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PubMed1982

Phospholipid turnover in isolated rat pancreatic acini. Consideration of the relative roles of phospholipase A2 and phospholipase C.

The purpose of the present study was to explore the interaction of phosphatidylinositol breakdown and the turnover of arachidonic acid in isolated rat pancreatic acini by using receptor agonists and the calcium ionophore ionomycin. Acini prelabelled with myo-[(3)H]inositol in vivo responded to carbachol with a rapid breakdown of phosphatidylinositol. In the presence of [(32)P]P(i), carbachol increased labelling of phosphatidic acid and phosphatidylinositol within 1 and 5 min respectively. Carbachol also rapidly stimulated the incorporation of [(14)C]arachidonic acid into phosphatidylinositol within 2 min, and the peptidergic secretagogue caerulein caused the loss of radioactivity from phospholipids prelabelled with arachidonic acid. Ca(2+) deprivation partially impaired the stimulatory action of carbachol on arachidonic acid turnover. In contrast with its stimulatory effects on [(32)P]P(i) and [(14)C]arachidonate incorporation, carbachol inhibited the incorporation of the saturated fatty acid stearic acid into phosphatidylinositol. Whereas ionomycin stimulation of phosphatidylinositol breakdown and [(32)P]P(i) labelling of phospholipids was slower in onset and less effective than carbachol stimulation, the ionophore effectively promoted (arachidonyl) phosphatidylinositol turnover within 2 min. These results implicate two separate pathways for stimulated phosphatidylinositol degradation in the exocrine pancreas, involving phospholipases A(2) and C. Whereas mobilization of cellular Ca(2+) appears sufficient to cause activation of phospholipase A(2) and amylase secretion, additional events triggered by receptor activation may be required to act in concert with Ca(2+) to optimally stimulate phospholipase C. The nature of the interaction between phospholipases A(2) and C and their specific physiological roles in pancreatic secretion remain to be elucidated.

Animals↗

PubMed1992

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Human or rat microsomal 5 alpha-reductase activity, as measured by enzymic conversion of testosterone into 5 alpha-dihydrotestosterone or by binding of a competitive inhibitor, [3H]17 beta-NN-diethulcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one ([3H]4-MA) to the reductase, is inhibited by low concentrations (less than 10 microM) of certain polyunsaturated fatty acids. The relative inhibitory potencies of unsaturated fatty acids are, in decreasing order: gamma-linolenic acid greater than cis-4,7,10,13,16,19-docosahexaenoic acid = cis-6,9,12,15-octatetraenoic acid = arachidonic acid = alpha-linolenic acid greater than linoleic acid greater than palmitoleic acid greater than oleic acid greater than myristoleic acid. Other unsaturated fatty acids such as undecylenic acid, erucic acid and nervonic acid, are inactive. The methyl esters and alcohol analogues of these compounds, glycerols, phospholipids, saturated fatty acids, retinoids and carotenes were inactive even at 0.2 mM. The results of the binding assay and the enzymic assay correlated well except for elaidic acid and linolelaidic acid, the trans isomers of oleic acid and linoleic acid respectively, which were much less active than their cis isomers in the binding assay but were as potent in the enzymic assay. gamma-Linolenic acid had no effect on the activities of two other rat liver microsomal enzymes: NADH:menadione reductase and glucuronosyl transferase. gamma-Linolenic acid, the most potent inhibitor tested, decreased the Vmax. and increased Km values of substrates, NADPH and testosterone, and promoted dissociation of [3H]4-MA from the microsomal reductase. gamma-Linolenic acid, but not the corresponding saturated fatty acid (stearic acid), inhibited the 5 alpha-reductase activity, but not the 17 beta-dehydrogenase activity, of human prostate cancer cells in culture. These results suggest that unsaturated fatty acids may play an important role in regulating androgen action in target cells.

5-alpha Reductase Inhibitors↗

PubMed1997

Oleic acid inhibits gap junction permeability and increases glucose uptake in cultured rat astrocytes.

