bluuebunny/crossref_metadata_2025 huggingface dataset:
Terpenes in sponge cell membranes: Cell separation and membrane fractionation studies with the tropical marine spongeAmphimedon sp.
Authors: Garson Mary J. , Thompson Janice E. , Larsen Rundi M. , Battershill Christopher N. , Murphy Peter T. , Bergquist Patricia R.
Published: November 2006

The differing sponge and symbiotic microbial cell types in the tropical marine spongeAmphimedon sp. were fractionated according to density, investigated by electron microscopy, and analyzed by high‐performance liquid chromatography and nuclear magnetic resonance for the presence of the terpene metabolite diisocyanoadociane (1) and Δ5,7‐sterols (2–7). A sample of whole sponge was dissected into superficial ectosome and deeper choanosome. The superficial tissue was found to be enriched in sterol relative to choanosome; however, extracts from both tissues contained terpene. Dissociation of whole sponge followed by Ficoll density gradient fractionation showed that there are two chemically distinct types of sponge cells inAmphimedon sp.—small non‐nucleolated cells of low density contain terpene 1 together with sterols, while larger nucleolated cells contain significant levels of terpene, but only traces of sterol. Membrane fractionation studies were undertaken to establish whether the terpene components were located specifically in the cell membranes of these two cell types. A membrane vesicle pellet spun down at 100,000×g from small sponge cells contained sterols, but only traces of terpene, whereas the membrane vesicle preparation from heavier cells contained both terpenes and sterols. Subsequently, the presence of terpenes together with sterols was demonstrated in a membrane vesicle preparation of purity >90% prepared from bacteria‐free sponge cells. These results provide the first experimental evidence that terpenes are associated with sponge cell membranes, where they may function as structural components.
High‐performance liquid chromatographic separation of enantiomeric benzyl glycerides
Authors: Foglia Thomas A. , Maeda Kazuhito
Published: November 2006

The enantiomeric resolution of a series of 1,2‐diacyl‐ and 1,2‐mixed acid‐diacyl‐3‐benzyl‐rac‐glycerols was investigated by high‐performance liquid chromatography (HPLC). Of the racemic benzylglycerols studied, the 1‐O‐benzyl‐2,3‐O‐iso‐propylidene‐rac‐glycerol 1‐acyl‐3‐benzyl‐rac‐glycerol and 2‐acyl‐3‐benzyl‐rac‐glycerol structures could be resolved into their enantiomers. The latter were resolved on a silica (10 μm) column coated with cellulose tribenzoate by isocratic elution with hexane/isopropanol mixtures as mobile phase. The effects of para substitution of the benzyl moiety on the resolution of the acylbenzylglycerols by this HPLC method were evaluated.
Geotrichum candidum NRRL Y‐553 lipase: Purification, characterization and fatty acid specificity
Authors: Baillargeon Mary Welch , McCarthy Stephen G.
Published: November 2006

Lipases fromGeotrichum candidum NRRL Y‐553 are of interest because of their unique specificity forcis‐9‐unsaturated fatty acids relative to both stearic and palmitic acids. The lipases were partially purified by chromatography on Octyl Sepharose, AG MP‐1 macroporous anion exchanger, and chromatofocusing resin. The preparation was found to contain multiple, glycosylated lipases varying slightly in pI (pI 4.88, 4.78, 4.65, 4.57 and 4.52) as judged by both activity and silver staining. The molecular mass determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis was 64 kilodaltons for the main species, with minor species of 60 and 57 kilodaltons present as well. The specificity of the crude lipases for hydrolysis of 4‐methylumbelliferyl esters of oleicvs. palmitic acid was 20‐to‐1. The specificity of the purified, partially separated lipases was similar to that of the crude preparation. Thus the lipases could be used even in crude form for the hydrolysis and restructuring of triacylglycerols on a large scale.
A novel method for the introduction of a methyl group into the furan ring of a 2,5‐disubstituted C18 furanoid fatty estervia a malonic acid function
Authors: Lie Ken Jie Marcel S. F. , Wong Ka‐Po
Published: November 2006

Furan ring opening with benzohydroxamic acid of methyl 9,12‐epoxy‐9,11‐octadecadienoate gave a mixture of positional isomers of conjugated methyl 3‐phenyl‐1,4,2‐dioxazolyl C18‐enone esters 6a,6b. Michael addition of diethyl malonate anion to the conjugated enone system of 6a,6b furnished the corresponding malonyl intermediates 7a,7b, which upon removal of the dioxazole ring by hydrolysis gave methyl 10‐ and 11‐dicarbethoxymethyl‐9,12‐dioxooctadecanoate 8a,8b. Cyclization of the latter gave the trisubstituted C18 furanoid fatty esters 9a,9b, containing the malonate ester function at the 3‐/4‐position of the furan ring. Base hydrolysis of compounds 9a,9b gave the corresponding tricarboxylic acid derivatives 10a,10b, which were esterified to the trimethyl esters 11a,11b in BF3/MeOH. When a mixture of 9a,9b was refluxed with Na2CO3/MeOH, hydrolysis of the malonate ester function was followed by decarboxylation to yield a‐CH2COOH substituent at the 3‐/4‐position of the furan ring (12a, 12b). Esterification of the latter with BF3/MeOH gave the corresponding methyl diester derivatives 13a,13b. When a mixture of tricarboxylic acids 10a,10b was heated at 160–180°C for 6 hr, exhaustive decarboxylation of malonic acid function furnished a methyl group at the 3‐/4‐position of the furan nucleus. Esterification of the decarboxylated product gave a mixture of trisubstituted furanoid compounds 14a,14b (overall yield 28%). The procedure constitutes a novel method for the introduction of a methyl groupvia a malonic acid group to the 3‐/4‐position of the furan ring of a 2,5‐disubstituted C18 furanoid fatty ester.
Preparation and some spectroscopic properties ofN‐heterocyclic derivatives of a novel 1‐pyrroline C18 fatty ester
Authors: Lie Ken Jie Marcel S. F. , Syed‐Rahmatullah M. S. K.
Published: November 2006

