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PubMed1993

Uptake of docosahexaenoic acid by microvessels from developing rat brain.

Uptake of polyunsaturated fatty acids by the rat brain occurs mainly during the three weeks before weaning. Docosahexaenoic acid [22:6], the predominant polyunsaturated fatty acid in the adult brain, appears to be preferentially taken up from the circulation by both the adult and developing rat brain. To test the hypothesis that this preferential incorporation was mediated by the cerebral microvasculature, we compared the incorporation of 22:6 to a saturated fatty acid, palmitic acid [16:0], in freshly isolated rat brain microvessels from the pooled brains of entire litters of two-week-old rats (n = 8 litters). For each litter duplicate incubations with 2 microCi of [1-14C]22:6 or [1-14C]16:0 were performed in 60% autologous rat serum for 2 hr at 37 degrees C. [3H]Sucrose was included in each incubation, allowing correction for non-specific uptake and trapping. An average of 2.7 +/- 2.0% (SD) of the radioactivity from 16:0 was found in the microvessels after 2 hr, vs 0.9 +/- 0.6% for 22:6. This yielded a three-fold enrichment of 16:0 over 22:6 (P = 0.02, paired t-test). There was preferential incorporation of 22:6 into phosphatidylethanolamine and of 16:0 into phosphatidylcholine, although most of the label from either substrate remained as fatty acid after the 2 hr incubation. These results do not indicate that brain capillaries mediate the preferential incorporation of polyunsaturated fatty acids into brain tissue that was seen in intact young rats.

Animals↗
PubMed1995

The composition and function of reptilian pulmonary surfactant.

In mammals, the surface tension of the fluid lining the inner lung greatly contributes to the work of breathing. Surface tension is modified by the secretion of a mixture of surface active lipids and proteins (termed pulmonary surfactant). A disaturated phospholipid (DSP), predominantly dipalmitoylphosphatidylcholine (DPPC), can eliminate surface tension under high dynamic compression. Cholesterol (CHOL) and unsaturated phospholipids (USP) promote respreading upon inflation by converting DPPC to the disordered liquid-crystalline state. It appeared to us that a surfactant rich in DPPC, which has a high phase transition temperature of 41 degrees C, is likely to be of only limited use in the lungs of reptiles, many of which have preferred body temperatures between 20 and 30 degrees C. We review here the presence and composition of surfactant in species from the three subclasses of the Reptilia and relate these to lung structure and function, phylogeny and environmental selection pressures such as body temperature. We also discuss the function of reptilian surfactant and the factors which control surfactant turnover. Large amounts of pulmonary surfactant have been found in all reptiles so far examined. In general, warmer reptiles have greater amounts of surfactant which is also relatively enriched in DSP. Cold lizards (18 degrees C) have significantly elevated levels of surfactant cholesterol. As in all vertebrates, PC is always the dominant phospholipid (60-80%). Unlike mammals, phosphatidylglycerol (PG) is absent, with the exception of one species. The remaining phospholipid groups are present to varying degrees. The saturated fatty acid, palmitic acid (16:0) is the dominant acyl group, oleic acid (18:1) is the dominant mono-unsaturated fatty acid, and polyunsaturates comprise only about 20% of the total fatty acid profile. For two species of dragon lizards, short term changes in temperature do not affect the fatty acids, but protracted periods of cold significantly decrease the presence of 16:0 in turtle lavage (Lau and Keough, Can.J. Biochem. 59: 208-219, 1981). Surfactant appears to function as an antiglue in most reptiles, serving to lower opening pressure, and decrease the work of breathing. However, surface tension forces generally do not influence reptilian lung compliance, suggesting that the primary functions of mammalian surfactant are not necessarily relevant to reptiles.

Animals↗
PubMed1995

Effects of various fatty acids alone or combined with vitamin E on cell growth and fibrinogen concentration in the medium of HepG2 cells.