The role of oleic acid in the modulation of gap junction permeability was studied in cultured rat astrocytes by the scrape-loading/Lucifer yellow transfer technique. Incubation with oleic acid caused a dose-dependent inhibition of gap junction permeability by 79.5% at 50 microM, and no further inhibition was observed by increasing the oleic acid concentration to 100 microM. The oleic acid-mediated inhibition of gap junction permeability was reversible and was prevented by bovine serum albumin. The potency of oleic acid-related compounds in inhibiting gap junction permeability was arachidonic acid > oleic acid > oleyl alcohol > palmitoleic acid > stearic acid > octanol > caprylic acid > palmitic acid > methyloleyl ester. Oleic acid and arachidonic acid, but not methyloleyl ester, increased glucose uptake by astrocytes. Neither oleic acid nor arachidonic acid increased glucose uptake in the poorly coupled glioma C6 cells. These results support that the inhibition of gap junction permeability is associated with the increase in glucose uptake. We suggest that oleic acid may be a physiological mediator of the transduction pathway leading to the inhibition of intercellular communication.

Animals↗

PubMed1994

Effects of long-chain polyunsaturated fatty acids on the contraction of neonatal rat cardiac myocytes.

Because of the ability of certain long-chain polyunsaturated fatty acids (PUFAs) to prevent lethal cardiac arrhythmias, we have examined the effects of various long-chain fatty acids on the contraction of spontaneously beating, isolated, neonatal rat cardiac myocytes. The omega 3 PUFA from fish oils, eicosapentaenoic acid [EPA; C20:5 (n-3)] and docosahexaenoic acid [DHA; C22:6 (n-3)], at 2-10 microM profoundly reduced the contraction rate of the cells without a significant change in the amplitude of the contractions. The fatty acid-induced reduction in the beating rate could be readily reversed by cell perfusion with fatty acid-free bovine serum albumin. Addition of either oxygenase inhibitors or antioxidants did not alter the effect of the fatty acids. Arachidonic acid [AA; C20:4 (n-6)] produced two different effects on the beating rate, an increase or a decrease, or it produced no change. In the case of the increased or unchanged beating rate in the presence of AA, addition of AA oxygenase inhibitors subsequently reduced the contraction rate. The nonmetabolizable AA analog eicosatetraynoic acid (ETYA) always reduced the beating rate, as did EPA or DHA. Two other PUFAs, linoleic acid [C18:2 (n-6)] and linolenic acid [C18:3 (n-3)] also exhibited similar but less potent effects compared with EPA or ETYA. In contrast, neither the monounsaturated fatty acid oleic acid [C18:1 (n-9)] nor the saturated fatty acids stearic acid (C18:0), myristic acid (C14:0), and lauric acid (C12:0) affected the contraction rate. The inhibitory effect of these PUFAs on the contraction rate was similar to that produced by the class I antiarrhythmic drug lidocaine. The fatty acids that are able to reduce the beating rate, particularly EPA and DHA, could effectively prevent and terminate lethal tachyarrhythmias (contracture/fibrillation) induced by high extracellular calcium concentrations or ouabain. These results suggest that free PUFAs can suppress the automaticity of cardiac contraction and thereby exert their antiarrhythmic effects.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1996

Evidence that free polyunsaturated fatty acids modify Na+ channels by directly binding to the channel proteins.

