useful for affinity labeling of desaturases in insect pheromone biosynthetic studies, a series of novel, selectively deuterated CPFA analogues was prepared and characterized. In methyl [16‐2H]12,13‐methylene‐12‐hexadecenoate, the incorporation of deuterium was achieved by treatment of the corresponding ω‐chloro derivative with sodium borodeuteride in dimethylsulfoxide at 70°C for 24 h (67% yield) following conventional procedures. Alkylation of the tetrahydropyranyl derivative of 13‐tridecynol in the presence of lithium diisopropylamide in tetrahydrofuran at −20°C with 1‐chloro‐3‐iodopropane in hexamethylphosphoramide, followed by Jones oxidation of the crude product, yielded 16‐chloro‐12‐hexadecynoic acid (54%), which was esterified to the corresponding methyl ester by treatment with potassium carbonate and methyl iodide in dimethylformamide. Treatment of this acetylenic ester with ethyldiazoacetate in the presence of activated copper‐bronze as catalyst followed by hydrolysis in KOH solution at room temperature yielded 16‐chloro‐12,13‐(carboxymethylene)‐12‐hexadecenoic acid. This diacid was treated with excess oxalyl chloride to give the corresponding diacyl chloride, which was decarbonylated in a diethyl ether solution with zinc chloride, and the cyclopropenium ions thus formed were added at −40°C to a methanolic sodium hydroxide solution of sodium borohydride to give methyl 16‐chloro‐12,13‐methylene‐12‐hexadecenoate. Analogous procedures were followed to prepare methyl [17‐2H]10,11‐methylene‐10‐hexadecenoate, methyl [17‐2H]11,12‐methylene‐11‐hexadecenoate and methyl [17‐2H]12,13‐methylene‐12‐hexadecenoate from the corresponding diacids using sodium borodeuteride in the reduction of the cyclopropenium ions. Alternatively, methyl [2,2,3,3‐2H4]hexadecynoate, prepared by reaction of methyl 2,11‐hexadecadiynoate with magnesium in deuterated methanol at room temperature, was submitted to the above cyclopropenylation and reductive decarbonylation sequence to give methyl [2,2,3,3,17‐2H5]‐11,12‐methylene‐11‐hexadecenoate. In summary, complementary methods for the selective incorporation of one to five deuterium atoms into cyclopropene fatty acids, at different sites, in moderate to high yields have been developed. The methods should easily be applicable to the preparation of the corresponding tritiated analogues.
Synthesis of arachidonic acid metabolites by syrian hamster platelets and peritoneal cells
Authors: Surette Marc E. , Whelan Jay , Lu G. ‐P. , Kinsella John E. 
Published: November 2006

AbstractIn this study, the metabolism of arachidonic acid by hamster platelets and peritoneal macrophages was assessed. Peritoneal macrophages stimulatedin vitro with the calcium ionophore A23187 or stimulatedin vivo by intraperitoneal injections of opsonized zymosan produced prostaglandin E2, thromboxane B2 (TxB2) and 6‐keto‐prostaglandin F1α, as determined by radioimmuno assays. Leukotriene B4 (LTB4), and 11‐ and 15‐hydroxyeicosatetraenoic acids (HETE), which were identified by reverse‐phase highperformance liquid chromatography coupled with diode array detection, were produced by peritoneal cells stimulatedin vitro with A23187 but were not found in the peritoneal exudate followingin vivo stimulation with opsonized zymosan. Synthesis of 11‐ and 15‐HETE, but not LTB4, was inhibited by 1 μM indomethacin but not by 10 μM nordihydroguaiaretic acid, which did inhibit LTB4 synthesis. Washed hamster platelets were prepared and shown to synthesize TxB2, 12‐HETE and 12‐hydroxyheptadecatrienoic acid following stimulation with thrombin. This paper is the first to report on eicosanoid metabolism in tissues related to atherosclerosis, thrombosis and inflammation in hamsters.
Gangliosides and atherosclerosis
Authors: Prokazova N. V. , Bergelson L. D. 
Published: November 2006

