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At least 19 recordsLinked to original sources
PubMed1990

Omega- and (omega-1)-hydroxylation of arachidonic acid, lauric acid and prostaglandin A1 by multiple forms of cytochrome P-450 purified from rat hepatic microsomes.

The metabolism of arachidonic acid, lauric acid and prostaglandin A1 by rat hepatic microsomes and multiple forms of cytochrome P-450 purified from rat hepatic microsomes was studied. Arachidonic acid was hydroxylated by hepatic microsomes of male rats by omega- and (omega-1)-hydroxylation. Phenobarbital treatment of rats decreased the hydroxylation activity slightly, but 3-methylcholanthrene treatment increased the hydroxylation activity 2-fold. However, lauric acid and prostaglandin A1 omega- and omega-1)-hydroxylation activities decreased after treatment with phenobarbital and 3-methylcholanthrene. Arachidonic acid and lauric acid were metabolized with similar ratios of omega- and (omega-1)-hydroxylation, but prostaglandin A1 was efficiently metabolized at the omega-position by hepatic microsomes of untreated male rats. In a reconstituted system with purified cytochromes P-450, P450 UT-1, UT-2 (P-450h), MC-1 (P-450d) and MC-5 (P-450c) effectively hydroxylated arachidonic acid at both the omega- and (omega-1)-position. P450 UT-8 hydroxylated arachidonic acid only at the omega-position. P450 DM (P-450j) hydroxylated arachidonic acid at the (omega-1)-position efficiently. Lauric acid was also hydroxylated by P450 UT-1, UT-2, PB-1, PB-2, MC-1, IF-3 (P-450a) and DM, at the (omega - 1)-position only. Only P450 UT-8 could hydroxylate laruic acid at the omega-position. Prostaglandin A1 was efficiently and specifically metabolized by P450 UT-8 with omega-hydroxylation. P450 UT-2 and PB-1 could hydroxylate prostaglandin A1 by (omega-1)-hydroxylation, but with low activity.

Animals↗
PubMed1982

Cytochrome P-450 induction by clofibrate. Purification and properties of a hepatic cytochrome P-450 relatively specific for the 12- and 11-hydroxylation of dodecanoic acid (lauric acid).

Hypolipidaemic drugs induce peroxisomal proliferation in the liver and many induce the formation of the hepatic endoplasmic reticulum in general and the formation of cytochrome P-450 in particular. We have induced the formation of rat liver microsomal cytochrome P-450 by the administration of the hypolipidaemic drug clofibrate, isolated the endoplasmic reticulum, solubilized the cytochrome P-450 from these membranes and subdivided the cytochrome P-450 into four fractions by the use of hydrophobic, anionic, cationic and adsorption chromatography. One of these fractions (cytochrome P-450 fraction 1) was highly purified to a specific content of 17nmol of cytochrome P-450/mg of protein and the protein was active in a reconstituted enzyme system towards the 12- and 11-hydroxylation of the fatty acid, dodecanoic (lauric) acid, with preferential activity towards the 12-hydroxy metabolite. This reconstituted activity was absolutely dependent on NADPH, NADPH-cytochrome P-450 reductase and cytochrome P-450, indicating the role of the mixed-function oxidase system in the metabolism of lauric acid. Another fraction of the haemoprotein (cytochrome P-450 fraction 2) preferentially formed 11-hydroxylauric acid, whereas a third fraction (cytochrome P-450 fraction 3) exhibited only trace laurate oxidase activity and was similar to the phenobarbitone form of the haemoprotein in that these last two cytochromes rapidly turned-over the drug benzphetamine. The molecular weights and spectral properties of these cytochrome P-450 fractions are reported, along with the phenobarbitone-induced form of the enzyme and the nature of the cytochrome(s) induced by clofibrate pretreatment are discussed in the terms of possible haemoprotein heterogeneity.

Animals↗
PubMed2007

Molecular cloning of CYP76B9, a cytochrome P450 from Petunia hybrida, catalyzing the omega-hydroxylation of capric acid and lauric acid.