A C18 1‐pyrroline fatty ester, methyl 8‐(5‐hexyl‐2‐pyrrolin‐1‐yl)octanoate (1), was prepared from methyliso‐ricinoleate. The C=N bond of the pyrroline ring was oxidized bym‐chloroperoxy‐benzoic acid to yield a mixture of oxaziridine isomers 2a,2b, which decomposed during gas chromatographic analysis to a 2,5‐disubstituted pyrrole derivative, methyl 8‐(5‐hexyl‐1H‐pyrrole‐2‐)octanoate (3). Compound 3 was also obtained by reaction of 2a,2b with dilute HCl in methanol. Reaction of compound 1 with iodo‐methane formed anN‐methyl iminium iodide intermediate 4, which on reduction with sodium borohydride furnished a mixture ofcis/trans‐N‐methyl‐2,5‐disubstituted pyrrolidine derivatives, methyl 8‐(cis/trans‐5‐hexyl‐N‐methyl‐pyrrolidine‐2‐)octanoates 5a,5b. Reduction of compound 1 with NaBH4 gave a mixture ofcis/trans‐isomers of 2,5‐disubstituted pyrrolidine derivatives, methyl 8‐(5‐hexyl‐pyrrolidine‐2‐)octanoates 6a,6b. Acetylation of compounds 6a,6b with acetic anhydride furnished the correspondingN‐acetyl pyrrolidines 7a,7b. When compound 1 was treated with perchloric acid, the corresponding iminium perchlorate derivative, methyl 8‐(5‐hexyl‐1‐pyrrolinium perchlorate‐2‐)octanoate 8 was obtained. The structures of the various derivatives were characterized by a combination of chromatographic, mass spectral and spectroscopic techniques.
Inhibition of ferrous‐induced lipid peroxidation by pyrimido‐pyrimidine derivatives in human liver membranes
Authors: de la Cruz J. P. , Carrasco T. , Ortega G. , de la Cuesta F. Sanchez
Published: November 2006

The effects of pyrimido‐pyrimidine derivatives (dipyridamole, RA‐642, and RA‐233) on lipid peroxidation, using d‐α‐tocopherol as standard, were studied in enriched membrane fractions from human and rat hepatocytes. Equimolar concentrations of ferrous sulfate and ascorbic acid were used to induce lipid peroxidation. The amount of peroxidized lipids observed in membrane fractions from human liver was smaller than in those from rat liver. In both species, however, pyrimido‐pyrimidine derivatives, except for RA‐233 in rat liver, inhibited lipid peroxidation dose‐dependently in the following sequence: RA‐642 > dipyridamole > d‐α‐tocopherol RA‐233.
α‐tocopherol oxidation mediated by superoxide anion (O2−) I. Reactions in aprotic and protic conditions
Authors: Csallany A. Saari , Ha Yeong L.
Published: November 2006

The reaction of α‐tocopherol (α‐T) with superoxide anion (O2−) in both dry acetonitrile and in aqueous acetonitrile solution is described. The O2− was generated by the electrochemical reduction of molecular oxygen in acetonitrile, using tetrabutylammonium bromide as an electrolyte. α‐T was reacted with O2− either in dry acetonitrile or in a 10% aqueous acetonitrile solution. In dry acetonitrile, α‐T was oxidized to a very unstable primary intermediate, which was further oxidized to a secondary, more stable intermediate. The formation of the secondary intermediate depended upon the presence of molecular oxygen. This intermediate readily converted into two compounds in equimolar amounts (designated A and B). The primary, very unstable intermediate was readily reduced again to α‐T by treatment with LiAlH4 or ascorbic acid. However, the secondary intermediate or the stable oxidation products could not be reduced to α‐T. In the 10% aqueous acetonitrile, α‐T was oxidized to α‐tocopheryl quinone, α‐tocopherol dimer and α‐tocopherol dihydroxy dimer, and an unknown compound. In the aqueous medium, no intermediates were formed by the action of O2−. The results of this study indicate that the reaction of α‐T with O2− under aprotic conditions is different from that observed under protic conditions.
α‐tocopherol oxidation mediated by superoxide anion (O2−). II. Identification of the stable α‐tocopherol oxidation products
Authors: Ha Yeong L. , Csallany A. Saari
Published: November 2006

The present paper describes the identification of two stable end products of α‐tocopherol oxidation that were previously detected among the products of the reaction of α‐tocopherol with superoxide anion (O2−) under aprotic conditions. One compound, previously designated compound A, was identified astrans‐7‐hydroxy‐trans‐8,8a‐epoxy‐α‐tocopherone, and the other, designated compound B, was identified ascis‐7‐hydroxy‐cis‐8,8a‐epoxy‐α‐tocopherone. It was also observed that under protic conditions (10% water in acetonitrile) the reaction of α‐tocopherol with O2− did not produce compounds A and B, but rather α‐tocopheryl quinone, α‐tocopherol dimer, α‐tocopherol dihydroxy dimer, and the previously designated compound C. Compound C was identified in the present study as α‐tocopheryl‐quinone‐2,3‐epoxide.
The inhibitory effect of water on the Co2+ and Cu2+ catalyzed decomposition of methyl linoleate hydroperoxides
Authors: Chen H. , Lee D. J. , Schanus E. G.
Published: November 2006

