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PubMed2002

Acidic phospholipids with unsaturated fatty acids inhibit the binding of origin recognition complex to origin DNA.

Origin Recognition Complex (ORC) is a candidate initiator of chromosomal DNA replication in eukaryotes. We recently reported that cardiolipin inhibits the interaction of Origin Recognition Complex ORC with origin DNA, as is the case of DnaA, the initiator of chromosomal DNA replication in prokaryotes. We report here that another acidic phospholipid, phosphatidylglycerol (PG), also inhibits the interaction. Synthetic PG with only unsaturated fatty acids inhibits ORC-binding to origin DNA more strongly than PG with only saturated fatty acids. On the other hand, phosphatidylcholine (neutral phospholipid) does not affect the ORC-origin interaction, regardless of the presence of saturated or unsaturated fatty acids. These results suggest that an acidic moiety and unsaturated fatty acids are important factors for the inhibitory effect of phospholipids on ORC binding to origin DNA, as is the case for DnaA. The inhibitory effect of cardiolipin on ORC binding to origin DNA was more apparent at 30 degrees C than at 4 degrees C. Furthermore, chlorpromazine restored the ORC-origin interaction in the presence of cardiolipin. Since the presence of unsaturated fatty acids, low incubation temperatures, and the addition of chlorpromazine all decrease membrane fluidity, these results suggest that membrane fluidity is important for the inhibitory effect of acidic phospholipids on ORC-binding to origin DNA, as is the case for DnaA.

Adenosine Triphosphate↗
PubMed1992

Quantitative fatty acid analyses in cultured porcine pulmonary artery endothelial cells: the combined effects of fatty acid supplementation and oxidant exposure.

Supplemental fatty acids can modify the oxidant susceptibility of pulmonary artery endothelial cells (PAEC) in monolayer culture. In addition, in vivo dietary modifications have altered tissue and animal susceptibility to a variety of forms of oxidant stress. These modifications of oxidant injury have been attributed to changes in the numbers of fatty acid double bonds in cell lipids. We tested this hypothesis by incubating porcine PAEC in culture medium supplemented with either 0.1 mM oleic acid (18:1 omega 9) or with an equivalent volume of ethanol vehicle alone (ETOH-0.1%) for 3 h. After supplementation, PAEC were exposed to either oxidant stress, 100 microM hydrogen peroxide (H2O2) in Hanks' balanced salt solution (HBSS), or to control condition, HBSS alone, for 30 min. Supplemental PAEC were exposed to HBSS or H2O2 either immediately or 24, 48, or 72 h after supplementation. Supplementation with 18:1 protected PAEC from H2O2-induced injury at all time points. The fatty acid composition of PAEC phospholipid (PL), triglyceride (TG), and free fatty acid (FFA) subclasses was determined using thin layer and gas chromatography. The PL fraction contained the majority of PAEC fatty acids, and H2O2 reduced the polyunsaturates in this fraction regardless of supplementation. Supplementation with 18:1 increased the 18:1 content of PAEC PL, TG, and FFA at all time points, modified other fatty acids to a lesser extent, but failed to alter the overall number of fatty acid double bonds at all time points. These results indicate that modification of double bond number does not fully explain the mechanisms by which changes in lipid composition can modulate oxidant injury.

Animals↗
PubMed2007

Characterization of a BODIPY-labeled fluorescent fatty acid analogue. Binding to fatty acid-binding proteins, intracellular localization, and metabolism.

The BODIPY-labeled fatty acid analogues are a useful addition to the tools employed to study the cellular uptake and metabolism of lipids. In this study, we show that BODIPY FL C(16) binds to purified liver and intestinal fatty acid-binding proteins with high affinity at a site similar to that for the physiological fatty acid oleic acid. Further, in human intestinal Caco-2 cells BODIPY FL C(16) co-localizes extensively with mitochondria, endoplasmic reticulum/Golgi, and L-FABP. Virtually no esterification of BODIPY FL C(16) was observed under the experimental conditions employed. We conclude that BODIPY FL C(16) may be a useful tool for studying the distribution and function of FABPs in a cellular environment.