The effects of free polyunsaturated fatty acids (PUFA) on the binding of ligands to receptors on voltage-sensitive Na+ channels of neonatal rat cardiac myocytes were assessed. The radioligand was [benzoyl-2,5-(3)H] batrachotoxinin A 20alpha-benzoate ([(3)H]BTXB), a toxin that binds to the Na+ channel. The PUFA that have been shown to be antiarrhythmic, including eicosapentaenoic acid (EPA; C20:5n-3), docosahexaenoic acid (DHA; C22:6n-3), eicosatetraynoic acid (ETYA), linolenic acid (C18:3n-3), and linoleic acid (C18:2n-6), inhibited [(3)H]BTXB binding in a dose-dependent fashion with IC50 values of 28-35 microM, whereas those fatty acids that have no antiarrhythmic effects including saturated fatty acid (stearic acid, C18:0), monounsaturated fatty acid (oleic acid; C18:1n-9), and EPA methyl ester did not have a significant effect on [(3)H]BTXB binding. Enrichment of the myocyte membrane with cholesterol neither affected [(3)H]BTXB binding when compared with control cells nor altered the inhibitory effects of PUFA on [(3)H]BTXB binding. Scatchard analysis of [(3)H]BTXB binding showed that EPA reduced the maximal binding without altering the Kd for [(3)H]BTXB binding, indicating allosteric inhibition. The inhibition by EPA of [(3)H]BTXB binding was reversible (within 30 min) when delipidated bovine serum albumin was added. The binding of the PUFA to this site on the Na+ channel is reversible and structure-specific and occurs at concentrations close to those required for apparent antiarrhythmic effects and a blocking effect on the Na+ current, suggesting that binding of the PUFA at this site relates to their antiarrhythmic action.

Animals↗

PubMed1999

The two calcium-binding proteins, S100A8 and S100A9, are involved in the metabolism of arachidonic acid in human neutrophils.

Recently, we identified the two myeloid related protein-8 (MRP8) (S100A8) and MRP14 (S100A9) as fatty acid-binding proteins (Klempt, M., Melkonyan, H., Nacken, W., Wiesmann, D., Holtkemper, U., and Sorg, C. (1997) FEBS Lett. 408, 81-84). Here we present data that the S100A8/A9 protein complex represents the exclusive arachidonic acid-binding proteins in human neutrophils. Binding and competition studies revealed evidence that (i) fatty acid binding was dependent on the calcium concentration; (ii) fatty acid binding was specific for the protein complex formed by S100A8 and S100A9, whereas the individual components were unable to bind fatty acids; (iii) exclusively polyunsaturated fatty acids were bound by S100A8/A9, whereas saturated (palmitic acid, stearic acid) and monounsaturated fatty acids (oleic acid) as well as arachidonic acid-derived eicosanoids (15-hydroxyeicosatetraenoic acid, prostaglandin E(2), thromboxane B(2), leukotriene B(4)) were poor competitors. Stimulation of neutrophil-like HL-60 cells with phorbol 12-myristate 13-acetate led to the secretion of S100A8/A9 protein complex, which carried the released arachidonic acid. When elevation of intracellular calcium level was induced by A23187, release of arachidonic acid occurred without secretion of S100A8/A9. In view of the unusual abundance in neutrophilic cytosol (approximately 40% of cytosolic protein) our findings assign an important role for S100A8/A9 as mediator between calcium signaling and arachidonic acid effects. Further investigations have to explore the exact function of the S100A8/A9-arachidonic acid complex both inside and outside of neutrophils.

Antigens, Differentiation↗

PubMed2003

Fusion of lamellar body with plasma membrane is driven by the dual action of annexin II tetramer and arachidonic acid.

Annexin II has been implicated in membrane fusion during the exocytosis of lamellar bodies from alveolar epithelial type II cells. Most previous studies were based on the fusion assays by using model membranes. In the present study, we investigated annexin II-mediated membrane fusion by using isolated lamellar bodies and plasma membrane as determined by the relief of octadecyl rhodamine B (R18) self-quenching. Immunodepletion of annexin II from type II cell cytosol reduced its fusion activity. Purified annexin II tetramer (AIIt) induced the fusion of lamellar bodies with the plasma membrane in a dose-dependent manner. This fusion is Ca2+-dependent and is highly specific to AIIt because other annexins (I and II monomer, III, IV, V, and VI) were unable to induce the fusion. Modification of the different functional residues of AIIt by N-ethylmaleimide, nitric oxide, or peroxynitrite abolished AIIt-mediated fusion. Arachidonic acid enhanced AIIt-mediated fusion and reduced its Ca2+ requirement to an intracellularly achievable level. This effect is due to membrane-bound arachidonic acid, not free arachidonic acid. Other fatty acids including linolenic acid, palmitoleic acid, myristoleic acid, stearic acid, palmitic acid, and myristic acid had little effect. AIIt-mediated fusion was suppressed by the removal of arachidonic acid from lamellar body and plasma membrane using bovine serum albumin. The addition of arachidonic acid back to the arachidonic acid-depleted membranes restored its fusion activity. Our results suggest that the fusion between lamellar bodies with the plasma membrane is driven by the synergistic action of AIIt and arachidonic acid.