A cDNA encoding a cytochrome P450 (CYP76B9) was isolated from Petunia hybrida. Northern blot analysis revealed preferential expression of the gene in flowers and leaves. The recombinant yeast microsomes expressing CYP76B9 was allowed to react with capric acid and lauric acid as substrates. One major metabolite was produced from each fatty acid after incubation with yeast microsomes expressing CYP76B9. The metabolites were identified by gas chromatography-mass spectrometry (GC-MS) as omega-hydroxy capric acid and omega-hydroxy lauric acid. The kinetic parameters of the reactions were Km=9.4 microM and Vmax=13.6 mol min(-1) per mol of P450 for capric acid, and Km=5.7 microM and Vmax=19.1 mol min(-1) per mol of P450 for lauric acid. We found that the omega-hydroxy metabolites of capric acid and lauric acid can affect the plant growth of Arabidopsis thaliana. Plants grown in the presence of omega-hydroxy fatty acids exhibited shorter root length than control plants with the corresponding non-hydroxylated fatty acids.

Amino Acid Sequence↗
PubMed2004

Solid-liquid phase behavior of binary fatty acid mixtures. 2. Mixtures of oleic acid with lauric acid, myristic acid, and palmitic acid.

Solid-liquid phase behavior was investigated for binary fatty acid mixtures composed of oleic acid (OA; cis-9-octadecenoic acid) and saturated fatty acids, lauric acid (LA; dodecanoic acid), myristic acid (MA; tetradecanoic acid), and palmitic acid (PA; hexadecanoic acid), by means of differential scanning calorimetry (DSC) and Fourier transform infrared spectroscopy (FT-IR). When the mixture was heated immediately after the solidification from the melt, the heat effect due to the gamma-to-alpha transformation of OA varied depending on the composition of the mixture. However, the mixture subjected to an annealing at the temperature slightly below the melting temperature provided the transformation at constant temperature which corresponds to the gamma-to-alpha transformation temperature of pure OA. This suggests that a solid phase formed by cooling of the melt of the mixture is not in an equilibrium state, but it relaxes to a stable solid during the annealing process. The T-X phase diagrams of these mixtures constructed from the DSC measurements demonstrate that the two fatty acid species are completely immiscible in a solid phase regardless of the type of polymorphs of OA, alpha- or gamma-form. According to a thermodynamic analysis of liquidus line basing on the regular solution model for the melt, the non-ideality of mixing tends to increase with the decrease in the acyl chain length of the saturated fatty acid, although the mixing is rather close to ideal.

Calorimetry, Differential Scanning↗
PubMed1993

Comparison of the effects of diets rich in stearic acid versus myristic acid and lauric acid on platelet fatty acids and excretion of thromboxane A2 and PGI2 metabolites in healthy young men.

The present study compared the effects of diets rich in stearic acid (C18:0) versus one high in lauric and myristic acid (C12:0, C14:0) on platelet phospholipid fatty acid levels and concentrations of urinary thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, which are stable metabolites of thromboxane A2 (TXA2) and PGI2 and indicators of cardiovascular hemostasis. A diet high in dairy butter (B) was the source of C12:0 and C14:0; C18:0 was provided by diets high in cocoa butter (CB), milk chocolate (CHOC) or CB+B in a 4:1 ratio (MIX). A randomized, crossover double-blind experimental design was used. Experimental subjects (n = 15) consumed each diet for 26 days, with a 1-month washout period between each experimental period. Urine and blood were collected from each subject at the beginning and end of each dietary period. Urinary TXB2 and 6-keto-PGF1 alpha were analyzed by radioimmunoassay (RIA). There were no effects of diet on the 24-hour excretion of either metabolite or on the ratio of 6-keto-PGF1 alpha/TXB2, even though there were significant changes in the eicosanoid precursor, arachidonic acid (C20:4n-6), in platelet phospholipids. C20:4n-6 levels increased (44.8% +/- 1.0% to 47.1% +/- 1.3%; P < .05) in the phosphatidylethanolamine phospholipid subclass in subjects on the B diet and decreased in the phosphatidylcholine subclass on the CB diet (16.5% +/- 1.0% to 14.2% +/- 1.1%; P < .05) compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Regioselectivity of a plant lauric acid omega hydroxylase. Omega hydroxylation of cis and trans unsaturated lauric acid analogs and epoxygenation of the terminal olefin by plant cytochrome P-450.