Boron Compounds↗
PubMed1994

Inhibition of two HMP shunt pathway enzymes by fatty acids and their CoA esters in developing human brain: role of fatty acid binding protein.

Inhibitory effects of fatty acids and their CoA esters on glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities of human fetal brain cytosol have been studied. Purified human fetal brain fatty acid binding protein reverses the inhibitory effects of palmitoyl-CoA and oleic acid on glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities in human fetal brain cytosol. This protein, when added alone, activates the enzymes. Levels of fatty acid binding proteins as well as the activities of these two HMP shunt pathway enzymes, which provide cofactors like NADPH for reductive biosynthesis, increase with gestation. These results indicate that a relationship exists between the high demand for fatty acids and synthesis of cofactors for lipid biosynthesis in developing brain.

Acyl Coenzyme A↗
PubMed1998

High transepidermal water loss induces fatty acid synthesis and cutaneous fatty acid-binding protein expression in rat skin.

Stratum corneum lipids (SCLs) are responsible for the water barrier function (WBF) of the skin in mammals. Recent studies have indicated that epidermal lipid synthesis might be regulated by WBF of stratum corneum and that cutaneous fatty acid-binding protein (C-FABP) plays an important role in fatty acid metabolism in epidermis. To clarify the regulatory mechanism of lipid synthesis, we assessed the effects of barrier disruption induced by either acetone treatment or linoleic acid deficiency on epidermal lipid synthesis in rat. Transepidermal water loss (TEWL) was measured with an evaporimeter before and after treatment. The time course of re-establishing SCLs was examined biochemically and histochemically and the expression of C-FABP in the epidermis was immunohistochemically examined. When the rat skin was covered with a vapor-impermeable membrane after the acetone treatment removing SCLs and inducing WBF disruption, the usual recovery of SCLs was blocked and TEWL was kept high by 24 h. In the uncovered area, rapid redeposition of SCLs within 24 h was found and associated with normal compositions of epidermal lipids including sphingolipids, free fatty acids and sterol and, immunohistochemically, C-FABP was very weakly expressed in epidermis at 0.5 and 2 h, and then strongly in the whole layers at 4 h, and returned to a normal pattern by 8 h. The epidermis of the covered rat skin was kept weak in C-FABP expression by 24 h. In the linoleic acid-deficient rats, TEWL did not increase and the expression pattern of C-FABP showed no notable change until 28 weeks after initiation of the diets, indicating that C-FABP expression may not be affected by altered essential fatty acid metabolism. These results suggest that increase of TEWL itself stimulates C-FABP expression, leading to activation of fatty acid metabolism.

Acetone↗
PubMedDate not supplied

Effect of ethanol on fatty acid metabolism in cultured hepatocytes: dependency on incubation time and fatty acid concentration.

In a previous report it was shown that ethanol increases the rate of accumulation of triacylglycerol by 90% in hepatocytes in primary culture. This represents the first known suitable model for in vitro studies of the ethanol-induced fatty liver. The biochemical alterations causing this accumulation of triacylglycerol remain to be elucidated, however. In the present report it is shown that (1) the effect of ethanol exhibits a time lag of 6-9 hours (2) the increment in the content of triacylglycerol caused by ethanol is increased by increased concentrations of fatty acids (3) the fatty acid uptake is not affected by ethanol (4) fatty acid synthesis is inhibited 20% by ethanol (5) the contents of diacylglycerol and phospholipids are not affected by ethanol (6) addition of ethanol increases the cytosolic and mitochondrial redox levels. It is concluded that ethanol is likely to exert its effect on the accumulation of triacylglycerol by redistributing fatty acids between oxidation and triacylglycerol synthesis and/or between storage and secretion of triacylglycerol.

Animals↗
PubMed1985

The induction of peroxisome proliferation in rat liver by perfluorinated fatty acids, metabolically inert derivatives of fatty acids.