AbstractThe ganglioside levels in atherosclerotic lesions of human aorta are considerably higher than those in unaffected areas of aorta, and atherosclerotic patients frequently have increased concentrations of serum gangliosides. The present review summarizes recent findings that suggest the possible involvement of aortic gangliosides in platelet activation and adhesion of platelets to the vessel wall. The effect of gangliosides on the structure of low density lipoproteins (LDL), on the interaction of LDL with macrophages and hepatic cells and on the LDL‐regulated biosynthesis of cholesterol is also discussed.In vitro experiments have demonstrated that a major ganglioside of the intima of atherosclerotic aorta induces rapid adhesion, aggregation and spreading of platelets. Moreover, gangliosides present in elevated amounts in the intercellular space of atherosclerotic aortic tissue modify the surface structure and stimulate aggregation of LDL. Ganglioside‐modified LDL are readily recognized and taken up by macrophages, while preincubation of LDL with low concentrations of gangliosides inhibits LDL binding to hepatic cells. Thus, ganglioside enrichment of LDL is likely to interfere with LDL clearancevia the hepatic cells. Thus, ganglioside enrichment of LDL is likely to interfere with LDL clearancevia the hepatic LDL receptor, and to stimulate binding of LDL to the scavenger receptor of macrophages. It is postulated that high ganglioside levels in the aorta and serum may be an additional risk factor in atherosclerosis.
Regulation of rat liver microsomal cholesterol ester hydrolase by reversible phosphorylation
Authors: Martínez María J. , Hernández María L. , Lacort Mercedes , Ochoa Begoña 
Published: November 2006

AbstractThe regulation of neutral cholesterol ester hydrolase activity by changes in its phosphorylation state was studied in rat liver microsomes. Treatment with cAMP‐dependent protein kinase resulted in increased enzyme activity, which was further enhanced by the addition of cAMP and MgATP. Consistent activations were also achieved with MgCl2 and MgATP, the magnesium effect being abolished by ethylenediaminetetraacetic acid and adenosine triphosphate. Cholesterol ester hydrolase was activated twofold by free calcium and Ca2+/calmodulin; this latter effect was blocked by the chelator ethyleneglycol‐bis(β‐aminoethyl ether)N,N,N′,N′‐tetraacetic acid and the calmodulin antagonist trifluoperazine. The phosphatase inhibitors pyrophosphate and glycerophosphate led to marked and dose‐dependent increases in esterase activity, whereas okadaic acid elicited no effect. Furthermore, pyrophosphate and okadaic acid did not change the increases in enzyme activity promoted by Ca2+, Ca2+/calmodulin, Mg2+ and MgATP. Cholesterol ester hydrolase was inactivated in a concentration‐dependent manner by nonspecific alkaline phosphatases. In cAMP‐dependent protein kinase/cAMP‐ or Ca2+/calmodulin‐activated microsomes, a time‐dependent loss of activation in cholesteryl oleate hydrolysis was caused by alkaline phosphatase. These findings suggest that microsomal cholesterol ester hydrolase is activated through cAMP and Ca2+/calmodulin phosphorylation, whereas enzyme deactivation is dependent on phosphatase action.
Biphasic modulation of choline uptake and phosphatidylcholine biosynthesis by vasopressin in rat cardiac myocytes
Authors: Man Adrian S. , Lee Edmund , Choy Patrick C. 
Published: November 2006

AbstractThe effect of vasopressin on choline uptake and phosphatidylcholine biosynthesis in isolated rat heart myocytes was investigated. Myocytes were incubated with labelled choline in the presence of 0.05–1.0 μM vasopressin. Uptake of choline was enhanced (25%) by a low concentration (0.2 μM) of vasopressin, but was attenuated (19%) by a higher vasopressin concentration (1.0 μM). The biosynthesis of phosphatidylcholine was also affected by vasopressin in a biphasic manner. At low concentrations of vasopressin, a general increase in cytosine triphosphate:phosphocholine cytidylyltranferase activity was observed that caused an enhanced conversion of phosphocholine to phosphatidylcholinevia the cytidine diphosphocholine pathway. At high vasopressin concentrations, a decrease in the activity of cytidylyltransferase was detected, which was caused by the translocation of the enzyme from the microsomal fraction to the cytosolic fraction. The decrease in enzyme activity coincides with a reduction in the conversion of labelled phosphocholine to phosphatidylcholine. In view of the fact that phospholipid biosynthesis in rat hepatocytes is inhibited by vasopressin at all concentrations, the biphasic modulation of phosphatidylcholine biosynthesis in rat heart myocytes illustrates the diverse effects of this hormone in different mammalian tissues.
Isolation, characterization and biological activity of inositol sphingophospholipids fromPhytophthora capsici
Authors: Pivot Véronique , Bruneteau Maud , Mas Pierre , Bompeix Gilbert , Michel Georges 
Published: November 2006