The inhibitory effect of water on the decomposition of methyl linoleate hydroperoxides (MLHP) catalyzed by Co2+ and Cu2+ was studied in a model system using proton nuclear magnetic resonance (NMR) spectroscopy. MLHP were prepared by photoxidation and purified by chromatographic methods. Proton NMR spectroscopy was used to measure reaction rates by monitoring changes in the intensity of the OOH signal. The rate constant of the reaction was obtained by plotting the natural logarithm of MLHP concentrationvs time. In the first part of the study, no transition metals were added to the model system, so that the effect of water could be attributed to the interaction between water and MLHP only. The rate constant of the reaction (K) was found inversely proportional to the concentration of water. There was a downfield chemical shift of both hydroperoxide and water peaks in the NMR spectra when water was added. As temperature increased to 40°C, the difference in K between the systems with 0% and 2% water disappeared. It is proposed that the hydroperoxides were solvated with water which retarded their decomposition. When Co2+ was added to the model system, K decreased as the concentration of water increased from 0% to 1.5%. As temperature increased from 18°C to 40°C, differences between the K for 0% and 2% water disappeared. A similar phenomenon was observed in reactions catalyzed with Cu2+. These findings would support a mechanism in which the protective effect of water involves both the solvation of OOH and hydration of the metal catalyst.
Comparison of free α‐tocopherol and α‐tocopheryl acetate as sources of vitamin E in rats and humans
Authors: Burton Graham W. , Ingold Keith U. , Foster David O. , Cheng Shee C. , Webb Ann , Hughes Lise
Published: November 2006

The uptake of α‐tocopherol from 2R,4′R,8′R‐α‐tocopherol and 2R,4′R,8′R‐α‐tocopheryl acetate has been compared in rats and humans. The two forms of vitamin E were compared simultaneously in each subject (rat and human) by using a combination of deuterium‐substitution and gas chromatography‐mass spectrometry (GC‐MS) to distinguish and measure the competitive uptake of α‐tocopherol from an orally ingested mixture of the acetate and the free phenol forms. When rats were dosed in a manner analogous to that used in traditional bioassays, i.e., providing the two forms of vitamin E one daily in tocopherol‐stripped corn oil for four successive days immediately prior to sacrifice, the net uptake of α‐tocopherol from the free phenol form was only half that from the acetate. This result is consistent with the greater activity of the acetate that had been observed previously in bioassays. However, when the two forms of tocopherol were intubated into rats as a single dose mixed in with an aqueous bolus of standard laboratory diet, the amount of α‐tocopherol taken up from the free form after 24 hr was very similar to that derived from the acetate. In five adult humans, competitive uptake studies of the two forms after a single dose taken with a meal showed that the amount of α‐tocopherol from the free phenol form was equal to that from the acetate in plasma and red blood cells. These findings illustrate the value and potential of using deuterium‐substituted α‐tocopherol and GC‐MS in evaluating the effectiveness of different forms of vitamin E in human studies. The results also stress the need for caution in using data obtained from animal bioassays when considering comparative human nutritional standards.
Differential effects of dietary linoleic and α‐linolenic acid on lipid metabolism in rat tissues
Authors: Garg M. L. , Sebokova E. , Wierzbicki A. , Thomson A. B. R. , Clandinin M. T.
Published: November 2006

Comparative effects of feeding dietary linoleic (safflower oil) and α‐linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α‐linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.
Biosynthesis of membrane cholesterol during peripheral nerve development, degeneration and regeneration
Authors: Yao Jeffrey K.
Published: November 2006

Biosynthesis of peripheral nerve cholesterol was investigated by the in vivo and in vitro incorporation of [1‐14C]‐acetate into sciatic endoneurium of normal rats during development, degeneration and regeneration. Labeled sterols were rapidly formed (<10 min) within the endoneurial portion of sciatic nerve after [1‐14C]acetate administration by intraneural injection. The majority of labeled sterols were initially found in lanosterol and desmosterol. After six hr, the14C‐labeling in both precursors was decreased to minimum, whereas cholesterol became the major labeled product of sterol. As myelination proceeded, the incorporation of [1‐14C]acetate into endoneurial cholesterol decreased rapidly and reached a minimum after six no. In mature adult nerve, an increased proportion of biosynthesis of lanosterol and desmosterol also was demonstrated. The in vitro incorporation of [1‐14C]acetate into cholesterol was inhibited during Wallerian degeneration. Instead, cholesteryl esters were labeled as the major sterol product. Such inhibition, however, was not observed in the adult Trembler nerve (Brain Res. 325, 21–27, 1985), which is presumed to be due to a primary metabolic disorder of Schwann cells. The cholesterol biosynthesis was gradually resumed in degenerated nerve by either regeneration of crush‐injured nerve or reattachment of the transected nerve. These results suggest that cholesterol biosynthesis in peripheral nerve relies on the axon to provide necessary substrates. De novo synthesis appears to be one of the major sources of endoneurial cholesterol that forms and maintains peripheral nerve myelin.
Fatty acid metabolism in renal ischemia
Authors: Ruidera E. , Irazu C. E. , Rajagopalan P. R. , Orak J. K. , Fitts C. T. , Singh I.
Published: November 2006

The increase in free fatty acids in the ischemic tissue is a consistent observation and these free fatty acids are considered, to play a role in the cellular toxicity. To elucidate the cause of higher levels of free fatty acids in ischemic tissue, we examined the catabolism of fatty acids. The β‐oxidation of lignoceric (24∶0), palmitic (16∶0) and octanoic (8∶0) acids and the peroxidation of fatty acids were measured at different times of renal ischemia in whole kidney homogenate. The enzymatic activities for the oxidation of fatty acids decreased with the increase in ischemia time. However, the lipid peroxide levels increased 2.5‐fold of control with ischemic injury. Sixty min of ischemia reduced the rate of oxidation of octanoic, palmitic and lignoceric acids by 57, 59 and 69%, respectively. Almost similar loss of fatty acid oxidation activity was observed in the peroxisomes and mitochondria. These data suggest that loss of mitochondrial and peroxisomal fatty acid β‐oxidation enzyme activities from ischemic injury may be one of the factors responsible for the higher levels of free fatty acids.
Effects of 2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) on de novo fatty acid and cholesterol synthesis in the rat
Authors: Lakshman M. R. , Campbell Barbara S. , Chirtel Stuart J. , Ekarohita Nisa
Published: November 2006