Dietary intake of fish oils, rich in the polyunsaturated fatty acids (PUFAs) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), has given inconsistent results as to their influence on the plasma fibrinogen level (1, 2, 3, 4, 5, 6). In the present study we have examined the effects of various fatty acids, the PUFAs and the saturated fatty acid palmitic acid (PA), alone or combined with the antioxidant vitamin E (Vit.E), on the fibrinogen concentration in the growth medium of human hepatoma (HepG2) cells. Vit.E alone decreased the amount of fibrinogen in the medium in a dose dependent fashion, where fibrinogen was measured as Fibrinopeptide A (FPA) releasable by thrombin. EPA and Vit.E decreased the amount of fibrinogen additively. PUFAs alone increased the fibrinogen concentration in a dose dependent manner. PUFAs combined with a fixed dose of Vit.E decreased the fibrinogen concentration, also dose dependently. OA and PA had an inhibitory effect, both alone and combined with Vit.E. These results indicate that Vit.E may be necessary for PUFAs to have a fibrinogen lowering effect, whereas both OA and PA apparently may decrease the fibrinogen concentration in the cell medium of HepG2 cells, both alone and combined with Vit.E. Possibly, peroxidation of the PUFAs may increase the fibrinogen production, that may be counteracted and reversed by the simultaneous presence of Vit.E.

Carcinoma, Hepatocellular↗
PubMed1993

Characterization of a cDNA encoding a human kidney, cytochrome P-450 4A fatty acid omega-hydroxylase and the cognate enzyme expressed in Escherichia coli.

A cDNA encoding a cytochrome P-450 4A (CYP4AII) was cloned from a human kidney cDNA library. Northern blot analysis and RNase protection assays indicate that related mRNAs occur in kidney and liver with the highest abundance found in kidney. The enzyme was expressed from its cDNA in Escherichia coli. A solubilized preparation of the enzyme reconstituted with cytochrome P-450 reductase catalyzed the omega-hydroxylation of lauric acid, palmitic acid, and arachidonic acid with turnover numbers of 9.8, 2.2 and 0.55 min-1, respectively. Little or no activity was detected toward prostaglandins A1 and E1.

Amino Acid Sequence↗
PubMed1994

Inhibition of cytokine-stimulated thymic lymphocyte proliferation by fatty acids: the role of eicosanoids.

The effect of individual fatty acids on the proliferation of thymic lymphocytes in response to interleukin-1 (IL-1) was investigated. Proliferation was estimated by measuring [3H]thymidine incorporation into the acid insoluble fraction of the thymocytes. A concentration-dependent inhibition (in the range 1-100 microM) in the IL-1-stimulated proliferation was observed with the C20 fatty acids dihomo-gamma-linolenic acid (DGLA), arachidonic acid and eicosapentaenoic acid (EPA). A less pronounced concentration-dependent inhibitory response was observed with the C18 fatty acids linoleic acid, alpha-linolenic acid and gamma-linolenic acid. Palmitic acid and oleic did not have any effect on either basal or IL-1-stimulated proliferation at concentrations up to 100 microM. The potencies of each fatty acid for this effect at a concentration of 100 microM were: arachidonic acid > EPA > or = DGLA > linoleic acid. DGLA, arachidonic acid and EPA also attenuated IL-2-stimulated proliferation. The inhibitory action of these fatty acids was not mediated by conversion to prostaglandins or other eicosanoids as the cyclooxygenase inhibitor, ketoprofen and NDGA did not alter their action. Incubation of thymocytes with radiolabelled DGLA and EPA followed by reverse-phase HPLC analysis revealed that DGLA is predominantly converted to a more polar metabolite which is not PGE1 whereas EPA does not appear to be converted to any other detectable metabolite. The data indicate that the inhibitory actions of fatty acids on cell proliferation do not occur as a result of conversion to other metabolites but may be direct effects. The inhibition of cytokine-stimulated lymphocyte proliferation by unsaturated fatty acids would imply that they may attenuate cell-mediated immune reactions.