AbstractSeveral inositol sphingophospholipids (ISPL) were isolated from mycelia ofPhytophthora capsici, a phytopathogenic fungus of pepper (Capsicum annuum c.v. Yolo Wonder). The sphingophospholipids induce a protective response by cotyledons of young peppers against necrotic lesions caused by the pathogenP. capsici. The ISPL structures were determined by chemical methods, fast atom bombardment mass spectrometry and by fast atom bombardment collision‐induced tandem mass spectrometry. All ISPL consisted of ceramides linked to inositol phosphate. The amidelinked fatty acids were found to have 16, 20 and 22 carbon chains. The long chain bases were identified as trimethylsilyl derivatives and shown to be C16‐sphingosine and C16‐dihydrosphingosine. The protective effect of the ISPL on cotyledons of young peppers against necrotic lesions caused by the pathogenP. capsici was shown not to be dependent on the unsaturation of the C16‐sphingosine base and the nature of the acyl chain. We also investigated the effect of growth conditions on the ISPL produced in three different, chemically defined media that are commonly used for fungi cultures. We showed thatP. capsici synthesized one major class of compounds with molecular weights of Mr=833 and 835 containing the 16∶1 base and the 22∶1 or the 22∶0N‐acyl group, independent of the growth medium used. The presence of phosphite or fosetyl‐A1 did not affect the result.
Interaction of dietary fatty acids and cyclosporine a in the borderline hypertensive rat: Tissue fatty acids
Authors: Mills David E. , de Antueno Roberto , Scholey James 
Published: November 2006

AbstractIn this study we examined (i) the effects of cyclosporine A (CS) on tissue lipid composition and (ii) the effect of changes in dietary n−6 fatty acids on tissue responses to CS. Fatty acid composition of liver, kidney, heart and brain were determined after 4 wk of treatment with CS (10 mg/kg·d p.o.) in male borderline hypertensive rats (BHR, n=4/group), whose diet was supplemented with either safflower oil or evening primrose oil (EPO). Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine/phosphatidylinositol, triglyceride and cholesteryl ester fatty acids were measured in kidney, heart, brain and liver. The same parameters were also measured in safflower‐fed BHR (n=4) receiving placebo. The effects of CS on liver microsomal Δ9, Δ6 and Δ5 desaturasesin vitro were also followed. CS affected the fatty acid composition of all tissues examined, with the greatest changes seen in the renal phosphatidylcholine and phosphatidylserine/phosphatidylinositol fractions. All CS‐induced changes that occurred in the liver, brain and renal fatty acids were reversed by EPO. CS elevated Δ9 desaturase but had no effect on Δ6 and Δ5 desaturase. In light of (i) the observation that EPO normalizes renal function and blood pressure in CS‐treated BHR, and (ii) the importance of the kidney in blood pressure regulation, the data suggest that the beneficial effects of EPO on CS toxicity may involve changes in renal phospholipid fatty acid profiles.
Effects of dietary protein and cholesterol on phosphatidylcholine and phosphatidylethanolamine molecular species in mouse liver
Authors: Koba Kazunori , Rozee Linda A. , Horrobin David F. , Huang Yung‐Sheng 
Published: November 2006

AbstractThe present study examined the effects of two atherogenic factors, animal protein and cholesterol, on the distribution of fatty acids and the molecular species of major liver phospholipids in mice. Weanling mice were fed a semisynthetic diet supplemented with either casein or soy protein (20%, w/w) in the presence or absence of 0.5% cholesterol for 4 wk. Results from mouse liver showed that animal protein and, more so, dietary cholesterol modified the fatty acid profiles of the phospholipids. Animal protein had no significant effect on the concentration of lipids, but it altered the relative distribution and fatty acid profiles of the phospholipids, phosphatidylcholine and phosphatidylethanolamine. Dietary cholesterol, on the other hand, significantly increased the concentration of liver lipids, but it did not alter the relative distribution of phosphatidylcholine and phosphatidylethanolamine. In cholesterol‐fed mice, the proportions of molecular species containing 18∶2n−6 were increased, whereas those containing 20∶4n−6 were decreased, indicating that dietary cholesterol suppressed linoleic acid metabolism. Since cholesterol feeding selectively decreased the ratio of 18∶0/20∶4n−6 in phosphatidylcholine, whereas it increased the 18∶0/18∶2n−6 ratio in phosphatidylethanolamine, this finding suggests that dietary cholesterol may affect the incorporation of fatty acids but not the rate of synthesis of phosphatidylcholine and phosphatidylethanolamine.
Effect of dietary fish oil on blood levels of free fatty acids, ketone bodies and triacylglycerol in humans
Authors: Dagnelie Pieter C. , Rietveld Trinette , Swart G. Roelof , Stijnen Theo 
Published: November 2006