The effects of 1, 5, 10 and 20 μg/kg dosages of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) upon de novo fatty acid and cholesterol synthesis in liver and adipose tissue were determined in pair‐fed rats. The incorporation of tritium from3H2O into tissue lipids was measured. Hepatic and adipose fatty acid synthetic rates (μmoles acetyl units g−1 hr−1 in the control groups were 19.6±4 and 75.7±18.5, respectively, and the liver cholesterol synthetic rate was 2.9±0.5 TCDD (1 μg/kg) inhibited fatty acid synthesis in the liver and adipose tissue, by 44% and 41% respectively, and the liver cholesterol synthesis was inhibited by 37%. The extent of these inhibitions increased with increasing dosages of TCDD. The effect of TCDD on sterol synthesis in adipose tissue could not be determined, because the tritium incorporation into the sterol fraction in this tissue was not detectable.
Dietary manipulation of macrophage phospholipid classes: Selective increase of dihomogammalinolenic acid
Authors: Chapkin Robert S. , Somers Scott D. , Erickson Kent L.
Published: November 2006

Because alterations in the dietary content of fatty acids are an important method for modulating macrophage eicosanoid production, we have quantitated the levels of n−6 and n−3 polyunsaturated fatty acids in peritoneal macrophage individual phospholipids from mice fed diets (3 wk) with either safflower oil (SAF), predominantly containing 18∶2n−6, borage (BOR) containing 18∶2n−6 and 18∶3n−6, fish (MFO) containing 20∶5n−3 and 22∶6n−3, and borage/fish mixture (MIX) containing 18∶2n−6, 18∶3n−6, 20∶5n−3 and 22∶6n−3. Dietary n−3 fattya cids were readily incorporated into macrophage phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS) and phosphatidylinositol (PI). The increase in n−3 fatty acid levels was accompanied by a decrease in the absolute levels of 18∶2n−6, 20∶4n−6 and 22∶4n−6 in PC, PE and PS. Interestingly, PI 20∶4n−6 levels were not significantly lowered (P>0.05) in MIX and MFO macrophages relative to SAF and BOR. These data demonstrate the unique ability of this phospholipid to selectively maintain its 20∶4n−6 levels. In BOR and MIX animals, 20∶3n−6 levels were significantly increased (P<0.05) in all phospholipids relative to SAF and MFO. The combination of borage and fish oils (MIX diet) produced the highest 20∶3n−6/20∶4n−6 ratio in all phospholipids. These data show that the macrophage eicosanoid precursor levels of 20∶3n−6, 20∶4n−6 and n−3 acids can be selectively manipulated through the use of specific dietary regimens. This is noteworthy because an increase in phospholipid levels of 20∶3n−6 and 20∶5n−3, while concomitantly reducing 20∶4n−6, may have therapeutic potential in treating inflammatory disorders.
Lipid abnormalities in pancreatic tissue of streptozotocin‐induced diabetic rats
Authors: Levy Emile , Roy Claude C. , Lepage Guy , Bendayan Moise
Published: November 2006

Pancreatic lipid and fatty acid composition was determined in streptozotocin‐induced diabetic rats and compared to control and insulin‐treated diabetic rats. A pronounced decrease of total fatty acids was recorded and mainly accounted for by a drop of fatty acids in glycerides. Cholesterol, on the other hand, was significantly increased two‐ to three‐fold, leading to an elevated cholesterol/phospholipid ratio. Morpho‐cytochemical studies confirmed these findings because the multiple lipid droplets present in acinar cells of diabetic animals were found to be of cholesterol nature. The major alterations in phospholipid‐fatty acid composition were characterized by an increase of linoleate coupled to a decrease of monounsaturates and arachidonate, suggesting defective metabolism of saturates and of linoleate. This was further supported by fatty acid ratios that suggested low Δ5 and Δ9 desaturation. Daily administration of insulin for 10 days restored and overcorrected the various lipid alterations. This study suggests that there are alterations in lipid composition and metabolism in the exocrine pancreas of chronic streptozotocin‐induced diabetic rats. Their possible role in the mechanism regulating pancreatic function and secretion remains to be elucidated.
Formation of trimers of α‐tocopherol and its model compound, 2,2,5,7,8‐pentamethylchroman‐6‐ol, in autoxidizing methyl linoleate
Authors: Yamauchi Ryo , Kato Koji , Ueno Yoshimitsu
Published: November 2006

The reaction products of α‐tocopherol and its model compound, 2,2,5,7,8‐pentamethylchroman‐6‐ol, during the autoxidation of methyl linoleate at 37 C were investigated. Two isomeric trimers were obtained as the major reaction products of α‐tocopherol, and a trimer was obtained as that of its model chroman. The structure of each trimer has been characterized by IR, UV,1H and13C NMR, and mass spectroscopy. The13C NMR spectra showed the presence of a quaternary carbon atom and a carbon atom bearing two oxy substituents in the molecule. On methanolysis of each trimer, equimolar amounts of the 5‐methoxymethyl compound and the dihydroxy dimer were formed, indicating the presence of a ketal group in the molecule. From these results, new trimeric structures are proposed. The reaction products of α‐tocopherol could be well‐separated by reverse‐phase high performance liquid chromatography. When methyl linoleate was autoxidized in the presence of 1 mol% α‐tocopherol, spirodiene dimer was the initial reaction product of α‐tocopherol, and trimers were formed with the decrease of α‐tocopherol.
Phospholipid analysis of human eosinophils: High levels of alkylacylglycerophosphocholine (PAF precursor)
Authors: Ojima‐Uchiyama Ayako , Masuzawa Yasuo , Sugiura Takayuki , Waku Keizo , Saito Hiroshi , Yui Yasuo , Tomioka Hisao
Published: November 2006

