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At least 199 records · Page 11Linked to original sources
PubMed1990

Molecular basis for the immunosuppressive action of stearic acid on T cells.

Studies were performed to determine the mechanism by which stearic acid (18:0) selectively inhibits T-dependent immune responses in vitro. Incubation of mitogen-activated B and T cells with 18:0 resulted in dissimilar patterns of incorporation of the saturated fatty acid into their membranes. High-performance liquid chromatography (HPLC) analyses of T cells showed an accumulation of disaturated [corrected] 18:0-containing phosphatidylcholine (PC) that replaced normal cellular PC. Less significant quantities of the same PC species were seen to accumulate in B-cell membranes; rather, they increased their proportion of oleic acid (18:1)-containing PC. The different lipid compositions of the lymphocyte cell membranes after exposure to 18:0 were correlated with their plasma membrane potentials. In T cells, the accumulation of disaturated [corrected], 18:0-containing PC coincided with a rapid (within 8 hr) collapse of membrane integrity, as determined by flow cytometry. The collapse of membrane integrity was found to be time and dose dependent. No such depolarization was observed in B cells which, by virtue of their desaturating ability, were able to avoid incorporating large amounts of disaturated [corrected] 18:0-containing phospholipids into their membranes. It is proposed that a lack of stearoyl-CoA desaturase in T cells precludes them from desaturating exogenously derived 18:0, thus leading to increased proportions of 18:0-containing disaturated [corrected] PC in their cell membranes. The increased abundance of this PC species may enhance membrane rigidity to an extent that plasma membrane integrity is significantly impaired, leading to a loss of membrane potential and ultimately cell function and viability.

Animals↗
PubMed2006

Shell cross-linked stearic acid grafted chitosan oligosaccharide self-aggregated micelles for controlled release of paclitaxel.

Stearic acid grafted chitosan oligosaccharide (CSO-SA) with different degree of amino substitution (SD) was synthesized by 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide (EDC)-mediated coupling reaction. The critical micelle concentration (CMC) of CSO-SA with different SD was about 0.06, 0.04, 0.01 mg/ml, respectively. With the increase of micelle concentration, the micelle size decreased, and the zeta potential increased. On the other hand, with the increase of SD of CSO-SA, the micelle size and zeta potential decreased due to the increased hydrophobic interaction of SA and the reduced free amino groups. To increase the stability of the micelle in vivo and controll drug release, the shells of micelles were cross-linked by glutaraldehyde. By controlling the molar ratio of CSO-SA to glutaraldehyde, the cross-linking of intra-micelle could be reached, and the nanoparticle with smaller size than that of its initial micelle was obtained. Paclitaxel was then used as model drug to incorporate into the micelles, and the surfaces of the micelles were further cross-linked by glutaraldehyde to form drug loaded and shell cross-linked nanoparticles. The effects of drug loading, SD of CSO-SA and cross-link degree on the size, zeta potential, drug entrapment efficiency and in vitro drug release behavior of micelles and its cross-linked nanoparticles were investigated. The higher drug entrapment efficiencies (above 94%) were observed in all case. The charged amounts of drug did not affect the drug release behavior. The drug release rate decreased with the increase of SD of CSO-SA and cross-link degree.

Biocompatible Materials↗
PubMed1990

Mapping of collision frequencies for stearic acid spin labels by saturation-recovery electron paramagnetic resonance.