8,11,14-Eicosatrienoic Acid↗
PubMed1990

Effect of albumin on oleic acid lymphatic absorption in rats.

1. The aim of this study was to investigate how fatty acid absorption was affected when exogenous fatty acids were complexed with albumin in absence of bile. Experiments were carried out in vivo, in order to study overall absorption processes. 2. An equimolar mixture of 14C oleic acid, palmitic acid and monopalmitin was infused intraduodenally in bile- and pancreatic juice-diverted rats. 3. Lipids were emulsified with either sodium taurocholate or fatty acids complexed with albumin. 4. Lymphatic lipid output was compared during the 6 hr following infusion of 90 mumol of the radioactive lipid mixture. 5. Lymphatic radioactive lipid recovery was significantly decreased by albumin. 6. Only 17% of the infused radioactivity was recovered in lymph when fatty acids were complexed with albumin against 37% when lipids were emulsified with sodium taurocholate. 7. Unrecovered lymph radioactivity was found at the distal part of intestine. Moreover, albumin significantly decreased lymph flow. 8. We conclude that undigested albumin acted at the luminal level of lipid absorption processes and specifically decreased fatty acid uptake.

Absorption↗
PubMed2006

Lipid peroxidation as a source of oxidative damage in Helicobacter pylori: protective roles of peroxiredoxins.

Oxidative stress conditions lead to enzymatic and non-enzymatic unsaturated fatty acid-initiated lipid peroxidation reactions. One exacerbating product is lipid hydroperoxide (LOOH) which itself promotes formation of several additional peroxyl radicals. Helicobacter pylori mutant strains with disruptions in genes encoding the peroxiredoxins, alkyl hydroperoxide reductase (ahpC) and the bacterioferritin comigratory protein (bcp), were more sensitive than the parent strain to oxidizing agents. These mutant strains were particularly sensitive, compared to the wild type, to killing by the unsaturated fatty acid linolenic acid but were not sensitive to the saturated fatty acid palmitic acid. A double mutant strain (ahpC bcp) accumulated more than 3-fold more lipid peroxides than the parent strain, indicating these peroxiredoxins together play a role in detoxifying lipid peroxides. The level of free iron accumulation, a signature of oxidative stress damage, was correlated specifically to organic peroxide-mediated stress by both in vivo and in vitro approaches. Free iron accumulation and concomitant destruction of [Fe-S] cluster-containing proteins (hydrogenase and aconitase) was correlated to damage mediated by exogenous t-butyl peroxide, or separately to intracellular accumulation of lipid peroxides in mutant strains. A major macromolecular target of accumulating lipid peroxides in H. pylori is DNA, as mutant analysis approaches combined with quantitative DNA fragmentation studies and specific DNA damage assessment (i.e. 8-oxoguanine formation) were used to demonstrate that such damage was especially associated with ahpC and ahpC bcp strains.

Bacterial Proteins↗
PubMed2005

Lysophospholipid and fatty acid inhibition of pulmonary surfactant: non-enzymatic models of phospholipase A2 surfactant hydrolysis.