The induction of peroxisome proliferation in rat liver was examined after administration of perfluoro-n-decanoic acid (PFDA, C10), perfluoro-n-octanoic acid (PFOA, C8), perfluoro-n-butyric acid (PFBA, C4), 1-H,1-H-pentadecafluoro-n-octanol (PFOL, C8) perfluorododecane (PFD, C12), and perfluorooctane (PFO, C8). The peroxisome proliferation in the liver was detected by the following methods; 1) measurement of liver weight, 2) assay of hepatic catalase activity, 3) analysis of 600 X g supernatant of liver homogenates by SDS-polyacrylamide gel electrophoresis to observe the induction of the bifunctional enoyl-CoA hydratase in peroxisomes (80K-protein) and 4) observation by electron microscopy. The oral administration of powdered chow containing 0.02%-PFOA and PFBA to male rats of the Sprague-Dawley strain for 2 weeks and the single intraperitoneal injection of corn oil mixed with PFDA, PFOA, and PFOL at the dose of 100 mg/kg induced peroxisome proliferation markedly. PFOL, which has two hydrogen atoms around the hydroxylated carbon, should be metabolized to PFOA, which is an active inducer. Perfluorinated paraffins, PFD and PFO, did not show any induction, indicating the importance of the carboxylic group in the molecule for the peroxisome proliferation. Although the participation of thyroid hormone cannot be excluded, PFOA appears to act directly on the liver.

Animals↗
PubMed2006

Different specificity of two types of Pseudomonas lipases for C20 fatty acids with a Delta5 unsaturated double bond and their application for selective concentration of fatty acids.

Two kinds of lipases, AK-lipase and HU-lipase, produced by two different Pseudomonas fluorescens strains, AK102 and HU380, respectively, were evaluated as to fatty acid hydrolysis specificity using six types of oil containing higher amounts of C20 fatty acids such as arachidonic acid (5,8,11,14-eicosatetraenoic acid, AA, or 20:4omega6), dihomo-gamma-linolenic acid (8,11,14-eicosatrienoic acid, DGLA, or 20:3omega6), 5,8,11,14,17-eicosapentaenoic acid (EPA or 20:5omega3), mead acid (5,8,11-eicosatrienoic acid, MA, or 20:3omega9), 8,11-eicosadienoic acid (20:2omega9) and 8,11,14,17-eicosatetraenoic acid (20:4omega3). Although HU-lipase did not show any specificity for C20 fatty acids with respect to the presence or absence of a Delta5 unsaturated bond, it exhibited comparatively low reactivity for 4,7,10,13,16,19-docosahexaenoic acid (DHA or 22:6omega3). In contrast, AK-lipase was less reactive for C20 fatty acids with a Delta5 unsaturated bond. However, the specificity of hydrolysis of AK-lipase gradually decreased as the reaction proceeded. Utilizing this fatty acid specificity, we concentrated either EPA or DHA from fish oils containing both EPA and DHA by means of lipase-catalyzed hydrolysis and urea adduction. Hydrolysis and urea adduction of refined cod oil including 12.2% EPA and 6.9% DHA with HU-lipase provided free fatty acids with 43.1% EPA and 7% DHA, respectively. The resulting yield of concentrated total fatty acids comprised 2.6% of the fatty acids from the cod oil. Thus, EPA was particularly concentrated in the fatty acids derived from refined cod oil on partial hydrolysis with HU-lipase followed by urea adduction. On the other hand, hydrolysis of cuttlefish oil with AK-lipase followed by urea adduction increase slightly the EPA composition from 14.2% to 16.8%, and markedly enhanced the composition of DHA from 16.3% to 44.6% in the hydrolyzed fatty acids. The yield of purified total fatty acids by urea concentrate was 9.4% of the fatty acids from the cuttlefish oil. Thus, DHA was particularly concentrated in the fatty acids derived from on partial hydrolysis with AK-lipase followed by urea adduction. We concluded that EPA and DHA concentrates can be easily and inexpensively obtained using HU-lipase and AK-lipase, respectively. Furthermore, it might be possible to separate and concentrate C20 polyunsaturated fatty acids (PUFAs) with or without a Delta5 double bond from PUFAs rich oils including both fatty acids.

Chemical Fractionation↗
PubMed2000

Specific phospholipid fatty acid composition of brain regions in mice. Effects of n-3 polyunsaturated fatty acid deficiency and phospholipid supplementation.

