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PubMed2003

Analysis of fatty oil in Semen Ziziphi Spinosae by capillary gas chromatography.

A simple and fast capillary gas chromatographic (CGC) method with flame ionization detection is developed for the analysis of fatty oil in Semen Ziziphi Spinosae. After methyl-esterification, eight components are identified by gas chromatography-mass spectrometry. The derivatization condition is investigated in order to validate this method. Palmitic acid and stearic acid are quantitated simultaneously. The limits of detection are 5.024 microg/mL for palmitic acid and 6.957 microg/mL for stearic acid, respectively. The limits of quantitation are 16.76 microg/mL for palmitic acid and 23.19 microg/mL for stearic acid, respectively. The percent recoveries of palmitic and stearic acid are 97.4% and 96.6%. CGC is shown to be a quick and informative tool for the analysis of fatty oil in Semen Ziziphi Spinosae.

Chromatography, Gas↗

PubMed1984

Identification of acyl donors and acceptor proteins for fatty acid acylation in BHK cells infected with Semliki Forest virus.

The modification of viral glycoproteins through the covalent attachment of fatty acids was studied in baby hamster kidney (BHK) cells infected with Semliki Forest virus (SFV). Comparative pulse-chase experiments with [3H]palmitic acid and [35S]methionine revealed that a precursor polypeptide, designated p62, of the structural SFV glycoprotein and E1 serve as the primary acceptors of acyl chains. Acylation of p62 occurs immediately prior to its proteolytical cleavage to E2 and E3 emphasizing the post-translational and specific nature of this hydrophobic modification. To trace the acyl donor(s) for protein acylation the covalent attachment of fatty acids to p62 was studied after extremely short labeling periods with [3H]palmitic acid and correlated to the metabolism of the exogenous tritiated fatty acid. The shortest possible labeling time, a 10 s pulse with [3H]palmitic acid, was sufficient to acylate SFV p62. Analysis of the labeled lipids extracted from the same cells revealed that palmitoyl-CoA and phosphatidic acid showed the highest specific radioactivity among the tritiated lipid species. Out of these lipid species palmitoyl-CoA was identified as the functional acyl donor lipid in a cell-free system for the acylation of polypeptides.

Acylation↗

PubMed1984

[Effect of mazindol on free fatty acid metabolism in the brain of rats].

The effects of mazindol which is known as a anorexigenic agent on the free fatty acid metabolism in the brain were studied. One-half mg of mazindol was orally administered to rats weighing 500 g for 5 days. Body weight was reduced by 10%, compared to the control. Serum levels of free fatty acid, triglyceride, total cholesterol and phospholipid were decreased. The effect of mazindol on the incorporation of [1-14C] palmitic acid into various lipids in the brain were studied. When mazindol (5 mg) was administered one hr before injection of [1-14C] palmitic acid to the internal carotid artery of rats ad libitum, incorporation of [1-14C] palmitic acid into free fatty acids in the cerebrum and diencephalon was lower than that of the control, but incorporation into phospholipid and triglyceride were higher than that of the control. When mazindol was injected into fasting rats, incorporation into free fatty acid in cerebrum and diencephalon was increased compared with the control, and the incorporations into phospholipid and triglyceride were decreased.

Animals↗

PubMed1976

Influence of the products of phospholipolysis of phosphatidylcholine on micellar solubilization of fatty acids in the presence of bile salts.

1. The solubility of fatty acids in aqueous solutions containing bile salts and lysolecithin at pH values between 2-0 and 7-4 was studied. Both the 1-acyl and 2-acyl isomers of lysolecithin increased the solubility of fatty acids to the same extent, the order of solubility being linoleic greater than oleic greater than elaidic greater than palmitic greater than stearic. 2. The influence of the products of phospholipolysis of lecithin on palmitic acid solubility was determined. On a molar basis, lysolecithin was more effective than were bile salts in promoting the solubilization of the fatty acid. 3. In bile salt solutions in which the phospholipid concentration was constant on a molar basis, in solubility of palmitic acid decreased linearly with the progressive replacement of lecithin by lysolecithin. Palmitic acid was solubilized to the same extent on replacing lecithin with lysolecithin on a constant weight basis. 4. In bile salt solution containing lysolecithin and oleic acid in equimolar amounts, the solubility of palmitic acid was similar to that in bile salt solution containing lecithin in equivalent proportion. 5. The results are discussed in relation to the action of phospholipolytic activity on the intestinal absorption of fatty acids in sheep.