Secretory A(2) phospholipases (sPLA(2)) hydrolyze surfactant phospholipids cause surfactant dysfunction and are elevated in lung inflammation. Phospholipase-mediated surfactant hydrolysis may disrupt surfactant function by generation of lysophospholipids and free fatty acids and/or depletion of native phospholipids. In this study, we quantitatively assessed multiple mechanisms of sPLA(2)-mediated surfactant dysfunction using non-enzymatic models including supplementation of surfactants with exogenous lysophospholipids and free fatty acids. Our data demonstrated lysophospholipids at levels >or=10 mol% of total phospholipid (i.e., >or=10% hydrolysis) led to a significant increase in minimum surface tension and increased the time to achieve a normal minimum surface tension. Lysophospholipid inhibition of surfactant function was independent of the lysophospholipid head group or total phospholipid concentration. Free fatty acids (palmitic acid, oleic acid) alone had little effect on minimum surface tension, but did increase the maximum surface tension and the time to achieve normal minimum surface tension. The combined effect of equimolar free fatty acids and lysophospholipids was not different from the effect of lysophospholipids alone for any measurement of surfactant function. Surfactant proteins did not change the percent lysophospholipids required to increase minimum surface tension. As a mechanism that causes surfactant dysfunction, depletion of native phospholipids required much greater change (equivalent to >80% hydrolysis) than generation of lysophospholipids. In summary, generation of lysophospholipids is the principal mechanism of phospholipase-mediated surfactant injury in our non-enzymatic models. These models and findings will assist in understanding more complex in vitro and in vivo studies of phospholipase-mediated surfactant injury.

Animals↗
PubMed2004

Anti-HCV activities of selective polyunsaturated fatty acids.

HCV infection can lead to chronic infectious hepatitis disease with serious sequelae. Interferon-alpha, or its PEGylated form, plus ribavirin is the only treatment option to combat HCV. Alternative and more effective therapy is needed due to the severe side effects and unsatisfactory curing rate of the current therapy. In this study, we found that several polyunsaturated fatty acids (PUFAs) including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) are able to exert anti-HCV activities using an HCV subgenomic RNA replicon system. The EC(50) (50% effective concentration to inhibit HCV replication) of AA was 4microM that falls in the range of physiologically relevant concentration. At 100microM, alpha-linolenic acid, gamma-linolenic, and linoleic acid only reduced HCV RNA levels slightly and saturated fatty acids including oleic acid, myristic acid, palmitic acid, and steric acid had no inhibitory activities toward HCV replication. When AA was combined with IFN-alpha, strong synergistic anti-HCV effect was observed as revealed by an isobologram analysis. It will be important to determine whether PUFAs can provide synergistic antiviral effects when given as food supplements during IFN-based anti-HCV therapy. Further elucidation of the exact anti-HCV mechanism caused by AA, DHA, and EPA may lead to the development of agents with potent activity against HCV or related viruses.

Antiviral Agents↗
PubMed2006

Simultaneous determination of saponins and fatty acids in Ziziphus jujuba (Suanzaoren) by high performance liquid chromatography-evaporative light scattering detection and pressurized liquid extraction.

The seed of Ziziphus jujube Mill. var. spinosa (Bunge) Hu ex H. F. Chou, Suanzaoren in Chinese, is one of commonly used Chinese medicines. Saponins and fatty oil contains several fatty acids in Suanzaoren are responsible for its therapeutic activities. In this study, a new HPLC coupled with evaporative light scattering detection (ELSD) and pressurized liquid extraction (PLE) method was developed for the simultaneous quantitative determination of 11 major components of 2 saponins and 9 fatty acids, namely jujuboside A, jujuboside B, lauric acid, myristic acid, palmitic acid, palmitoleic acid, stearic acid, oleic acid, linoleic acid, arachidic acid and docosanoic acid in Suanzaoren. Simultaneous separation of these eleven compounds was achieved on a C18 analytical column. The mobile phase consisted of (A) 0.1% aqueous acetic acid and (B) methanol with 0.1% acetic acid using a gradient elution. The drift tube temperature of ELSD was set at 75 degrees C, and nitrogen flow-rate was 1.8l/min. All calibration curves showed good linearity (r(2)>0.9955) within test ranges. This method showed good reproducibility for the quantification of these eleven components in Suanzaoren with intra- and inter-day variations of less than 3.41 and 4.37%, respectively. The validated method was successfully applied to quantify 11 investigated components in nine commercial samples of Suanzaoren.

Calibration↗
PubMed2005

Alpha-linolenic acid and riluzole treatment confer cerebral protection and improve survival after focal brain ischemia.