AbstractAlthough the reduction of serum triacylglycerol concentrations by dietary fish oil is a well‐known effect, the exact mechanism of this effect has not been previously studied in human subjects. Therefore, the aim of this study was (i) to examine the effect of short‐term fish oil supplementation on blood concentrations of ketone bodies, free fatty acids and triacylglycerol in healthy humans and (ii) to verify whether the observed relationships between these variables would be consistent with reduced lipolysis and/or enhanced hepatic fatty acid oxidation after fish oil supplementation. Twenty subjects (21–23 years, normal liver function tests) were randomly divided into two groups to supplement their usual diet with either 30 g/d of fish oil (n=11) or olive oil (n=9). Venous blood samples were drawn after an overnight fast, before and after 1, 3 and 7 d of fish oil/olive oil supplementation. Blood concentrations of triacylglycerol and free fatty acids decreased consistently after fish oil supplementation; the reduction was already significant after one day of fish oil (P<0.001 for triacylglycerol andP=0.01 for free fatty acids). In contrast, neither of these blood values changed after olive oil supplementation (P>0.10). No significant changes in glucose, insulin or ketone body levels were observed in either group after supplementation. After fish oil, but not after olive oil supplementation, the ratio of blood ketone body levels to free fatty acid levels increased significantly (P<0.05). Furthermore, after fish oil supplementation only, free fatty acid levels were significantly correlated with levels of ketone bodies (day 7 of supplementation: r=0.90,P<0.001) and triacylglycerol (maximum value on day 3: r=0.77,P<0.01). These findings suggest that reduced lipolysis and increased hepatic β‐oxidation/ketogenesis may contribute to reduced triacylglycerol levels after ω3 fatty acid supplementation in humans. Turnover studies are needed in order to further quantitate these processes.
Lipid peroxidation and antioxidant status is affected by different vitamin E levels when feeding fish oil
Authors: Cho Sung‐Hee , Choi Young‐sun 
Published: November 2006

AbstractThe protective role of vitamin E and changes in the status of several physiological antioxidants after feeding rats a fish oil diet were investigated. Six‐week‐old male Sprague‐Dawley rats were divided into four groups and fed experimental diets for 8 wk. Three fish oil (FO) groups were fed a menhaden fish oil and soybean oil (SO) (9∶1) mixture as 10% (w/w) of the diet. These groups were provided with ≤3, 45 or 209 IU of vitamin E/kg diet. One SO group was used as control and was fed ≤45 IU of vitamin E/kg diet. Plasma vitamin E levels, when expressed as vitamin E per mL plasma, were extremely low in the group fed FO and ≤3 IU of vitamin E, and were lower in the groups fed FO than in the group fed SO. However, plasma vitamin E levels when expressed per mg plasma lipid were higher in the FO groups provided with ≤45 and 209 IU of vitamin E than in the SO group. Compared with the SO group, plasma levels of thiobarbituric acid reactive substances (TBARS), when expressed per mg lipid, were higher in the three FO groups, plasma retinol levels were lower in the FO groups provided with ≤3 and 45 IU of vitamin E, and ascorbic acid levels were lower only in the FO group provided with ≤3 IU of vitamin E. Blood glutathione (GSH) levels were lower in all three FO groups than in the SO group. Liver vitamin E levels increased as the dietary level of vitamin E increased, but all FO groups had higher liver levels of TBARS than the SO group. The dietary vitamin E levels were correlated positively with plasma vitamin E (r=0.71) and negatively with TBARS in both the plasma and liver of rats fed FO. Among the antioxidants measured, correlations were found between plasma retinol and vitamin C (r=0.64), and plasma vitamin C, uric acid (r=0.72) and blood GSH (r=0.60). Weaker correlations were found between plasma retinol, uric acid and blood GSH. It is concluded that vitamin E requirements are higher when feeding fish oil. Vitamin E seems necessary to prevent enhanced lipid peroxidation and to maintain appropriate levels of other physiological antioxidants.
Effects of high corn oil diet on preneoplastic murine colons: Prostanoid production and lipid composition
Authors: Robblee Nancy M. , Bird Ranjana P. 
Published: November 2006