The study of the stereochemistry and regioselectivity of plant fatty acid hydroxylases is hampered by the difficulty to purify plant cytochrome P-450 enzymes. To provide an alternative, we have now defined an experimental plant system which expresses only one hydroxylase activity towards lauric acid: microsomes from clofibrate-induced Vicia sativa seedlings hydroxylate this fatty acid exclusively at the methyl terminus. To explore the catalytic capabilities of this laurate oxidase, a series of 1-14C-radiolabeled unsaturated lauric acid analogs (7-, 8-, 9-, 10- and 11-dodecenoic acids) were synthesized. Microsomes from clofibrate induced Vicia sativa seedling catalyzed the omega-oxidation of the lauric acid analogs in the presence of O2 and NADPH. The cis and trans forms of the four in-chain unsaturated analogs of lauric acid were 12-hydroxylated with similar efficiency. The terminal olefin was readily converted to the epoxide with only marginal autocatalytic inactivation of the enzyme. The formation of each metabolite was inhibited to the same extend when microsomes were incubated in presence of carbon monoxide or a suicide-substrate for omega LAH, suggesting that a single cytochrome P-450 isoenzyme from Vicia sativa microsomes is able to omega hydroxylate lauric acid and in-chain unsaturated analogs, and to epoxygenate 11-dodecenoic acid.

Alkenes↗
PubMed2004

Labeling of major plant lipids and jasmonic acid using [1-(14C)] lauric acid.

A medium chain length fatty acid, [1-(14C)] lauric acid (12:0) was administered to the detached leaves of Artemisia and was incorporated into major lipids, including phospholipids and galactolipids. [1-(14C)]12:0 was elongated and desaturated into linolenic acid (18:3). In detached leaves of both Artemisia and Arabidopsis thaliana ecotype Columbia, radioactivity from [14C]18:3 was incorporated into jasmonic acid (JA) and methyl jasmonate (MJ). Higher amounts of [14C]JA were measured in Artemisia than Arabidopsis leaves. In Artemisia, [14C]JA was actively metabolized into [14C]MJ. Extracts prepared from the leaves of Artemisia, exhibited higher in vitro JA methyltransferase activity than those from Arabidopsis.

Arabidopsis↗
PubMed1992

Stereochemistry of oxidized fatty acids generated during catalytic oxygenation of lauric acid and unsaturated analogs by plant microsomes.

The capacity of microsomes from aminopyrine-induced Jerusalem artichoke (Helianthus tuberosus L.) to oxidize saturated and unsaturated fatty acids has been investigated using lauric acid and a series of unsaturated lauric acid analogs (7-, 8-, 9- and 10-dodecenoic acids) as radiolabeled substrates. In the presence of NADH, lauric acid was mono-hydroxylated principally at carbon 9. Steric analysis of this product showed a low enantiomeric excess of 28%. Mono-hydroxylated and mono-epoxidated reaction products were formed from the unsaturated analogs. The epoxidation/hydroxylation ratio was related to the position of the double bond in the aliphatic chain. The oxidation of 7-dodecenoic acid (7-DDNA) and 10-DDNA produced mainly 9-hydroxy-7-DDNA and 9-hydroxy-10-DDNA plus minor amounts of 7,8-epoxy- or 10,11-epoxylauric acid, respectively. In contrast, 8- and 9-DDNAs yielded essentially 8,9-epoxy- and 9,10-epoxylauric acids and smaller amounts of 10-hydroxy-9-DDNA and 8-hydroxy-9-DDNA, respectively. The optical purity and the absolute configuration of the major metabolites were investigated. Epoxidation of Z 8-DDNA and Z 9-DDNA occurs with high enantiomeric excesses. When the double bond was in the Z configuration, (8S,9R)/(8R,9S) 8,9-epoxylauric acid (93/7) or (9R,10S)/(9S,10R) 9,10-epoxylauric acid (89/11) were produced. In contrast, when the double bond was in the E configuration, steric analysis showed an enantiomeric ratio of 52/48 for E 8,9-epoxide and of 59/41 for E 9,10-epoxide. Z 7-DDNA led to the formation of 98% of the 9(S)-hydroxy-Z 7-DDNA enantiomer, while 9-hydroxy-Z 10-DDNA derived from Z 10-DDNA was 35% (R) and 65% (S).