Animals↗

PubMed1988

The functional glycoprotein CD9 is variably acylated: localization of the variably acylated region to a membrane-associated peptide containing the binding site for the agonistic monoclonal antibody 50H.19.

Recent studies have shown that [3H]palmitic acid strongly labels both glycosylated forms (gp22 and gp24) of the signal-initiating cell surface glycoprotein CD9. We performed a two-dimensional limited proteolysis analysis with Staphylococcus aureus V8 proteinase in order to localize the palmitylation sites to final peptides on both glycosylated forms of CD9. Analysis of [3H]leucine- and [3H]amino acid mixture-labeled gp22 delineated 4 final peptides of 11, 8, 7 and 4 kDa. gp24 produced a similar pattern with the exception that the 11 kDa peptide was replaced by an N-glycosylated 13 kDa peptide. Since all four final peptides (total molecular mass of 30/32 kDa) could not be accommodated by a parent molecule of 22/24 kDa, it is likely that one of the final peptide coexists in two differently modified states. Palmitic acid labeled the 11 kDa/13 kDa final peptides, and the 7 kDa final peptide, with equal intensity, but was not incorporated into the 4 kDa final peptide, demonstrating that fatty acid is ligated in two distinct regions of the molecule. The 8 kDa final peptide was strongly labeled by [3H]palmitic acid, but only weakly by [3H]leucine. We present evidence that this peptide is derived by further acylation of the region defined by the 7 kDa peptide, and that this occurs in only 15% of the molecules. Palmitic acid is turned over faster at these additional sites, indicating that they may be more accessible to membrane transacylases. Proteolysis of CD9 on the intact cell with papain enabled the highly acylated region to be localized to a membrane-associated fragment which contains the binding site for the agonistic monoclonal antibody 50H.19. The co-localization of a functional domain with a region of variable acylation suggests that acylation events may play a role in the transduction of the signal initiated by interaction of the antibody with CD9.

Acylation↗

PubMed2002

Influence of the physical states of membrane surface area and center area on lysosomal proton permeability.

The physical state of the lysosomal membrane was modulated with the membrane fluidizers n-propanol and n-octanol and with the membrane rigidifiers cholesteryl hemisuccinate and cholesterol. Membrane fluidity was examined by the steady-state fluorescence anisotropy of 2-(9-anthroyloxy) palmitic acid and 16-(9-anthroyloxy) palmitic acid. Fluidizing the membranes at the surface and center areas increased the proton permeability coefficient by 92.8 and 18.0%, respectively. Rigidifying the membranes at the surface and center areas decreased the coefficient by 68.2 and 40.2%, respectively. Proton leakage of the lysosomes increased and decreased similar to the coefficient changes with the treatments. The results indicate that lysosomal proton permeability is affected by its membrane's physical state, and the physical state of the membrane surface area affects the proton permeability more markedly. The proton permeability coefficient of liposomes was similar to that of lysosomes, suggesting that efflux of lysosomal protons might occur through the lipid part of the bilayer but not transmembrane proteins.

1-Octanol↗

PubMed1992

Influence of lipid composition on the orientational order in Acholeplasma laidlawii strain B membranes: a deuterium NMR study.

2H NMR techniques have recently been developed to determine the complete orientational order profile of lipid bilayers employing lipids containing perdeuteriated palmitic acid [Lafleur, M., Fine, B., Sternin, E., Cullis, P.R., & Bloom, M. (1989) Biophys. J. 56, 1037-1041]. In this work, these techniques have been applied to study order profiles in intact membranes derived from Acholeplasma laidlawii strain B. It is shown that complete orientational order profiles can be readily obtained from the intact membranes of A. laidlawii B grown on equimolar amounts of perdeuteriated palmitic acid and a nondeuteriated fatty acid of varying length and unsaturation. By variation of the fatty acid composition employing mixtures of perdeuteriated palmitic acid with myristic, elaidic, oleic, or linoleic acid, a range of hydrocarbon order compatible with high rates and extents of cell growth has been obtained where the average order parameter, mean value of S, varies over the range 0.140-0.176. This same variation in order is seen for liposomes derived from total lipids extracted from these intact membranes. 2H NMR studies on liposomes composed of individual species of the extracted lipids indicate that modulation of the membrane lipid headgroup composition has the potential to play an important role in maintaining the membrane order within this range.