AbstractIn the present study, the effect of normal (5% by wt) and high (23.5% by wt) corn oil diets on prostanoid production and on the lipid composition of preneoplastic colonic epithelium was investigated. CF1 mice (female, 3–4‐weeks‐old) were fed a normal corn oil dietad libitum and were treated with the colon carcinogen 1,2‐dimethylhydrazine (DMH, 20 mg/kg/wk) or saline (control) for 24 wk. At this stage, all animals received the AIN‐76 diet (normal corn oil)ad libitum. Following the last injection, half of the animals from each treatment group were randomly allocated to a high corn oil diet for 5 to 10 wk, whereas the remaining animals continued on the normal corn oil diet. After 5 wk of feeding, the colonic mucosa of carcinogentreated animals had a higher level of bicyclic prostaglandin E2 (PGE2) than had the animals in the control groups; prostanoid synthesis in the colonic mucosa of control animals was unaffected by the high corn oil diet. Preneoplastic colonic mucosa of animals fed the high corn oil diet had a significantly higher level of PGE2 than corresponding control colonic mucosa. The 6‐keto‐prostaglandin F1α/thromboxane B2 ratio was significantly lower in the DMH‐treated groups than in the control groups, and was unaffected by dietary treatments. After 10 wk of feeding a particular diet, the differences in the fatty acid composition between the control and DMH‐treated groups were minor. Our findings demonstrate that the preneoplastic colonic epithelium differs from that of normal epithelium with respect to prostanoid synthesis.
Famesylamine: An inhibitor of famesylation and growth ofras‐transformed cells
Authors: Kothapalli Ravi , Guthrie Najla , Chambers Ann F. , Carroll Kenneth K. 
Published: November 2006

AbstractFarnesylamine, an analogue of farnesol, was shown to inhibit growth of PAP2 cells (ras‐transformed NIH 3T3 cells) in a dose‐dependent manner. This inhibition was overcome by adding farnesol to the culture medium, but not by adding geranylgeraniol, squalene, cholesterol, dolichol, myristic acid or palmitic acid. Farnesylamine inhibited both farnesyl/protein transferase and geranylgeranyl/protein transferase in whole cell extracts and also inhibited the prenylation of proteins, particularlyras p21, in PAP2 cells. Inhibition of prenylation was associated with increased biosynthesis of other products of the mevalonate biosynthetic pathway. These observations suggest that inhibition of the growth of PAP2 cells by farnesylamine may be due to blocking ofras‐mediated signal transduction. This offers a means of investigating mechanisms involved inras action and raises the possibility of developing novel strategies for anticancer therapy.
Different resistance of mammalian red blood cells to hemolysis by bile salts
Authors: Salvioli G. , Gaetti E. , Panini R. , Lugli R. , Pradelli J. M. 
Published: November 2006

AbstractTo evaluate why hemolysis of red blood cells (RBC) by bile acids varies in different mammalian species, we determined the mean corpuscular volume (MCV), lipid content and the concentrations of the conjugates of deoxycholate and of NaCl inducing 50% hemolysis of RBC from healthy humans, pigs, horses, cows, sheep and jaundiced humans. A volume of 0.05 mL of washed RBC at 1% hematocrit, which has the same lipid content but different phospholipid composition and number of erythrocytes (owing to the variable MCV), was incubated in taurodeoxycholate (TDC) solution (0–5 mM) to determine the TDC concentration inducing 50% hemolysis (TDC50). The TDC50 was highest in RBC of sheep and decreased within the series sheep>pig>cow>horse>healthy human>jaundiced human, which have generally increasing MCV. The osmotic resistance followed an inverse order, with jaundiced human >healthy human>horse>cow>pig>sheep. Although we found no correlation between the TDC50 and phospholipid composition of the erythrocytes tested, the extent of bile salt‐induced hemolysis seemed to depend on both the MCV and the number of erythrocytes in the incubation medium.
Fatty acid content and composition ofOenothera hookeri seeds containing mutant plastids
Authors: Epp Melvin D. , Pollard Michael R. 
Published: November 2006

AbstractThe effects of plastid mutations on seed oil content and fatty acid composition are of considerable interest. Seeds of a number of plastome mutants produced by thepm plastome mutator line ofOenothera hookeri were therefore harvested to investigate these effects. The mutants were altered solely in their plastome: each seed lot had the same nuclear background. To facilitate the study, a rapid single‐step method was developed to simultaneously assay both oil content and fatty acid composition of small quantities ofOenothera seed. The lipid analyses showed that the mutated plastome often changed the oil content of the seeds, and that such changes always reduced oil content. Strong negative correlations were observed between oil content and palmitate or γ‐linolenate, and a strong positive correlation was observed between oil content and linoleate. This is the first instance to our knowledge in which plastid mutations have been unequivocally demonstrated to affect seed oil content and composition. Such effects would be indirect, since the mutated plastid genes would not be the structural genes for enzymes on the pathway of oil biosynthesis. The plastid mutations demonstrate another layer of potential complexity in understanding oilseed genetics.