Fatty Acids↗
PubMed2005

A degradation study of PLLA containing lauric acid.

Addition of lauric acid to poly (L-lactide) (PLLA) has resulted in a new family of enhanced degradation biomaterials. Presented is PLLA4.5 (PLLA containing 4.5 wt% lauric acid), the fastest degrading of the family. Degradation was studied via mass changes, gel-permeation chromatography, wide- and small-angle X-ray scattering (WAXS and SAXS), simultaneous SAXS and tensile testing, and visual observation. The undegraded PLLA4.5 deformed by crazing, recognisable from the characteristic shape of the SAXS pattern. As water up-take and degradation proceeded, samples crystallised, decreasing the SAXS long period, until by 4 days the deformation mechanism had become that of crystal-mediated deformation. This resulted in a 'peanut-lemon'-shaped SAXS pattern, interpreted in terms of cavitation and fibrillated shear. Further degradation up to 12 days resulted in the same deformation mechanism at different sample displacements, with samples failing earlier during tensile testing until a ductile-brittle transition occurred. At 30-40 days water up-take and mass-loss increased significantly and global whitening of samples occurred, while the crystallinity and long period stabilised. Complete degradation had not occurred by the end of the study at 73 days. Through an understanding of how the changes in morphology during degradation affect the micromechanisms of deformation, it may be possible to design microstructures to give a tailored evolution of mechanical response in the body.

Absorbable Implants↗
PubMed1996

Simultaneous radiometric and fluorimetric detection of lauric acid metabolites using high-performance liquid chromatography following esterification with 4-bromomethyl-6,7-dimethoxycoumarin in human and rat liver microsomes.

The formation of (omega-1)-hydroxylauric acid from lauric acid (LA) can be used as an indicator of the activity of cytochrome P450 2E1 (CYP2E1) in rat and human liver microsomes. A high-performance liquid chromatographic (HPLC) method that is capable of identifying and measuring the two main metabolites of lauric acid, (omega-1)- and omega-OH-LA, has been developed and used in the study of rat and human liver microsomes. Measurement of the enzymatic activities, based on the esterification of the metabolites and substrate with the fluorescent agent, 4-bromomethyl-6, 7-dimethoxycoumarin, is described using both radiometric and fluorimetric detection methods. Extraction efficiencies of metabolites and residual substrate were calculated using radioactivity and were greater than 85%. The assay is accurate and reproducible and has a detection limit of 75 pg (0.37 pmol). Additionally, a strong correlation between the two techniques was found in both human (r = 0.945, n = 15, p < 0.01) and rat (r = 0.949, n = 18, p < 0.01) livers, for the (omega-1)-hydroxylauric acid.

Animals↗
PubMed1972

Quantitative analysis of uptake of free fatty acid by mammalian cells: lauric acid and human erythrocytes.

Quantitative aspects of the binding of free fatty acid to human erythrocytes were studied by measuring the distribution of various amounts of [1-(14)C]lauric acid between washed human erythrocytes and defatted human plasma albumin. Incubations were done at 37 degrees C in an isotonic phosphate-buffered salt solution. Laurate uptake approached a steady state value within 1 hr of incubation over the range of laurate-albumin molar ratios that were tested. Uptake was due primarily to a transfer of laurate from albumin to the cell, not to incorporation of the intact laurate-albumin complex. The fatty acid binding sites of the erythrocyte are located predominantly on or within the cell membrane. The binding model which best fitted the laurate uptake data consisted of two classes of erythrocyte binding sites. This model contains a small number of sites, 2.0 x 10(-13) moles/10(6) cells, that have an average apparent association constant of 1.8 x 10(6) m(-1) for laurate. Thus, the average strength of these sites is of the same order of magnitude as the stronger laurate binding sites of albumin. The binding model also contains a relatively large number of weaker fatty acid binding sites, 1.3 x 10(-11) moles/10(6) cells, that have an average apparent association constant of 1.3 x 10(4) m(-1) for laurate. These sites are too weak to bind appreciable amounts of laurate unless the fatty acid-albumin molar ratio is elevated.