We investigated here the effects of alpha-linolenic acid and riluzole, both activators of the 2P-domain K+ channel family TREK/TRAAK, in a model of focal ischemia clinically relevant to stroke, not only assessing neuronal protection, but also long term survival. Moreover, all the drug treatments were initiated post-ischemia. Mice were subjected to transient middle cerebral artery occlusion (1 h) and reperfusion according to the intraluminal filament model. Drugs were injected into the jugular vein according to three protocols: (i) a single dose of 4 mg/kg riluzole or 500 nmol/kg alpha-linolenic acid at different reperfusion time; (ii) a three-day therapy (a single dose of 2 mg/kg riluzole and 250 nmol/kg alpha-linolenic acid given 1-2, 48 and 72 h after reperfusion); (iii) a three-week therapy (a single dose of 2 mg/kg riluzole and 250 nmol/kg alpha-linolenic acid given once a week during three weeks after reperfusion. A combined treatment with 2mg/kg riluzole+250 nmol/kg alpha-linolenic acid injected 2 h after reperfusion was also tested. A single dose of riluzole (4 mg/kg) or alpha-linolenic acid (500 nmol/kg) injected up to 3 h after reperfusion reduced drastically the stroke volume by 75% and 86%, respectively. Neurological deficits 24 h after ischemia were significantly improved by alpha-linolenic acid500 or riluzole4 with a neurological score of 1.8 as compared with 2.5 observed in vehicle-treated mice. Alpha-linolenic acid- and riluzole treatment were associated with a reduction in cytopathological features of cell injury, including DNA fragmentation and Bax expression in the cortex and the caudate putamen. With regard to the survival rate at 30 days, the best protections were obtained with the alpha-linolenic acid-injection in the three-week therapy as well as with a single dose of the combined treatment (2 mg/kg riluzole+250 nmol/kg alpha-linolenic acid). Palmitic acid, a saturated fatty acid that does not activate the 2P-domain K-channel TREK/TRAAK family, did not provide any neuroprotection. Taken together, these data suggest that the TREK/TRAAK K-channel family may be a promising target for neuroprotection, and that riluzole and alpha-linolenic acid could be of therapeutic value against focal ischemia/reperfusion injury to the brain.

Animals↗
PubMed1986

Qualitative and quantitative analysis of peanut oil triacylglycerols by reversed-phase liquid chromatography.

Triacylglycerols (TGs) from an african peanut oil were analysed and fractionated by reversed-phase liquid chromatography (RPLC) using a differential refractometer as a detector. The fatty acids of the 33 collected fractions were analysed by gas chromatography after pentadecanoic acid (15:0) was added as an internal standard to quantitate the TG fractions. The three major fatty acids in the oil were octadecenoic acid (oleic acid, 44.5%), octadecadienoic acid (linoleic acid, 32.3%) and hexadecanoic acid (palmitic acid, 13.9%) together amounting to ca. 90% of the total fatty acids. Very long-chain saturated fatty acids (20:0-26:0) were also found. Thirty TGs could be easily identified from the fatty acid composition of the fractions alone. Dioleoyllinoleoylglycerol (18:1, 18:1, 18:2) was the main TG, amounting to nearly 17% of the oil, followed by palmitoyloleoyllinoleoylglycerol (16:0, 18:1, 18:2) (13%), oleoyldilinoleoylglycerol (18:2, 18:2, 18:1) (12%) trioleoylglycerol (18:1, 18:1, 18:1) (10%) and palmitoyldioleoylglycerol (16:0, 18:1, 18:1) (8%). These five TGs, which were virtually the only TGs in their respective fractions, together represented ca. 60% of the peanut oil TGs. Straight parallel lines were found for different series of TGs on plotting the logarithm of the relative retention time of the identified TGs (and those further identified) versus the number of double bonds. Other straight parallel lines were also observed on plotting the carbon numbers versus the equivalent carbon numbers of the oil TGs. These linear relationships were used to predict the different TGs present in the complex fractions. Their proportions in most instances were easily determined from the fatty acid composition of the fractions. In a very few instances a mathematical method had to be applied to solve the problem. Using the above-mentioned methods, 84 TGs could be identified and their percentages determined in the studied peanut oil. The very long-chain saturated fatty acids were always found associated with unsaturated fatty acids, preferentially with two molecules of linoleic acid. On the other hand, correction factors, determined from commercial simple TGs, were applied to peak areas before calculating the percentages of the 33 eluted TG fractions. For the major fractions of the oil, the series of values thus obtained was comparable to the series determined by the internal standardization procedure. Data reported here for peanut oil TGs are likely to be useful in identifying and quantifying the component TGs of other oils analysed by RPLC under the reported conditions.