The phospholipid composition and fatty acid profiles of human eosinophils were studied. Extremely high levels of ether phospholipids were found in this type of cell, such as alkylacylglycerophosphocholine (GPC) and alkenyl‐acylglycerophosphoethanolamine (GPE); these two ether phospholipids accounted for about three‐fourths of the choline and ethanolamine glycerophospholipids (CGP and EGP), respectively. Fatty acid analyses revealed that very large portions of arachidonic acid (20∶4) were esterified to alkylacyl‐GPC (92.0% in CGP) and alkenylacyl‐GPE (86.6% in EGP), respectively. While high amounts of alkylacyl‐GPC and the abundance of 20∶4 in this ether phospholipid have been observed in other types of blood cells of various animals, these percentages for human eosinophils are the highest among such cells. These results suggest that alkyl and alkenyl ether phospholipids play essential roles in human eosinophils in various physiological and pathological conditions.
Divinyl ethers and hydroxy fatty acids from three species ofLaminaria (brown algae)
Authors: Proteau Philip J. , Gerwick William H.
Published: November 2006

Three species of brown algae,Laminaria sinclairii, L. saccharina andL. setchellii, have been investigated for the presence of oxylipins. From one,L. sinclairii, three new divinyl ether fatty acids have been characterized as methyl ester derivatives (methyl 12‐[1′ (Z),3′(Z)‐hexadienyloxy]‐6(Z), 9(Z), 11(E)‐dodecatrienoate, methyl 12‐[1′ (Z), 3′ (Z)‐hexadienyloxy]‐9(Z), 11(E)‐dodecatrienoate, and methyl 14‐[1′ (Z),3′ (Z)‐hexadienyloxy]‐9(Z),11(E)‐dodecadienoate, and methyl 14‐[1′ (Z),3′(Z)‐hexadienyloxy]‐5(Z),8(Z),11(Z),13(E)‐tetradecatetraenoate) by a variety of spectroscopic methods. In addition, one new [13(S)‐hydroxy‐6(Z),9(Z),11(E),15(Z)‐octadecatetraenoic acid] and four known monohydroxy polyunsaturated fatty acids have been isolated from all three species as their methyl ester derivatives. The occurrence of these compounds in brown algae strongly suggests that these organisms possess an active lipoxygenase(s) with ω6 specificity.
Separation of bile acid methyl esters by high‐performance liquid chromatography
Authors: Kuhajda K. , Kandrac J. , Dobanović‐Slavica S. , Hranisavljević J. , Miljković D.
Published: November 2006

Conjugated bile acids, namely glyco‐ and tauro‐3α,6α‐dihydroxy‐5β‐cholanoic acid (hyodeoxycholic acid), 3α,7α‐dihydroxy‐5β‐cholanoic acid (chenodeoxycholic acid), 3α,6α,7α‐trihydroxy‐5β‐cholanoic acid (hyocholic acid) and 3α‐hydroxy‐6‐oxo‐5β‐cholanoic acid (6‐keto‐litocholic acid) were isolated from pig bile, and subsequently transformed into the corresponding methyl esters. Separation of the methyl esters of the isolated bile acids by high‐performance liquid chromatography (HPLC) was accomplished on a ZORBAX‐CN column (Dupont, Boston, MA) withn‐hexane/2‐propanol/methylene chloride (89∶6∶5, by vol) as the mobile phase containing traces (≈1%) of amyl alcohol and water as moderators. HPLC analysis of the methyl esters also showed the presence of methyl 3α‐hydroxy‐6‐oxo‐5α‐cholanoate, which was probably produced in the course of alkaline hydrolysis of the conjugated bile acids.
In vitro oxidation of vitamins C and E, cholesterol, and thiols in rat brain synaptosomes
Authors: Vatassery G. T.
Published: November 2006

Free radical‐induced oxidation of vitamins C, E, sulfhydryl compounds, and cholesterol in brain synaptosomes from Fisher 344 rats was studied. The synaptosomes were incubated at 37°C with 2,2′‐abobis‐(2‐amidinopropane) dihydrochloride (AAPH), which undergoes thermal decomposition to yield free radicals. After incubation, the synaptosomes were sedimented, saponified, and extracted with hexane to isolate tocopherol and cholesterol. Ascorbate and tocopherol were assayed by liquid chromatography, cholesterol by gas chromatography, and total sulfhydryls by spectrophotometry. Under thein vitro conditions used in this study, the approximate order for the ease of oxidation of the various compounds was: ascorbate ≫tocopherol>sulfhydryl compounds⋙cholesterol. However, tocopherol and sulfhydryl oxidation occurred even before all of the ascorbate had been consumed. Therefore, the fate of a specific antioxidant at a particular cellular location cannot be predicted with complete accuracy using thein vitro order for ease of oxidation shown here. Ascorbate may play a major role in protecting brain against oxidative damage because: (i) ascorbate concentration is high in brain, (ii) it can regenerate vitamin E from its radical oxidation product, and (iii) it is one of the first antioxidants to be consumed during oxidative reactions.
Sesame seed and its lignans produce marked enhancement of vitamin E activity in rats fed a low α‐tocopherol diet
Authors: Yamashita Kanae , Iizuka Yoshie , Imai Tomoko , Namiki Mitsuo
Published: November 2006