Short pulse saturation-recovery electron paramagnetic resonance methods have been used to measure interactions of 14N:15N stearic acid spin label pairs in multilamellar liposomal dispersions composed of dimyristoyl-phosphatidylcholine (DMPC) and dielaidoylphosphatidylcholine (DEPC). Pairs consisting of various combinations of [14N]-16-, [14N]-12- or [14N]-5-doxylstearate, and [15N]-16-, [15N]-12-, or [15N]-5-doxylstearate were studied. SR experiments were performed at 27 degrees and 37 degrees C, and recovery signals were analyzed for initial conditions and multiexponential time constants by computer fitting using a damped least-squares approach. The time constants contain combinations of the electron spin lattice relaxation time, Tle, for each member of the spin-label pair, and the Heisenberg exchange rate constant, Kx. Spin-lattice relaxation times for each of the 14N and 15N stearic acid spin labels were determined, and it is noted that Tle for a given 15N-SASL was always slightly greater than that of the corresponding 14N-SASL. From Kx the bimolecular collision frequency was calculated, providing a detailed picture of molecular interactions. For both lipid systems the bimolecular collision rates were ordered as 12:5 less than 16:5 less than 5:5 less than 16:12 less than 12:12 less than 16:16. For all spin-label pairs studied, interaction frequencies were greater in DMPC than in DEPC. For the 16:16, 12:12, and 16:12 pairs, Kx was approximately 30% greater in DMPC than in DEPC, a significantly greater difference than is observed by conventional EPR methods. Further confirmation of the existence of vertical fluctuation of nitroxide moieties that are at the 16- (or 12) position toward the polar surfaces was obtained, with the frequency of 16:5 (or 12:5) interactions ~40% of the 16:16 (or 12:12) interaction frequency. In both DMPC and DEPC, Kx for homogeneous pairs increases as the doxyl moiety is moved further down the alkyl chain (i.e.,5:5 < 12:12 < 16:16), suggesting that steric effects or the local rotational mobility of the nitroxide group influence the frequency at which spin exchange occurs.

Cyclic N-Oxides↗
PubMed1994

Metabolism of dietary stearic acid relative to other fatty acids in human subjects.

This paper reviews results obtained by stable-isotope-tracer methods for stearic acid (18:0) and palmitic acid (16:0) metabolism and the influence of dietary linoleic acid on the metabolism of these saturated fatty acids in humans subjects. The results, based on stable-isotope-tracer data, show that absorption of 18:0 is not significantly different from 16:0; percent desaturation of 18:0 to 9-cis 18:1 (9.2%) is 2.4 times higher than for 16:0 to 9-cis 16:1 (3.9%) and 9-desaturation is not greatly influenced by the amount of linoleic acid in typical US diets. Additionally, compared with 16:0, 18:0 incorporation is 30-40% lower for plasma triglyceride and cholesterol ester and approximately 40% higher for phosphatidylcholine; beta-oxidation of saturated fatty acids was slower than for unsaturated fatty acids and increasing the intake of dietary linoleic acid decreased beta-oxidation of saturated fatty acids. These results indicate that metabolic differences between 18:0 and 16:0 only partially explain the difference in the cholesterolemic effect reported for these saturated fatty acids.

Absorption↗
PubMed1976

An ESR study of the anchoring of spin-labeled stearic acid in lecithin multilayers.

In egg lecithin-water lamellar phases, spin-labeled stearic acid gives two superimposed ESR spectra which are only well resolved when the temperature is greater than 30 degrees C. These two spectral components are attributed to the dissociated and non-dissociated forms of the fatty acid carboxylic group, anchored at two different positions in the polar interface constituted by the hydrated lipid polar heads. Results on such interactions of other functional groups (spin-labeled fatty ester and fatty alcohol) are also presented.

Binding Sites↗
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↗
PubMed1993

Interrelationship of stearic acid content and triacylglycerol composition of lard, beef tallow and cocoa butter in rats.

We investigated modes whereby stearic acid (18:0) exerts a neutral or cholesterol-lowering effect using dietary fats which provided graded levels of 18:0 and distinct triacylglycerol (TAG) profiles. Male Sprague-Dawley rats (150-175 g) were fed diets containing 0.2% cholesterol and 16% fat from corn oil, or from 1% corn oil plus 15% lard (13.2% 18:0), beef tallow (19.2% 18:0) or cocoa butter (34.7% 18:0) for 3 wk, and then killed in a fasted or fed state. Chylomicron (CM) fatty acid profiles suggested reduced absorption of 18:0 with greater 18:0 intake. CM TAG profiles indicated a reduction or loss of two TAG species compared to the TAG profiles of the stearate-rich diets: 1-palmitoyl-2-oleoyl-3-stearoyl glycerol (POS) and 1,3-distearoyl-2-oleoyl glycerol (SOS). Hepatic total cholesterol concentrations were 54-77% lower (P < 0.01) in the cocoa butter-fed than the lard-and beef tallow-fed groups. The cocoa butter group showed a significantly lower ratio of high-density lipoprotein esterified/free cholesterol than all other groups. Hepatic stearoyl-CoA and oleoyl-CoA concentrations, the substrate and product for hepatic delta 9 desaturase, were not significantly different for corn oil-fed and cocoa butter-fed groups in spite of a large difference in 18:0 intake. These data suggest that the neutral or cholesterol-lowering effect of 18:0 is not due to hepatic conversion of stearic to oleic acid, and that POS and SOS are poorly absorbed from stearate-rich dietary fats.