This study examined the effects of dietary alpha-linolenic acid deficiency followed or not by supplementation with phospholipids rich in n;-3 polyunsaturated fatty acid (PUFA) on the fatty acid composition of total phospholipids in 11 brain regions. Three weeks before mating, mice were fed a semisynthetic diet containing both linoleic and alpha-linolenic acid or deficient in alpha-linolenic acid. Pups were fed the same diet as their dams. At the age of 7 weeks, a part of the deficient group were supplemented with n;-3 polyunsaturated fatty acids (PUFA) from either egg yolk or pig brain phospholipids for 2 months. Saturated and monounsaturated fatty acid levels varied among brain regions and were not significantly affected by the diet. In control mice, the level of 22:6 n-3 was significantly higher in the frontal cortex compared to all regions. alpha-Linolenic acid deficiency decreased the level of 22:6 n-3 and was compensated by an increase in 22:5 n-6 in all regions. However, the brain regions were affected differently. After the pituitary gland, the frontal cortex, and the striatum were the most markedly affected with 40% reduction of 22:6 n-3. Supplementation with egg yolk or cerebral phospholipids in deficient mice restored a normal fatty acid composition in brain regions except for the frontal cortex. There was a regional distribution of the fatty acids in the brain and the impact of deficiency in alpha-linolenic acid was region-specific. Dietary egg yolk or cerebral phospholipids are an effective source of n-3 PUFA for the recovery of altered fatty acid composition induced by a diet deficient in n-3 PUFA.

Animals↗
PubMed2002

A synthetic strategy for ON-resin amino acid specific multiple fatty acid acylation of peptides.

Covalent modification with fatty acids is observed in several proteins that play crucial roles in cellular physiology. In this paper, a convenient method for the generation of multiple fatty acylated synthetic peptides is described. Peptides were synthesized using solid phase procedures with fluorenylmethoxycarbonyl a-amino protected amino acids. Acetamidomethyl protected cysteines were employed. The thiol protecting group was selectively deprotected and acylation was carried out on the resin-bound peptides. The strategy described in this report is applicable to any peptide sequence.

Acylation↗
PubMed2001

Effects of delta5 polyunsaturated fatty acids of maritime pine (Pinus pinaster) seed oil on the fatty acid profile of the developing brain of rats.

Conifer (pine) seeds are a potential source of dietary oils, but their safety and nutritional properties are not well established. Conifer seed oils differ from common edible vegetable oils in having a series of unusual polyunsaturated fatty acids (PUFA) with a polymethylene-interrupted (PMI) double bond system and a double bond at the delta5 position. A rat study was conducted to assess whether delta5 PMI-PUFA of conifer seeds could alter the levels of n-6 and n-3 long-chain polyunsaturated fatty acids (LC-PUFA) in mothers' milk and the developing brain of fetuses and pups. Feeding maritime pine (Pinus pinaster) seed oil (MPO) diet with a delta5 PMI-PUFA content of 1.4 g/100 g throughout pregnancy and lactation resulted in a large incorporation of delta5 PMI-PUFA in mothers' milk (5.1 +/- 0.5% of total fatty acids). The fetus (17 d old) and pup (22 d) brains, however, accumulated very little (0.6 and 0.4% of total fatty acids, respectively) delta5 PMI-PUFA. Mother's milk and pup's brain of the MPO group contained normal levels of 20:4n-6, 22:4n-6, and 20:5n-3 compared to a reference group of rats fed a fat blend of sunflower, high-oleic sunflower, and canola oils. The level of 22:6n-3, however, was slightly but significantly (P < 0.05) higher in milk and pup brain of the MPO group. These results show that delta5 PMI-PUFA of MPO exert no negative effect on the levels of n-6 and n-3 LC-PUFA in rat brain during its early development.

Animals↗
PubMed1995

Long-chain polyene status of preterm infants with regard to the fatty acid composition of their diet: comparison between absolute and relative fatty acid levels in plasma and erythrocyte phospholipids.