Three series of experiments demonstrated that sesame seed and its lignans cause significant elevation of α‐tocopherol content in rats. In Experiment 1, 20% sesame seed (with a negligible amount of α‐tocopherol) supplementing 10 (low), 50 (normal), or 250 (high) mg/kg α‐tocopherol diets (protein and fat concentrations in diets were adjusted to 200 and 110 g/kg, respectively) all caused a significant increase of α‐tocopherol in the blood and tissue of rats. In Experiment 2, groups of rats were fed five different diets: a vitamin E‐free control diet, a low α‐tocopherol diet, and three low α‐tocopherol diets supplemented with 5, 10, and 15% sesame seed. Changes in lipid peroxides in liver, red blood cell hemolysis, and pyruvate kinase activity, as indices of vitamin E deficiency, were examined. These indices were high in the low α‐tocopherol diet, whereas supplementation with even 5% sesame seed suppressed these indices completely and caused a significant increase of α‐tocopherol content in the plasma and liver. In Experiment 3 two diets containing sesame lignan (sesaminol or sesamin) and low α‐tocopherol were tested. Results in both of the sesame lignan‐fed groups were comparable to those observed in the sesame seed‐fed groups as shown in Experiment 2. These experiments indicate that sesame seed lignans enhance vitamin E activity in rats fed a low α‐tocopherol diet and cause a marked increase in α‐tocopherol concentration in the blood and tissue of rats fed an α‐tocopherol‐containing diet with sesame seed or its lignans.
Suppression by carotenoids of microtenoids of microcystin‐induced morphological changes in mouse hepatocytes
Authors: Matsushima‐Nishiwaki Rie , Shidoji Yoshihiro , Nishiwaki Shinji , Yamada Tetsuya , Moriwaki Hisataka , Muto Yasutoshi
Published: November 2006

Microcystin‐LR is a liver tumor promoter in the okadaic acid class, a group of potent inhibitors of protein phosphatases 1 and 2A. Because of inhibition of protein phosphatases, microcystin‐LR induces hyperphosphorylation of cellular proteins, including cytoskeletal proteins—cytokeratins 8 and 18—and causes morphological changes in mouse hepatocytes in primary culture. We studied the effects of carotenoids to antagonize microcystin‐LR‐induced morphological changes in hepatocytes. β‐Carotene (100 nM to 100 μM), suppressed the morphological changes induced by 100 nM microcystin‐LR in a dose‐dependent manner. Other carotenoids tested exerted similar suppressive effects, although retinoids, such as all‐trans retinol, all‐trans retinoic acid, and 9‐cis retinoic acid, were only weakly suppressive. The relative potency of the suppression correlated significantly with the number of conjugated double bonds in thetrans configuration. β‐Carotene strongly suppressed the hyperphosphorylation of cellular proteins induced by microcystin‐LR without significant changes in the basal phosphorylation level. Other antioxidants, such as α‐tocopherol, did not protect the cells against microcystin‐LR. Taken together, the antagonistic effects of carotenoids against microcystin‐LR are difficult to explain by their antioxidant or provitamin A activities. Suppression of the hyperphosphorylation of cellular proteins may be a novel mechanism by which carotenoids inhibit tumor promotion.
Urinary Malondialdehyde‐Equivalents during ingestion of meat cooked at high or low temperatures
Authors: Brown Ellen D. , Morris Virginia C. , Rhodes Donna G. , Sinha Rashmi , Levander Orville A.
Published: November 2006

Excretion of malondialdehyde (MDA)‐generating substances in the urine has been suggested as an indicator ofin vivo lipid peroxidation. However, MDA in the urine also reflects the amount of lipid peroxidation products consumed in the diet. We determined MDA as the thiobarbituric acid (TBA)‐MDA complex in urine of 19 healthy adults (10 male and 9 female) fed large quantities (3.6–4.1 g/kg body weight) of ground beef cooked at a low or a high temperature. Subjects are a controlled diet with no alcohol or nutritional supplements. For 7 d they consumed ground beef cooked at 100°C for 20 min (low‐temperature meat) followed by 7 d with meat fried at 250°C for 22 min (high‐temperature meat). Prior to the study, subjects consumed their normal free choice diet with moderate amounts of meat. The concentration of MDA in urine at baseline was 2.1±0.3 μmol TBA‐MDA equivalents/day (mean±SEM). After 7 d of low‐temperature meat, urinary TBA‐MDA equivalents increased to 23.1±1.4 μmol/d. Urinary TBA‐MDA equivalents were consistently lower (6.9–8.0 μmol/d) 1, 2, 3, and 7 d after subjects changed to high‐temperature meat. After 7 d of treatment, 97% of the MDA‐equivalents in the meat was recovered in 24‐h urine samples. The low temperature meat had 3–4 times more MDA than did the high‐temperature meat. These data indicate that the amount of meat eaten and the cooking procedures used can dramatically alter urinary MDA. Dietary sources of MDA must be controlled if urinary MDA is to be used as an indicator of oxidative stress.
Diabetes and proteolysis: Effects on carnitine palmitoyltransferase‐I and malonyl‐CoA binding
Authors: Kashfi Khosrow , Cagen Lauren , Cook George A.
Published: November 2006