Animals↗

PubMed2003

Selected nutritional biomarkers predict diet quality.

OBJECTIVE: To examine associations of biomarkers of nutrient intake with overall diet quality. SUBJECTS: A convenience sample of 102 healthy postmenopausal women in Seattle, Washington (USA). DESIGN AND METHOD: Participants attended a study centre where they provided fasting blood specimens and completed a 122-item validated food-frequency questionnaire (FFQ). Data from the FFQ were used to calculate Diet Quality Index (DQI) scores and categorise women as having diets of excellent, good, fair or poor quality. The blood specimens were analysed for nine phospholipid fatty acids (as percentage of total) and serum concentrations of vitamin C, alpha-tocopherol, gamma-tocopherol, vitamin B12, folate and six carotenoids. Multivariate linear regression was used to model associations of the nutrient biomarkers with DQI scores. RESULTS: Compared with women with poor-quality diets, women with excellent diets, as measured by the DQI, had higher plasma concentrations of vitamin C (P for trend=0.01), alpha-tocopherol (P for trend=0.02) and beta-cryptoxanthin (P for trend=0.03). Women with excellent diets also had lower proportions of plasma phospholipid fatty acids of two potentially atherogenic fatty acids: stearic acid (P for trend=0.01) and behenic acid (P for trend=0.03). A group of six biomarkers explained a moderate proportion of the total variability in DQI scores (36%). CONCLUSIONS: These objective measures of dietary intake support the use of the DQI as a useful tool to measure dietary patterns.

Aged↗

PubMed2006

Lipid microencapsulation in starch.

Short microwave heating of granular potato, waxy corn and tapioca starches with such lipids as cis-9-octadecenoic acid (oleic acid), cis,cis-9,12-octadecadienoic acid (linoleic acid), octadecanoic acid (stearic acid), ethyl cis-9-octadecenoate, ethyl cis,cis-9,12-octadecadienoate and methyl octadecanoate provided microcapsules in which encapsulated guest molecules did not interact with starch microcapsules. On the formation of microcapsules, the lipid guest molecules did not react to starches. The encapsulation yield varied between almost 11-94%.

Calorimetry, Differential Scanning↗

PubMed2001

Final report on the safety assessment of Corylus Avellana (Hazel) Seed Oil, Corylus Americana (Hazel) Seed Oil, Corylus Avellana (Hazel) Seed Extract, Corylus Americana (Hazel) Seed Extract, Corylus Avellana (Hazel) Leaf Extract, Corylus Americana (Hazel) Leaf Extract, and Corylus Rostrata (Hazel) Leaf Extract.