Acyl Coenzyme A↗
PubMed1982

The effects of cholesterol on the time-resolved emission anisotropy of 12-(9-anthroyloxy)stearic acid in dipalmitoylphosphatidylcholine bilayers.

The time-resolved fluorescence emission anisotropy of 12-(9-anthroyloxy)stearic acid (12-AS) and 1,6-diphenyl-1,3,5-hexatriene (DPH) have been measured in dipalmitoylphosphatidylcholine liposomes in the presence and absence of 40 mol% cholesterol at temperatures above and below the phase transition temperature (41 degrees C). By using a synchronously-pumped mode-locked frequency-doubled dye laser and single photon counting detection with an excitation response function of 300 picosecond, rotational correlation times down to less than 1 nanosecond could be resolved. Whereas DPH showed only small changes in the limiting anisotropy on the addition of cholesterol, 12-AS showed significant increases in this parameter with the effect being potentiated at higher temperatures. This difference in behaviour has been attributed to a fluorophore-cholesterol interaction that resulted in a change in the fluorophore geometry. Not only do DPH and 12-AS sense different depolarizing rotations due to the different directions of their emission dipoles but also differ in their lipid interactions which alter their limiting anisotropies. The implication is that the comparison of steady-state anisotropy measurements between chemically identical fluorophores in different lipid environments may be complicated by molecular distortions that change the motions to which the steady-state fluorescence parameters will be sensitive.

Cholesterol↗
PubMed1986

Determination of partition and lateral diffusion coefficients of ubiquinones by fluorescence quenching of n-(9-anthroyloxy)stearic acids in phospholipid vesicles and mitochondrial membranes.

The quenching of fluorescence of n-(9-anthroyloxy)stearic acids and other probes by different ubiquinone homologues and analogues has been exploited to assess the localization and lateral mobility of the quinones in lipid bilayers of model and mitochondrial membranes. The true bimolecular collisional quenching constants in the lipids together with the lipid/water partition coefficients were obtained from Stern-Volmer plots at different membrane concentrations. A monomeric localization of the quinone in the phospholipid bilayer is suggested for the short side-chain ubiquinone homologues and for the longer derivatives when cosonicated with the phospholipids. The diffusion coefficients of the ubiquinones, calculated from the quenching constants either in three dimensions or in two dimensions, are in the range of (1-6) X 10(-6) cm2 s-1, both in phospholipid vesicles and in mitochondrial membranes. A careful analysis of different possible locations of ubiquinones in the phospholipid bilayer, accounting for the calculated diffusion coefficients and the viscosities derived therefrom, strongly suggests that the ubiquinone 10 molecule is located within the lipid bilayer with the quinone ring preferentially adjacent to the polar head groups of the phospholipids and the hydrophobic tail largely accommodated in the bilayer midplane. The steady-state rates of either ubiquinol 1-cytochrome c reductase or NADH:ubiquinone 1 reductase are proportional to the concentration of the quinol or quinone substrate in the membrane. The second-order rate constants appear to be at least 3 orders of magnitude lower than the second-order constants for quenching of the fluorescent probes; this is taken as a clear indication that ubiquinone diffusion is not the rate-determining step in the quinone-enzyme interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

12-(9-Anthroyl)stearic acid, a fluorescent probe for the ubiquinone region of the mitochondrial membrane.