The long-chain polyene (LCP) status of thirty-nine premature infants (birth weight < 1800 g) was evaluated. Twenty-seven infants were fed on an artificial formula, twelve received their own mother's breast milk. Fatty acid compositions of both plasma and erythrocyte (RBC) phospholipids (PL) were determined in umbilical venous blood and in weekly postnatal blood samples until the 28th day of life. Individual fatty acid levels were expressed as absolute quantities (mg fatty acid/l plasma or RBC suspension) and as relative (mg/100 mg total fatty acids) values. The changes with time in the absolute values for 22:6n-3 and 20:4n-6 in plasma were strikingly different from those of the relative values for these fatty acids. In plasma PL the inter-group differences in the absolute postnatal values for 22:6n-3 (P < 0.0005) and 20:4n-6 (P < 0.05) and the relative values for 22:6n-3 (P < 0.02) were significant, with lower fatty acid values in the formula-fed infants. In RBC PL, no significant inter-group differences in the postnatal 22:6n-3 and 20:4n-6 values were found. Based on the assumption that it is desirable for formula-fed infants to achieve postnatal plasma LCP values at least comparable with those found in infants fed on human milk, the findings of the present study indicate that both n-3 and n-6 LCP should be added to preterm infant formulas. Moreover, the additional importance of absolute fatty acid levels was demonstrated, although analytical procedures need to be standardized to enable effective comparison of results from different research groups.

Dietary Fats↗
PubMed2005

Fatty acid transduction of nitric oxide signaling: multiple nitrated unsaturated fatty acid derivatives exist in human blood and urine and serve as endogenous peroxisome proliferator-activated receptor ligands.

Mass spectrometric analysis of human plasma and urine revealed abundant nitrated derivatives of all principal unsaturated fatty acids. Nitrated palmitoleic, oleic, linoleic, linolenic, arachidonic and eicosapentaenoic acids were detected in concert with their nitrohydroxy derivatives. Two nitroalkene derivatives of the most prevalent fatty acid, oleic acid, were synthesized (9- and 10-nitro-9-cis-octadecenoic acid; OA-NO2), structurally characterized and determined to be identical to OA-NO2 found in plasma, red cells, and urine of healthy humans. These regioisomers of OA-NO2 were quantified in clinical samples using 13C isotope dilution. Plasma free and esterified OA-NO2 concentrations were 619 +/- 52 and 302 +/- 369 nm, respectively, and packed red blood cell free and esterified OA-NO2 was 59 +/- 11 and 155 +/- 65 nm. The OA-NO2 concentration of blood is approximately 50% greater than that of nitrated linoleic acid, with the combined free and esterified blood levels of these two fatty acid derivatives exceeding 1 microm. OA-NO2 is a potent ligand for peroxisome proliferator activated receptors at physiological concentrations. CV-1 cells co-transfected with the luciferase gene under peroxisome proliferator-activated receptor (PPAR) response element regulation, in concert with PPARgamma, PPARalpha, or PPARdelta expression plasmids, showed dose-dependent activation of all PPARs by OA-NO2. PPARgamma showed the greatest response, with significant activation at 100 nm, while PPARalpha and PPARdelta were activated at approximately 300 nm OA-NO2. OA-NO2 also induced PPAR gamma-dependent adipogenesis and deoxyglucose uptake in 3T3-L1 preadipocytes at a potency exceeding nitrolinoleic acid and rivaling synthetic thiazo-lidinediones. These data reveal that nitrated fatty acids comprise a class of nitric oxide-derived, receptor-dependent, cell signaling mediators that act within physiological concentration ranges.

3T3-L1 Cells↗
PubMed1976

The interaction of fatty acid synthetase with cytoplasmic protein in the control of the chain-length of fatty acids synthesised by the lactating rabbit mammary gland.