Acholeplasma laidlawii↗

PubMed1997

Dexamethasone induces posttranslational degradation of GLUT2 and inhibition of insulin secretion in isolated pancreatic beta cells. Comparison with the effects of fatty acids.

GLUT2 expression is strongly decreased in glucose-unresponsive pancreatic beta cells of diabetic rodents. This decreased expression is due to circulating factors distinct from insulin or glucose. Here we evaluated the effect of palmitic acid and the synthetic glucocorticoid dexamethasone on GLUT2 expression by in vitro cultured rat pancreatic islets. Palmitic acid induced a 40% decrease in GLUT2 mRNA levels with, however, no consistent effect on protein expression. Dexamethasone, in contrast, had no effect on GLUT2 mRNA, but decreased GLUT2 protein by about 65%. The effect of dexamethasone was more pronounced at high glucose concentrations and was inhibited by the glucocorticoid antagonist RU-486. Biosynthetic labeling experiments revealed that GLUT2 translation rate was only minimally affected by dexamethasone, but that its half-life was decreased by 50%, indicating that glucocorticoids activated a posttranslational degradation mechanism. This degradation mechanism was not affecting all membrane proteins, since the alpha subunit of the Na+/K+-ATPase was unaffected. Glucose-induced insulin secretion was strongly decreased by treatment with palmitic acid and/or dexamethasone. The insulin content was decreased ( approximately 55 percent) in the presence of palmitic acid, but increased ( approximately 180%) in the presence of dexamethasone. We conclude that a combination of elevated fatty acids and glucocorticoids can induce two common features observed in diabetic beta cells, decreased GLUT2 expression, and loss of glucose-induced insulin secretion.

Animals↗

PubMed1997

The mechanism and functional roles of protein palmitoylation in the nervous system.

Palmitoylation refers to the covalent attachment of long-chain fatty acids, mostly palmitic acid, to the side chain of cysteine residues of proteins. In recent years, a considerable number of functionally relevant nervous system proteins including ion channels, neurotransmitter receptors, signal transduction components and cell-adhesion molecules have been found to be palmitoylated. However, the lack of a generalized and unambiguous role for the fatty acids in these proteins has questioned the importance of palmitoylation in the functioning of the nervous system. Last year, it was found that the deficiency of palmitoyl-protein thioesterase (PPT), one of the enzymes responsible for the removal of palmitate from proteins, is the underlying cause of infantile neuronal ceroid lipofuscinosis (INCL). This finding not only constitutes a step forward in elucidating the pathogenesis of INCL, but it also provides new impetus in the search for the function(s) of protein palmitoylation. This work succinctly outlines the molecular mechanisms involved in dynamic acylation and the potential biological role(s) of this modification, and it constitutes an introduction to those presentations in this issue which specifically deal with the pathogenic mechanisms of INCL.

Adolescent↗

PubMed1991

Inhibition of long-chain acyl-CoA synthetase by the peroxisome proliferator perfluorodecanoic acid in rat hepatocytes.

Perfluorodecanoic acid (PFDA) is a potent peroxisome proliferator and is known to affect hepatic lipid metabolism in rats. The effects of PFDA on fatty acid utilization were examined in isolated rat hepatocyte suspensions and in rat liver mitochondria and microsomes. PFDA inhibited the oxidation of palmitic acid but not octanoic or pyruvic acids when hepatocytes were incubated with 1 mM PFDA. At this PFDA concentration the esterification of palmitic acid into triacylglycerols was also reduced. The activity of long-chain acyl-CoA synthetase (ACS), an enzyme essential for both oxidation and esterification of fatty acids, was reduced in hepatocytes incubated with 1 mM PFDA. Carnitine palmitoyltransferase (CPT), an important enzyme for the oxidation of long-chain fatty acids, was not altered in hepatocytes incubated with this PFDA concentration. In rat liver mitochondria, palmitate oxidation and ACS activity were reduced significantly (P less than 0.01) at a PFDA concentration that had no effect on CPT activity. The inhibition of ACS by PFDA was similar in liver mitochondria and microsome preparations. In mitochondria incubated with PFDA, the inhibition of ACS appears to be noncompetitive for the substrates palmitic acid and CoA. However, the ACS inhibition by PFDA appeared to be competitive for the ATP binding site of the enzyme. Several chain length perfluorinated fatty acids were examined for their ability to inhibit mitochondrial ACS. Short-chain perfluorinated fatty acids (perfluoroproprionic and -butyric acid) did not inhibit ACS activity. However, medium-chain perfluorinated acids (perfluorooctanoic, -ananoic and -decanoic acid) were found to be potent inhibitors of ACS in isolated mitochondria. Whether ACS inhibition is causally related to PFDA-induced peroxisome proliferation and altered lipid metabolism seen in vivo is yet to be determined.