Malonyl‐CoA binding and malonyl‐CoA inhibition of carnitine palmitoyltransferase‐1 (CPT‐I) were measured in hepatic mitochondria from normal and diabetic rats and in protease‐treated mitochondria from fed rats to test the hypothesis that proteolysis represents a mechanism by which diabetes produces changes in the sensitivity of CPT‐I to inhibition by malonyl‐CoA. As in diabetes, protease treatment increased the apparent Ki values for malonyl‐CoA. Palmitoyl‐CoA greatly diminished malonyl‐CoA specific binding in the mitochondrial system being studied, suggesting strong competition at the malonyl‐CoA binding site. Proteolysis decreased capacity for specific binding of malonyl‐CoA by 60–80%, but it had no effect on binding affinity. In contrast, the decreased specific binding of malonyl‐CoA seen in the diabetic state is accompanied by increased binding affinity. Furthermore, observed Kd values differed from Ki values by a factor of 10 or more, suggesting that measured Kd and Ki may represent different ligand‐protein complexes. These data suggest that alterations in inhibition of CPT‐I by malonyl‐CoA occurring in the diabetic state may involve mechanisms other than simple proteolytic removal of malonyl‐CoA binding sites.
Iron‐catalyzed reaction products of α‐tocopherol with methyl 13(S)‐hydroperoxy‐9(Z),11(E)‐octadecadienoate
Authors: Yamauchi Ryo , Yamamoto Norio , Kato Koji
Published: November 2006

α‐Tocopherol was reacted with methyl 13(S)‐hydroperoxy‐9(Z),11(E)‐octadecadienoate in the presence of an iron‐chelate, Fe(III)‐acetylacetonate, at 37°C in benzene. The reaction was carried out either aerobically or anaerobically. The main products of α‐tocopherol under air were isolated and identified as two stereoisomers of 4a,5‐epoxy‐8a‐hydroperoxy‐α‐tocopherone, four stereoisomers of methyl 9‐(8a‐dioxy‐α‐tocopherone)‐12,13‐epoxy‐10(E)‐octadecenoate, four stereoisomers of methyl 11‐(8a‐dioxy‐α‐tocopherone)‐12,13‐epoxy‐9(Z)‐octadecenoate, two stereoisomers of methyl 13(S)‐(8a‐dioxy‐α‐tocopherone)‐9(Z),11(E)‐octadecadinoate, and α‐tocopherol dimer. Besides the 8a‐(lipid‐peroxy)‐α‐tocopherones, two stereoisomers of methyl 11‐(α‐tocopheroxy)‐12(S),13(S)‐epoxy‐9(E)‐octadecenoate, two stereoisomers of methyl 9‐(α‐tocopheroxy)‐12(S),13(S)‐epoxy‐10(E)‐octadecenoate, and two isomers of methyl (α‐tocopheroxy)‐octadecadienoate were obtained under nitrogen atmosphere. The results indicate that the peroxyl radicals from lipid hydroperoxides prefer to react with the 8a‐carbon radical of α‐tocopherol and the carbon‐centered radicals react with the phenoxyl radical of α‐tocopherol.
Dietary fats rich in saturated fatty acids (12∶0, 14∶0, and 16∶0) enhance gallstone formation relative to monounsaturated fat (18∶1) in cholesterol‐fed hamsters
Authors: Jonnalagadda Satya S. , Trautwein Elke A. , Hayes K. C.
Published: November 2006

To test the possibility that dietary palmitic acid (16∶0) may be lithogenic, different fats were blended to exchange 18∶1 in olive oil with either 16∶0 in palm stearin, 12∶0+14∶0 in coconut oil, or 14∶0+16∶0 in butterfat. Dietary 18∶2 was held constant at 1.2% energy (en) (with extra safflower oil as needed) in these four purified diets containing low fat (11% of total energy) and 0.4% cholesterol. A fifth, high‐fat diet provided 40% of the total energy as the 16∶0‐rich blend. All hamsters fed the low‐fat, 16∶0‐rich blend for six weeks developed cholesterol gallstones (8/8). Although the gallstone incidence was lower for the 12∶0+14∶0‐rich diet (5/8), the severity of stone formation in affected hamsters was equal to that in the low‐fat, 16∶0‐rich group. Mucin accumulation in gallbladder bile was often associated with cholesterol gallstones in diets containing 16∶0, but was minimal in 18∶1‐rich and 12∶0+14∶0‐rich groups. Neither the lithogenic index (all>1.0), plasma lipids, nor liver cholesterol was a selective predictor of stone formation. The high‐fat, 16∶0‐rich diet actually decreased cholesterol stone incidence (3/8) and severity, but yielded a high incidence of pigment stones (5/8). Thus, saturated fat and 16∶0per se were not responsible for the exaggerated lithogenesis. Because the antilithogenic 18∶1‐rich diet also normalized the 18∶2 intake (1.2% en) relative to previous butter diets (0.3% en), the potential importance of essential fatty acids (EFA) deficiency in the model was tested in a second study by feeding graded amounts of 18∶2 (0.3, 0.6, 0.9, and 1.2% en) as safflower oil in four low‐fat, butter‐rich diets (11% en as fat) without alleviating gallstone incidence or severity. These studies indicate that substitution of 18∶1 for saturated fatty acids in low‐fat diets reduces gallstone formation without affecting the lithogenic index. Furthermore, intake of 18∶2 at or below the EFA requirement does not appear to be a major factor in this model.
Reduction of hyperlipidemia in hepatoma‐bearing rats by dietary fish oil
Authors: Kawasaki Masashi , Yagasaki Kazumi , Miura Yutaka , Funabiki Ryuhei
Published: November 2006

The effect of dietary fish oil on serum lipid levels was studied by comparing it with dietary corn oil in Donryu rats subcutaneously implanted with an ascites hepatoma cell line (AH109A). The hepatoma‐bearing rats exhibited hyperlipidemia charactarized by a rise in both serum cholesterol and triglyceride levels. Increased cholesterogenesis in the host liver and decrease steroid excretion into feces are suggested to be responsible for the hepatoma‐induced hypercholesterolemia, and increased fatty acid mobilization from peripheral adipose tissues and decreased triglyceride clearance from the blood circulation are considered causes for the hepatoma‐induced hypertriglyceridemia. Dietary fish oil reduced the hyperfipidemia in these animals, suppressed the hepatoma‐induced increase in hepatic cholesterogenesis and fatty acid mobilization from adipose tissue. Dietary fish oil also tended to increase fatty acid oxidation in the liver. Such diverse effects of fish oil may lead to the reduction of the hepatoma‐induced hyperlipidemia. These results suggest that studies on dietary fish oil may be warranted in patients with cancer‐related hyperlipidemia.
Dietary deficiency of docosahexaenoic acid impairs vision at low light intensities in juvenile herring (Clupea harengus L.)
Authors: Bell Michael V. , Batty Robert S. , Dick James R. , Fretwell Karen , Navarro Juan Carlos , Sargent John R.
Published: November 2006