Arachis↗
PubMed2001

Eicosanoids mediate microaggregation reactions to bacterial challenge in isolated insect hemocyte preparations.

Nodule formation is the quantitatively predominant insect cellular defense reaction to bacterial challenges, responsible for clearing the largest proportion of infecting bacteria from circulation. It has been suggested that eicosanoids mediate several steps in the nodulation process, including formation of hemocyte microaggregates, an early step in the process. While fat body and hemocytes are competent to biosynthesize eicosanoids, the source of the nodulation-mediating eicosanoids remains unclear. To investigate this issue, we studied hemocyte microaggregation reactions to bacterial challenge in vitro. Hemocyte suspensions from the tobacco hornworm, Manduca sexta, were treated with the phospholipase A(2) inhibitor, dexamethasone, then challenged with the bacterium Serratia marcescens. Preparations treated with dexamethasone yielded fewer hemocyte microaggregations than untreated, control preparations. Furthermore, the influence of dexamethasone was reversed by amending experimental (dexamethasone-treated) preparations with the eicosanoid biosynthesis precursor, arachidonic acid. Palmitic acid, which is not a substrate for eicosanoid biosynthesis, did not reverse the influence of dexamethasone on the microaggregation reaction. The influence of dexamethasone was also reversed by adding filtered media from challenged hemocyte preparations to dexamethasone-treated preparations. Finally, most hemocyte preparations treated with selected eicosanoid biosynthesis inhibitors formed fewer hemocyte microaggregations than control preparations. The 5- and 12-lipoxygenase inhibitor, esculetin, did not influence the formation of hemocyte microaggregations in this system. These results are consistent with similar investigations performed in vivo, and we infer that hemocytes are responsible for forming and secreting eicosanoids, which subsequently initiate nodulation by mediating hemocyte microaggregation.

Journal Article↗
PubMed1996

Adipose tissue fatty acids and size and number of fat cells from birth to 9 years of age--a cross-sectional study in 96 boys.

We studied interrelations between the size and number of fat cells and the composition of fatty acids in 96 boys from birth to 9 years of age. The size of fat cells increased during the first months of life and decreased over the second 6 months, in parallel with the tissue fat concentration and the skinfold thickness of subcutaneous fat. From the end of the first year of life, the size of the fat cell increased slowly. The number of fat cells did not begin to increase until the end of the first year of life, maintaining a continuous increase until 9 years of age. During the first years of life, important changes occurred in the concentration of adipose tissue fatty acids. Palmitic acid had the greatest concentration in adipose tissue at the moment of birth and then decreased, becoming stabilized from the age of 2 or 3 years. The concentrations of lauric, myristic, and myristoleic acids followed a course similar to that of adipocyte growth, probably reflecting changes in the accumulation of fat by the adipocyte. At the moment of birth, the concentrations of linoleic acid (C18:2), an essential fatty acid not synthesized by the organism, were low, increasing from the very first months of life. This increase correlated with the increase in fat cell size and number. These interrelations between the size and number of fat cells and the composition of adipose tissue fatty acids suggest the important role dietary fat can play in the childhood endowment of adipocytes.