These ingredients are all derived from hazelnut trees. The two seed oils are expressed from the nuts of the hazelnut tree of the particular species identified. Most current reported cosmetic uses are of the seed oils. The seed extracts are the extract of the nuts of the identified species tree. There is one current report of use of seed extract in cosmetics. The leaf extracts are the extract from the leaves of the particular species tree. There are no current reports of use of these extracts in cosmetics. Analysis of seed oil from one species identified Oleic Acid, Palmitoleic Acid, Linoleic Acid, Eicosaenoic Acid, Docosenoic Acid, Eicosanoic Acid, Palmitic Acid, Linolenic Acid, Stearic Acid, and Tetraeicosanoic Acid. Little information is available to characterize the extracts, however. The functions of most of these ingredients in cosmetics are not reported. In studies of hazelnuts from Spain and Egypt, aflatoxin was reported as a possible contaminant. Aflatoxins are considered carcinogenic in humans. Virtually no safety test data are available on these ingredients. Negative results in one comedogenicity study using a seed oil are reported. Cross-sensitivity to proteins in peanuts and those in hazelnuts are reported, but the presence or absence of protein in nut extract and plant extract from hazelnut trees is not known. Additional data were provided regarding concentration of use, method of extraction and contaminants, comedogenicity, and ultraviolet (UV) radiation absorption, but these data related to nut oil from only one species, and were not overall sufficient to resolve questions about irritation, sensitization, and photosensitization. Because of the absence of data, it is concluded that the available data are insufficient to support the safety of these ingredients in cosmetic products. Because of the limited information that characterizes any of these oils or extracts, data are needed on each (except that items 1, 2, and 3 below are not needed for Hazel [Corylus Avellana] Nut Oil). The additonal data needs include: (1) current concentration of use; (2) method of extraction/manufacture and quality control (i.e., chemical analyses); (3) contaminants and methods of extraction (especially pesticides and heavy metals); (4) dermal irritation and sensitization; (5) UV absorption; if there is significant absorption, then a photosensitization study will be needed; (6) 28-day dermal toxicity; (7) reproductive and developmental toxicity; and (8) two genotoxicity assays, one in a mammalian system; if positive, then a 2-year dermal carcinogenesis study using National Toxicology Program (NTP) methods may be needed.

Acne Vulgaris↗

PubMed1997

Alterations in eighteen-carbon saturated, monounsaturated and polyunsaturated fatty acid peroxisomal oxidation in mouse brain during development and aging.

Peroxisomal oxidation was measured in mouse brain homogenate by adding cyanide to the test tube (which inhibits mitochondrial oxidation). Eighteen-carbon fatty acids (saturated, monounsaturated and polyunsaturated) were oxidized by brain peroxisomes. At nearly all ages, oxidation of oleic acid was higher (about 2 fold) than oxidation of other eighteen-carbon fatty acids. In contrast to other fatty acids, stearic acid oxidation decreased regularly up to weaning (6 fold) and was stable thereafter. Oleic acid oxidation increased up to weaning, decreased during development up to day 70 and remained subsequently nearly stable. Linoleic acid and alpha-linolenic acid oxidation increased up to weaning, decreased up to day 105 and was nearly stable thereafter. Alpha-linolenic acid oxidation about was two fold lower than linoleic acid oxidation. Interestingly, peroxisomal oxidation for all fatty acids examined declined during aging, between day 365 and day 450.

Aging↗

PubMed1979

Diet-related toxemia in pregnancy. I. Fat, fatty acids, and cholesterol.

Toxemia in pregnancy (preeclampsia)is characteristerized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In three successive trials over three consecutive years, the dietary intake of a selected number of young pregnant women attending a Maternal and Infant Care Program at Tuskegee Institute were evaluated for total lipids, individual fatty acids, and cholesterol. Women with toxemia or with any of the individual symptoms were identified and women without toxemia or these symptoms served as controls. Results were variable from repetition to repetition in all but the toxemia group and the edema group. The consumption of total lipids and cholesterol was significantly greater in all three trials by both the toxemia and edema groups. Also, total saturated, monounsaturated, and polyunsaturated fatty acids were eaten in greater amounts. The greatest differences were in palmitic acid, stearic acid, oleic acid, and linoleic acid. The proportion of unsaturated fatty acids consumed in all groups was very low. All differences could be attributed primarily to breakfast and dinner meals and were found in the milk, meat, and egg food groups. Although satistical correlations were found between lipid intake and toxemia of pregnancy any specific relationship between the two is still unclear.

Adolescent↗

PubMed1997

Some Food and Drug Administration perspectives of fat and fatty acids.