1. Fatty acid synthetase from rabbit mammary gland can be separated from the protein which modifies the chain-length at which fatty acids are released from the enzyme complex in the soluble fraction. This can be achieved by ultracentrifugation, precipitation with specific antibody or ammonium sulphate. 2. The chain-length modifying protein in the supernatant fraction from rabbit mammary gland was less active towards cow mammary gland fatty acid synthetase than rabbit mammary gland fatty acid synthetase in the synthesis of medium-chain fatty acids. The fatty acid synthetases from these two tissues are also immunologically non-identical. 3. It is proposed that there is a loose but specific interaction of rabbit mammary gland fatty acid synthetase with the chain-length modifying protein in regulating product chain length which is dependent on the concentration of interacting proteins. 4. The chain-lengthening effect of added malonyl-CoA decreases with increasing concentration of interacting proteins, but differences in the fatty acid chain-length with malonyl-CoA synthesised in situ by acetyl-CoA carboxylase and with added malonyl-CoA indicate that the product chain-length is sensitive to the availability of malonyl-CoA for enlongation in all but the most tightly coupled situations.

Acetyl Coenzyme A↗
PubMed1994

Stimulation of fatty acid biosynthesis by dietary cholesterol and of cholesterol synthesis by dietary fatty acid.

We reported previously that dietary cholesterol produces hypertriglyceridemia in the rat, accompanied by reduced oxidation and increased incorporation of exogenous fatty acid into hepatic triglyceride and increased secretion of very low density lipoprotein. We now report that dietary cholesterol also increases net hepatic fatty acid synthesis and the incorporation of newly synthesized fatty acid into hepatic triglyceride in vivo. Male rats were fed a cholesterol-free, semisynthetic diet (5% [w/w] corn oil) for 7 days, or the same diet supplemented with 0.5% cholesterol. On the day of the experiments, fed animals received 5 mCi 3H2O intraperitoneally (i.p.) either at 1200 h (6 h into the light cycle) or at 2400 h (6 h into the dark cycle). Animals were killed 1 h after receiving the radioisotope. Feeding cholesterol increased hepatic triglyceride and cholesteryl ester concentrations, moderately elevated the content of free cholesterol, but did not affect phospholipid levels. Increased net synthesis of fatty acids by livers of animals receiving cholesterol was observed during the dark period; a similar increase during the light period was also observed for incorporation of newly synthesized fatty acid into hepatic phospholipid and cholesteryl ester, although incorporation into triglyceride was of borderline significance (P < 0.06). In other experiments male rats were fed similar diets for 3, 7, or 21 days. Fed animals received 10 mCi 3H2O, i.p. (900-1000 h), and were killed 24 h later. Duration of feeding did not influence rates of net fatty acid synthesis or the stimulation by cholesterol of incorporation of newly synthesized fatty acid into hepatic triglyceride and cholesteryl ester.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Partial purification and characterization of fatty acid binding protein(s) in Escherichia coli membranes and reconstitution of fatty acid transport system.

Fatty acid binding protein(s) in E. coli membranes was solubilized and partially purified by oleate-AH Sepharose 4B column chromatography. The binding of palmitate to the protein was saturable. The protein bound all fatty acids with chain lengths of 10-18 tested, and its maximum activity was observed with palmitate. The incorporation of the protein into liposomes which contained a system for acyl-CoA synthesis significantly increased the uptake of the extracellular [14C] palmitate by the liposomes in comparison with the liposomes without the protein. The uptake of [14C] palmitate was also saturable, and the accumulated radioactive compound was found to be palmitoyl-CoA.

Biological Transport↗
PubMed1993

Methoxylated fatty acids reported in Rhizobium isolates arise from chemical alterations of common fatty acids upon acid-catalyzed transesterification procedures.

We obtained from a phospholipid extract of wild-type Rhizobium leguminosarum bv. trifolii ANU843 methoxylated fatty acids that had been previously reported as constitutive unusual Rhizobium fatty acids. The use of deuterated reagents and subsequent gas-liquid chromatography-mass spectrometry analyses showed that these methoxylated fatty acid derivatives are the products of chemical alterations of common cyclopropane-containing and unsaturated fatty acids occurring during various acid-catalyzed transesterification treatments aimed at producing the methyl ester derivatives. Similar results were obtained from a phospholipid extract of Escherichia coli K-12. In contrast, these chemical alterations were not induced by an alkaline methanolysis method of transesterification. If an acidic treatment is needed to release the fatty acids from the source molecule, the finding of unusual methoxylated fatty acids should be carefully confirmed with deuterated reagents.

Acids↗