Adipocytes↗
PubMed2003

Identification of some plasticizers compounds in landfill leachate.

In this work it was described a simple method for extraction of plasticizer compounds (mainly phthalate esters and bisphenol A (BPA)) from landfill leachate samples. The samples were submitted to an extraction procedures based on precipitation, solid phase extraction (SPE) and ionic exchange chromatography (IEC). Firstly the landfill leachate sample was acidified by addition of HCl concentrated, in order to precipitate the organic compounds that are less soluble in water. The precipitate was washed with several solvents. The aqueous phase was then submitted to SPE with XAD-4 resin and IEC with Amberlyst A-27 resin. The instrumental analysis was performed by gas chromatography with mass spectrometer detector (GC/MSD) and the compounds were identified by the GC/MSD library (Wiley) and by using some standard substances. These methodologies allow the isolation and identification of the following compounds: dioctylphthalate, diisobutilphthalate, BPA, benzoic acid, palmitic acid and diisopentylphthalate. The methods are very simple, rapid and selective, for plasticizers extraction from landfill leachate matrices.

Brazil↗
PubMed2002

Ranking the toxicity of fatty acids on Jurkat and Raji cells by flow cytometric analysis.

The fatty acids have an important role in the control of leukocyte metabolism and function. Higher concentrations of certain fatty acids, particularly polyunsaturated fatty acids (PUFAs) and volatile fatty acids, can cause cell death via apoptosis or, when concentrations are greater, necrosis. In this study, we determined the highest concentrations of various fatty acids that are non-toxic to two human leukemic cell lines, Jurkat (T-lymphocyte) and Raji (B-lymphocyte). Toxicity was evaluated by either loss of membrane integrity and/or DNA fragmentation using flow cytometric analysis. There were no remarkable differences for the toxicity of the fatty acids between B and T cell lines. The cytotoxicity of the fatty acids was related to the carbon chain length and number of double bonds: docosahexaenoic acid=eicosapentaenoic acid=arachidonic acid=gamma-linolenic acid=stearic acid=palmitic acid > linoleic acid=palmitoleic acid > vacenic acid=lauric acid > oleic acid > elaidic acid > capric acid > butyric acid > caprylic acid=caproic acid=propionic acid. The proportion of cells undergoing apoptosis or necrosis, induced by the fatty acids tested, remains to be investigated.

Apoptosis↗
PubMed1997

Stable nitroxide radicals protect lipid acyl chains from radiation damage.

The present study focused on protective activity of two six-membered-ring nitroxide radicals, 2,2,6,6-tetramethylpiperidine-1-oxyl (Tempo) and 4-hydroxy-Tempo (Tempol), against radiation damage to acyl chain residues of egg phosphatidylcholine (EPC) of small unilamellar vesicles (SUV). SUV were gamma-irradiated (10-12 kGy) under air at ambient temperature in the absence and presence of nitroxides. Acyl chain composition of the phospholipids before and after irradiation was determined by gas chromatography. Both Tempo and Tempol effectively and similarly protected the acyl chains of EPC SUV, including the highly sensitive polyunsaturated acyl chains, C20:4, C22:5, and C22:6. The conclusions of the study are: (a) The higher the degree of unsaturation in the acyl chain, the greater is the degradation caused by irradiation. (b) The fully saturated fatty acids palmitic acid (C16) and stearic acid (C18) showed no significant change in their levels. (c) Both Tempo and Tempol provided similar protection to acyl chain residues. (d) Nitroxides' lipid-bilayer/aqueous distribution is not validly represented by their n-octanol/saline partition coefficient. (e) The lipid-bilayer/aqueous partition coefficient of Tempo and Tempol cannot be correlated with their protective effect. (f) The nitroxides appear to protect via a catalytic mode. Unlike common antioxidants, such as alpha-tocopherol, which are consumed under irradiation and are, therefore, less effective against high radiation dose, nitroxide radicals are restored and terminate radical chain reactions in a catalytic manner. Furthermore, nitroxides neither yield secondary radicals upon their reaction with radicals nor act as prooxidants. Not only are nitroxides self-replenished, but also their reduction products are effective antioxidants. Therefore, the use of nitroxides offers a powerful strategy to protect liposomes, membranes, and other lipid-based assemblies from radiation damage.