Because of public health concerns about the amount of fat in the American diet, the Food and Drug Administration and the US Department of Agriculture have emphasized use of the recently reformed food label to inform consumers about the fat and fatty acid contents of foods. The health effects of specific fatty acids continue to be the subject of much research, discussion, and debate. Issues that must be addressed to further improve the communication effectiveness of the food label include health effects of n-3 and n-6 fatty acids; appropriate labeling of trans fatty acids, stearic acid, and other non-cholesterol-raising fatty acids; partially absorbed fats; and label claims, especially health claims, for specific fatty acids and fatty acids of biotechnologically altered foods.

Diet↗

PubMed1997

Individual fatty acid effects on plasma lipids and lipoproteins: human studies.

The purpose of this review is to summarize our current understanding of the cholesterolemic effects of individual fatty acids. Although historically there has been great interest in the fatty acid classes, it has been only recently that emphasis has shifted to individual fatty acids. Consequently, and in conjunction with the methodologic challenges inherent in studying individual fatty acids, our database is relatively modest. Nonetheless, it is clear that saturated fatty acids are hypercholesterolemic and that unsaturated fatty acids elicit a hypocholesterolemic effect compared with saturated fatty acids. The question at hand is, What are the relative cholesterolemic effects of the major saturated and unsaturated fatty acids in the diet? On the basis of a limited number of well-controlled studies, it appears that myristic acid is the most potent saturated fatty acid. Of the saturated fatty acids, stearic acid is uniquely different in that it appears to be a neutral fatty acid. Monounsaturated fatty acids appear to exert a neutral effect or to be mildly hypocholesterolemic. trans Fatty acids elicit effects that are intermediate to those of the hypercholesterolemic saturated fatty acids and the cis-monounsaturated and cis-polyunsaturated fatty acids. Polyunsaturated fatty acids elicit the most potent hypocholesterolemic effects. Studies are needed to establish the potency with which each fatty acid affects plasma total and lipoprotein cholesterol concentrations as well as the mechanisms that account for their markedly different effects. This information will be useful in making dietary recommendations for individual fatty acids that may further reduce risk of chronic diseases in the United States.

Cholesterol, LDL↗

PubMed2001

Characterization of a novel triphosphonooctaosylceramide from the eggs of the sea hare, Aplysia kurodai.

We have reported the existence of a triphosphonoglycosphingolipid, EGL-I, in the eggs of a sea gastropod, Aplysia kurodai [Yamada, S., Araki, S., Abe, S., Kon, K., Ando, S., and Satake, M. (1995) J. Biochem. 117, 794-799]. We have now isolated a novel glycosphingolipid, named EGL-II, from the eggs of Aplysia. By component analysis, sugar analysis, permethylation studies, fast atom bombardment-mass spectrometry, secondary ion mass spectrometry, and proton magnetic resonance spectrometry, its structure was revealed to be as follows: Galalpha1-->3(GlcNAcalpha1-->2)Galalpha1-->3(3-O-MeGalalpha1-->2)Galalpha1-->3[6'-O-(2-aminoethylphosphonyl)Galalpha1-->2](2-aminoethylphosphonyl-->6)Galbeta1-->4(2-aminoethylphosphonyl-->6)Glcbeta1-->1ceramide. The major aliphatic components of the ceramide are palmitic acid, stearic acid, and anteisononadeca-4-sphingenine.

Animals↗

PubMed1986

1H-NMR study on the interactions of human serum albumin with free fatty acid.