In the retina of herring (Clupea harengus L.), rods are recruited from about 8 wk after hatching, and from this time there is a linear relationship between the number of rods in the photoreceptor cell population and the content of di22∶6n−3 molecular species of phospholipids. Juvenile herring were reared from four weeks' post‐hatching for 15 wk on eitherArtemia nauplii deficient in 22∶6n−3 or on enrichedArtemia nauplii containing 4.3% 22∶6n−3. The visual performance of the fish was then determined at three light intensities (0.01, 0.1, and 1.0 lux) by observing their frequency of striking at liveArtemia nauplii using infrared video recording. Herring reared on the diet containing no 22∶6n−3 were less active predators, especially at the lowest light intensity where very few strikes were observed. The eyes of these fish contained greatly reduced levels of di22∶6n−3 molecular species of total phospholipid, 2.1% vs. 12.0% in fish supplemented with 22∶6n−3. The contribution of saturated and monounsaturated fatty acids in the molecular species of phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylcholine (PC) was virtually unchanged, while 20∶5n−3 and 22∶5n−3 largely replaced 22∶6n−3. There was an almost complete disappearance of di22∶6n−3 PC, while the amounts of di22∶6n−3 PE and PS fell by 18.1 and 20.6% to 2.7 and 7.6%, respectively. The dipolyunsaturated molecular species di20∶5n−3, 20∶5n−3/22∶5n−3, and di22∶5n−3 made up a substantial part of the deficit. We conclude that a dietary deficiency of 22∶6n−3 during the period early in rod development impairs visual performance such that the fish can no longer feed at low light intensities.
Eicosanoid generating capacities of different tissues from the rainbow trout,Oncorhynchus mykiss
Authors: Knight John , Holland Jason W. , Bowden Linda A. , Halliday Katrina , Rowley Andrew F.
Published: November 2006

The eicosanoid generating potential of the brain, gills, skin, ovary, muscle, eye, liver, spleen, heart, and alimentary canal in the rainbow trout,Oncorhynchus mykiss, was examined. All the organs/tissues examined synthesized the 12‐lipoxygenase products, 12‐hydroxyeicosatetraenoic acid (12‐HETE), and 12‐hydroxyeicosapentaenoic acid (12‐HEPE), implying the widespread nature of this enzyme in trout. Both prostaglandin E and LTC were also found in variable amounts in the organs, with the greatest amount of PGE found in the gill. Leukotriene (LT) B4 and LTB5 were found in supernatants from calcium ionophore‐challenged brain, skin, ovary, liver, spleen, and heart, but the lipoxins A4 and A5 were only present in brain, ovary, and spleen in relatively small amounts. As lipoxins have previously been shown to be synthesized by macrophages in rainbow trout [Pettittet al., J. Biol. Chem. 266, 8720–8726 (1991)], and related cells (microglial cells) are found in the brain of mammals, the localization of macrophage‐like cells in trout brain was investigated immunocytochemically. Monoclonal antibodies specific for trout leucocytes failed to identifity any microglial‐like cells in sections of the brain, although microvessels containing immuno‐positive reaction products were observed. A number of distinct lipoxygenase products were found in supernatants of ionophore‐challenged gill, including 14‐hydroxydocosahexaenoic acid, 12‐HETE, and 12‐HEPE, and a large number of dihydroxy fatty acid derivatives with conjugated triene chromophores. One of these products was tentatively identified as 8(R),15(S)‐dihydroxyeicosatetraenoic acid, a dual 12‐ and 15‐lipoxygenase product, but apparently no LTB4 was generated by this tissue.
New branched‐chain fatty acids from the senegalese gorgonianLeptogorgia piccola (white and yellow morphs)
Authors: Mirallès Joseph , Barnathan Gilles , Galonnier Renée , Sall Thioro , Samb Abdoulaye , Gaydou Emile Marcel , Kornprobst Jean‐Michel
Published: November 2006

Fatty acids from total lipids of the gorgonianLeptogorgia piccola (white and yellow morphs), collected from the same area at two different periods with regard to the average water temperature, were studied. More than fifty fatty acids were identified as methyl esters andN‐acyl pyrrolidides by gas chromatography and gas chromatography/mass spectrometry. Three new, branched‐chain unsaturated fatty acids were identified in addition to the unusual 7‐methyl‐6‐hexadecenoic acid, namely 10‐methyl‐6‐hexadecenoic, 7,9‐dimethyl‐6‐hexadecenoic, and 10‐methyl‐6,9‐heptadecadienoic acids. Also 6,9‐heptadecadienoic acid was identified. The fatty acid patterns of specimens harvested in colder waters were quite different from those harvested in warmer waters in that the former contained high amounts of methylene‐interrupted polyunsaturated acids, including tetracosapolyenoic acids, especially 6,9,12,15,18–24∶5 (up to 15.8% of the total acid mixture) and 6,9,12,15,18,21–24∶6 (up to 5.3%). Arachidonic acid was, nevertheless, a major component in all the fatty acid mixtures studied (13.6–20.5%). Based on gas chromatography/Fourier transform infrared experiments, the double bonds were assigned the (Z) configuration. Several fatty aldehydes and their dimethyl acetals were also detected, of which the most abundant was octadecanal.