Antioxidants↗
PubMed1997

Enhanced hepatic fatty acid oxidation and upregulated carnitine palmitoyltransferase II gene expression by methyl 3-thiaoctadeca-6,9,12,15-tetraenoate in rats.

This study reports the effects of a novel polyunsaturated 3-thia fatty acid, methyl 3-thiaoctadeca-6,9,12,15-tetraenoate on serum lipids and key enzymes in hepatic fatty acid metabolism compared to a saturated 3-thia fatty acid, tetradecylthioacetic acid. Palmitic acid treated rats served as controls. Fatty acids were administered by gavage in daily doses of 150 mg/kg body weight for 10 days. The aim of the present study was: (a) To investigate the effect of a polyunsaturated 3-thia fatty acid ester, methyl 3-thiaoctadeca-6,9,12,15-tetraenoate on plasma lipids in normolipidemic rats: (b) to verify whether the lipid-lowering effect could be consistent with enhanced fatty acid oxidation: and (c) to study whether decreased activity of esterifying enzymes and diversion to phospholipid synthesis is a concerted mechanism in limiting the availability of free fatty acid as a substrate for hepatic triglyceride formation. Repeated administration of the polyunsaturated 3-thia fatty acid ester for 10 days resulted in a reduction of plasma triglycerides (40%), cholesterol (33%) and phospholipids (20%) compared to controls. Administration of polyunsaturated and saturated 3-thia fatty acids (daily doses of 150 mg/kg body weight) reduced levels of lipids to a similar extent and followed about the same time-course. Both mitochondrial and peroxisomal fatty acid oxidation increased (1.4-fold- and 4.2-fold, respectively) and significantly increased activities of carnitine palmitoyltransferase (CPT) (1.6-fold), 2,4-dienoyl-CoA reductase (1.2-fold) and fatty acyl-CoA oxidase (3.0-fold) were observed in polyunsaturated 3-thia fatty acid treated animals. This was accompanied by increased CPT-II mRNA (1.7-fold). 2,4-dienoyl-CoA reductase mRNA (2.9-fold) and fatty acyl-CoA oxidase mRNA (1.7-fold). Compared to controls, the hepatic triglyceride biosynthesis was retarded as indicated by a decrease in liver triglyceride content (40%). The activities of glycerophosphate acyltransferase, acyl-CoA: 1,2-diacylglycerol acyltransferase and CTP:phosphocholine cytidylyltransferase were increased. The cholesterol lowering effect was accompanied by a reduction in HMG-CoA reductase activity (80%) and acyl-CoA:cholesterol acyltransferase activity (33%). In hepatocytes treated with methyl 3-thiaoctadeca-6,9,12,15-tetraenoate, fatty acid oxidation was increased 1.8-fold compared to controls. The results suggest that treatment with methyl 3-thiaoctadeca-6,9,12,15-tetraenoate reduces plasma triglycerides by a decrease in the availability of fatty acid substrate for triglyceride biosynthesis via enhanced fatty acid oxidation, most likely attributed to the mitochondrial fatty acid oxidation. It is hypothesized that decreased phosphatidate phosphohydrolase activity may be an additive mechanism which contribute whereby 3-thia fatty acids reduce triglyceride formation in the liver. The cholesterol-lowering effect of the polyunsaturated 3-thia fatty acid ester may be due to changes in cholesterol/cholesterol ester synthesis as 60% of this acid was observed in the hepatic cholesterol ester fraction.

Alkenes↗