Binding Sites↗
PubMed1991

Involvement of lauric acid hydroxylase in the activation of beta-substituted nitrosamines.

The mutagenicity of N-nitrosobis (2-hydroxypropyl) amine (BHP), N-nitrosobis(2-oxopropyl)amine (BOP) and N-nitroso-(2-hydroxy-propyl) (2-oxopropyl) amine (HPOP) was measured in V79 cells. Hepatocytes, used to metabolize (activate) the nitrosamines, were isolated from untreated Syrian hamsters (control) and hamsters treated with clofibrate (CLO) or dehydroepiandrosterone (DHEA) in vivo. BHP and HPOP mutagenicity increased 3- and 2-fold when hepatocytes from CLO- and DHEA-treated hamsters were used. BOP mutagenicity did not increase. 10-Undecynoic acid, a lauric acid hydroxylase inhibitor, inhibited the increase in BHP and HPOP mutagenicity by 80-90% but did not affect that of BOP. Antimycin A1, a fatty acyl coenzyme A beta-oxidase inhibitor did not affect the mutagenicity of these nitrosamines. Lauric acid hydroxylase, probably omega-1 hydroxylase (cytochrome P-450 IVA2), appears to be involved in the activation of BHP and HPOP.

Acyl-CoA Oxidase↗
PubMed1994

Fat high in stearic acid favorably affects blood lipids and factor VII coagulant activity in comparison with fats high in palmitic acid or high in myristic and lauric acids.

The effect of fats high in individual, prevalent saturated dietary fatty acids on lipoproteins and hemostatic variables in young healthy subjects was evaluated in a randomized strictly controlled metabolic feeding study. Three experimental diets: shea butter (S; 42% stearic acid), palm oil (P; 43% palmitic palmitic acid), and palm-kernel oil with high-oleic sunflower oil (ML; 10% myristic acid, 30% lauric acid) were served to 15 men for 3 wk each, separated by washout periods. Diet S compared with diet P resulted in significant reduction in plasma cholesterol (22%) LDL cholesterol (26%), apolipoprotein B (18%), HDL cholesterol (12%), apolipoprotein A-I (13%), and a 13% lower factor VII coagulant activity (P = 0.001). Similar differences were observed between diets S and ML. In conclusion, intake of shea butter high in stearic acid favorably affects blood lipids and factor VII coagulant activity in young men, compared with fats high in saturated fatty acids with 12-16 carbons.

Adult↗
PubMed2004

Ion pair formation as a possible mechanism for the enhancement effect of lauric acid on the transdermal permeation of ondansetron.

Transdermal application can be an alternative drug delivery route for ondansetron, an antiemetic drug. Previous studies found that fatty acids, namely oleic and lauric, were the most effective penetration enhancers. The aim of this study was to investigate the formation of an ion pair between ondansetron and lauric acid as a possible mechanism of its enhancing action. Several techniques were used to reveal the formation of an ion pair complex. Partitioning experiments, where the n-octanol/water coefficient was measured, showed an increase in the distribution coefficient in the presence of the acid, possibly as a result of the formation of more lipophilic ion pairs between the charged molecules of ondansetron and lauric acid. Further evidence of complex formation between ondansetron and lauric acid, was gained from the 13C-nuclear magnetic resonance (13C-NMR) spectra of ondansetron, lauric acid, and their mixture (molar ratio 1:1). The NMR spectra revealed alterations to the magnetic environment of the carbon atoms adjacent to the ionized group, which are the carbonyl group of the acid and the nitrogen of the imidazole ring of ondansetron. This evidence substantiates the theory of ion pair formation. Finally, thermal analysis of the binary mixtures of ondansetron and lauric acid revealed the formation of an additional compound, with different melting point from pure ondansetron and lauric acid, which is thermodynamically favored.