1. 12-(9-Anthroyl)stearic acid can be incorporated into mitochondrial membranes. 2. The fluorescence properties of the membrane-bound probe are different from those of the free molecule. 3. The intensity of emission and fluorescence life-time of the probe is enhanced when, in the presence of substrate, the electron-transport chain is reduced. 4. This change in intensity has been demonstrated to be a result of collisional quenching by oxidised ubiquinone in the oxidised membrane but not when the respiratory chain is in the reduced state. 5. In pulsing anaerobic mitochondria with oxygen the rate of the fluorescence change is found to be slower than the rate of ubiquinone oxidation, suggesting that the probe detects a structural transition in the mitochondrial inner membrane. 6. This transition results in a constraint on ubiquinone motion in the reduced system. Model experiments, using lipid dispersions, have been carried out to test some of the interpretations.

Animals↗
PubMed1994

Fatty acid binding site of the mitochondrial uncoupling protein. Demonstration of its existence by EPR spectroscopy of 5-DOXYL-stearic acid.

Fatty acid binding site on isolated mitochondrial uncoupling protein (UcP) is demonstrated using EPR spectroscopy of 5-DOXYL-stearic acid (5-SASL), which also activated H+ transport in proteoliposomes containing UcP. In the presence of UcP the EPR spectrum showed reproducible broadening of the low field peak as well as an increase in h+1I/h+1M ratio, rotational correlation time and in order parameter. The half-height width of the low field peak was even doubled in the presence of another UcP ligand, GDP. Palmitic acid reversed the effect of 5-SASL and non-ionizable 5-DOXYL-decane did not exhibit it.

Adipose Tissue, Brown↗
PubMedDate not supplied

[The early and late effects of a radiation lesion by 14C(14C-stearic acid)].

In experiments with mice a study was made of the biological effect of radiocarbon (14C-stearic acid) injected intraperitoneally in doses of 2.2, 1.2 and 0.5 MBq/g. The doses absorbed within the body made up an average of 13.4 and 1.7 Gy respectively. The animals of the 1st group exhibited a severe degree of radiation affection and those of the 2nd and 3d groups median and mild degrees. Metabolism peculiarities and formation of absorbed 14C doses, as well as early and remote effects of radiation were investigated.

Animals↗
PubMedDate not supplied

[Relative location of anthroyl derivatives of stearic acid in low density lipoproteins].

Effective quenching constants (K'sv) of 2-, 7- and 12-(9-anthroyloxy)stearic acid (n-AS) fluorescence in LDL were determined. Spin probes I(m, n) (n = 3, 7, 10, 14) and I- anions were used as quenchers. Quenching of 2-AS and 12-AS fluorescence by I(m, n) was the more effective, the deeper spin probe nitroxyl fragment was located (the greater n was); maximal K'sv value corresponded to I(1,14). By contrast, for 7-AS the quenching by I(12,3) was the most effective. 2-AS and 12-AS spectra maxima and fluorescence polarization were similar. We concluded that the 2-AS chromophore was located deeper in LDL phospholipid monolayer than chromophore of 7-AS (as was the case for 12-AS).

Electron Spin Resonance Spectroscopy↗
PubMed1960

Interactions of veratrum alkaloids, procaine, and calcium with monolayers of stearic acid and their implications for pharmacological action.

The interactions of veratridine, cevadine, veracevine, and veratramine with monolayers of stearic acid show marked differences. Veratridine and cevadine, at concentrations that are known from potential, ionic flux, and other measurements to affect living membranes, react strongly with the film and appear to cause an "interfacial dissolution" whereby both the alkaloid and the stearate leave the surface. Veracevine at the same concentration does not interact with the film. The veratramine reaction is weak, much like that of the local anesthetic procaine. The veratridine and cevadine effects are antagonized by 10(-3)M Ca(++), low pH, and 3.7 and 7.4 x 10(-3)M procaine. These differences among the veratrum alkaloids and the antagonisms parallel effects observed in living systems. Such parallelism suggests that similar physical interactions are involved in the stearate film and in natural membranes.

Anesthetics, Local↗