Binding of free fatty acid (FFA) to human serum albumin (HSA) was studied by 1H-NMR spectroscopy. Addition of FFA to defatted HSA at a mole ratio (FFA/HSA) up to 4 caused a small change in the NMR spectrum of HSA. The integrated intensity of sharp signals of the histidine C2 proton region of HSA decreased as the mole ratio was increased from 0 to 4 for both medium chain (lauric acid) and long chain (palmitic acid, stearic acid, and oleic acid) FFA's. By contrast, when the mole ratio was increased above 4, several histidine C2 proton signals coalesced and sharpened. Therefore, the HSA molecule appears to have a different conformation on binding with more than 4 FFA molecules, which allows increased local motions of HSA. By analyzing the NMR difference spectra of HSA with various amounts of FFA, the conformational change of HSA was investigated in more detail. The difference spectrum between [HSA + 2FFA] and [HSA + FFA] was almost the same as the difference spectrum between [HSA + FFA] and [HSA], which suggests that one primary site binds a pair of FFA molecules. These results are consistent with those of a spectroscopic study with polyene fatty acids (Berde, C.B., et al. (1979) J. Biol. Chem. 254, 391-400). The existence of a bimolecular complex of FFA molecules in aqueous solution may facilitate this type of binding. Similarly, it was found that the third and fourth FFA molecules were bound to a secondary site on HSA, because the difference spectrum between [HSA + 4FFA] and [HSA + 3FFA] was nearly equal to the difference spectrum between [HSA + 3FFA] and [HSA + 2FFA]. Further addition of FFA resulted in a drastic spectral change of HSA. The NMR difference spectrum between HSA solutions with perdeuterated FFA and those with undeuterated FFA gave the 1H-NMR spectra of FFA molecules bound to HSA. Titration of FFA revealed that, in the binding to the primary site of HSA, the carboxyl group of FFA is tightly bound to the protein, whereas the methyl group is not so firmly bound. In contrast, in the binding to low affinity sites, the methyl group is bound to HSA as tightly as other portions of the molecule.

Binding Sites↗

PubMed1995

Structural analysis of a novel triphosphonoglycosphingolipid from the egg of the sea hare, Aplysia kurodai.

A novel phosphonoglycosphingolipid which contains three residues of 2-aminoethylphosphonate (2-AEP) was isolated from eggs of a sea gastropoid, Aplysia kurodai, and its structure was identified as follows. [see text] The major aliphatic components of ceramide were palmitic acid, stearic acid, 4-sphingenine, and 16-methyl-4-sphingenine. Antibodies which recognize 3-O-methylgalactose linked beta-glycosidically to phosphonoglycosphingolipids failed to react to the egg glycolipid. By comparing 1H-NMR spectra of native and HF-treated glycolipids, steric interactions of two residues of 2-AEP with ring protons of the glucose and the internal galactose were indicated.

Aging↗

PubMed2003

Fatty acids and glucose increase neutral endopeptidase activity in human microvascular endothelial cells.

Neutral endopeptidase (NEP), a membrane-bound metallopeptidase enzyme that degrades neuropeptides, bradykinin, atrial natriuretic factor, enkephalins, and endothelin may regulate response to injury. We have previously demonstrated increased NEP localization and enzyme activity in diabetic wounds and skin compared with normal controls. We hypothesized that hyperlipidemia and hyperglycemia associated with type 2 diabetes mellitus may induce excessive NEP activity and thereby diminish normal response to injury. Human microvascular endothelial cells were treated with five different fatty acids (40 microM) with varying degrees of saturation, including oleic acid, linoleic acid, palmitic acid, stearic acid, and linolenic acid and/or glucose (40 mM) for 48 h. The effect of the antioxidative agents vitamin E and C on NEP enzyme activation was determined by treating the cultured cells with alpha-tocopherol succinate and/or L-ascorbic acid. Cell membrane preparations were assayed for NEP activity by incubation with glutaryl-Ala-Ala-Phe-4-methoxy-beta naphthylamide to generate a fluorescent degradation product methoxy 2 naphthylamine. High glucose or fatty acid concentration upregulated NEP activity. The highest NEP activity was observed with combined elevated glucose, linoleic acid, and oleic acid (P < 0.05). Antioxidant vitamin E and C treatment significantly reduced NEP enzyme activity after fatty acid exposure (P < 0.05). Thus, hyperglycemia and hyperlipidemia associated with type 2 diabetes mellitus may increase endothelial cell NEP activity and thereby decrease early pro-inflammatory responses. The modulator effect of vitamin E and C on NEP membrane enzyme activity after exposure to fatty acid stimulation suggests that lipid oxidation may activate NEP.

Antioxidants↗