Algorithms↗
PubMed2001

Effect of fatty acids on arenavirus replication: inhibition of virus production by lauric acid.

To study the functional involvement of cellular membrane properties on arenavirus infection, saturated fatty acids of variable chain length (C10-C18) were evaluated for their inhibitory activity against the multiplication of Junin virus (JUNV). The most active inhibitor was lauric acid (C12), which reduced virus yields of several attenuated and pathogenic strains of JUNV in a dose dependent manner, without affecting cell viability. Fatty acids with shorter or longer chain length had a reduced or negligible anti-JUNV activity. Lauric acid did not inactivate virion infectivity neither interacted with the cell to induce a state refractory to virus infection. From mechanistic studies, it can be concluded that lauric acid inhibited a late maturation stage in the replicative cycle of JUNV. Viral protein synthesis was not affected by the compound, but the expression of glycoproteins in the plasma membrane was diminished. A direct correlation between the inhibition of JUNV production and the stimulation of triacylglycerol cell content was demonstrated, and both lauric-acid induced effects were dependent on the continued presence of the fatty acid. Thus, the decreased insertion of viral glycoproteins into the plasma membrane, apparently due to the increased incorporation of triacylglycerols, seems to cause an inhibition of JUNV maturation and release.

Animals↗
PubMed2001

Consumption of a solid fat rich in lauric acid results in a more favorable serum lipid profile in healthy men and women than consumption of a solid fat rich in trans-fatty acids.

Solid fats are used in food manufacturing to provide texture and firmness to foods. Such fats are rich in either saturated or trans-fatty acids, both of which increase the risk of coronary heart disease. Epidemiological and experimental studies suggest that trans-fatty acids increase risk more than do saturates because they lower serum high density lipoprotein (HDL) cholesterol. However, there appear to be differences between saturates in their effect on HDL cholesterol. We investigated whether the consumption of a solid fat rich in lauric acid (C12:0) would result in a more favorable blood lipid profile than the consumption of a solid fat rich in trans-fatty acids. We fed 32 healthy men and women two controlled diets in a 2 x 4-wk randomized crossover design. The diets consisted of a background diet supplemented with margarines. In the trans-diet, 9.2% of energy was provided by trans-fatty acids and 12.9% by saturated fatty acids. In the Sat-diet, energy intake was 0% from trans-fatty acids and 22.9% from saturated fatty acids. Lauric acid composed one third of all saturates in the Sat-diet. Serum HDL cholesterol was 0.36 mmol/L lower at the end of the trans-diet than at the end of the Sat-diet (95% confidence interval, -0.46 to -0.26), whereas serum low density lipoprotein cholesterol and triglyceride concentrations remained stable. Serum total cholesterol was 0.31 mmol/L (95% confidence interval, -0.48 to -0.14) lower at the end of the trans-diet than at the end of the Sat-diet. Consumption of a solid fat rich in lauric acid gives a more favorable serum lipoprotein pattern than consumption of partially hydrogenated soybean oil rich in trans-fatty acids. Thus, solid fats rich in lauric acids, such as tropical fats, appear to be preferable to trans-fats in food manufacturing, where hard fats are indispensable.

Adolescent↗
PubMed2006

Comparison of the hydrolytic degradation and deformation properties of a PLLA-lauric acid based family of biomaterials.

Addition of lauric acid to PLLA results in a significantly increased rate of hydrolytic degradation, with the time-to-loss of tensile strength directly related to the concentration of lauric acid. In this study, the hydrolytic degradation profiles of four materials were studied: amorphous PLLA, amorphous PLLA containing 1.8 wt % lauric acid, amorphous PLLA containing 4.5 wt % lauric acid, and pre-crystallized PLLA containing 1.8 wt % lauric acid. Hydrolytic degradation was monitored through mass profiles, molecular weight profiles, crystallinity and the development of mechanical properties and deformation mechanisms (through simultaneous small-angle X-ray scattering and tensile testing), and a "phase diagram" of properties suggested. The key factor in determining the development of properties was found to be the time at which crystallization occurred in relation to the loss of molecular weight, with the two factors most affecting this being the lauric acid content and the pre-degradation annealing treatment.

Biocompatible Materials↗