Animals↗

PubMed2000

Effect of palm oil on plasma lipoprotein concentrations and plasma low-density lipoprotein composition in non-human primates.

Palm oil (PO) contains approximately 43% of palmitic acid. It is the most abundant saturated fatty acid in the diet and it is generally considered the primary cholesterol (C)-raising fatty acid. However, the effect of palmitic acid on plasma cholesterol appears to depend on the cholesterol content of the diet. The aim of this study was to determine the effect of PO with either a high-fat, high-C or moderate-fat, moderate-C diet on lipoprotein C and low-density lipoprotein (LDL) composition. Fifty adult, male vervet monkeys were randomly assigned to the high-fat diet group (HFD: 35%E fat, approximately 0.106 mg C/kJ; n = 30) and the moderate-fat diet group (MFD: 30%E fat, approximately 0.027 mg C/kJ; n = 30). Baseline LDL-C, high-density lipoprotein (HDL)-C and body weight were used to stratify the vervets into comparable experimental groups within each dietary group. The HFD group was divided into two groups of 10 each: one group continued with the HFD in which 8.1%E was derived from lard (AF); in the other group, AF was substituted isocalorically with PO. The MFD group was divided into three groups of 10 each: one group continued with the MFD in which 11.8%E was derived from AF; in the other two groups, the AF was substituted isocalorically with either sunflower oil (SO) or PO. This article presents preliminary results on plasma lipoproteins and LDL composition after 6 months of dietary intervention. Plasma total and LDL-C was higher in all the groups, but the mean changes elicited by PO with either the HFD or MFD were no different from that observed with AF and SO. There was no difference in the mean change of LDL molecular weight within the HFD and MFD. It is concluded that PO is no different from AF (HFD and MFD) or SO (MFD) in its cholesterolaemic effect.

Animal Nutritional Physiological Phenomena↗

PubMed2000

Varying incorporation of fatty acids into phospholipids from muscle, adipose and pancreatic exocrine tissues and thymocytes in adult rats fed with diets rich in different fatty acids.

Despite numerous studies, the importance which the tissue or the composition of the diet may have in the biological distribution of each fatty acid is not well known. To determine the importance of tissue origin and dietary fatty acids in the fatty acid composition of cell phospholipids, 54 male adult rats were fed isocaloric diets for one month varying only in their fatty acid compositions. The fat component of the six experimental groups was derived from olive oil, sunflower oil, fish oil, soybean oil, palmitic acid, or 82% palmitic acid plus 18% soybean oil, supplying the essential fatty acid. The fatty acid composition of phospholipids from thymocytes, pancreatic exocrine, muscle and adipose tissues was studied by gas-chromatography. The tissue of origin was a more important source of variation than diet in the fatty acid content of the cell phospholipids except for palmitic acid (16:0), eicosapentaenoic acid (20:5 n-3), and docosahexaenoic acid (22:6 n-3). This study points out the complexity of the interrelations between different families of fatty acids and of the specificity of each tissue to changes in the composition of dietary fatty acids, as well as the inconvenience of speaking from the dietary point of view of groups of fatty acid families based on the position of the double bond, since their individual behaviour, including saturated fatty acids, is very different in the face of dietary manipulation. The study also highlights the different behaviour of each of the fatty acids in relation to the others in the diet in each of the tissues, a circumstance which should be taken into account when evaluating the biological effects in both epidemiological and experimental studies.

Adipose Tissue↗

PubMed2005

Comparative study of sex pheromone composition and biosynthesis in Helicoverpa armigera, H. assulta and their hybrid.

Two Helicoverpa species, H. armigera and H. assulta use (Z)-11-hexadecenal and (Z)-9-hexadecenal as their sex attractant pheromone components but in opposite ratios. Since both female and male interspecific hybrids produced by female H. assulta and male H. armigera have been obtained in our laboratory, we can make a comparative study of sex pheromone composition and biosynthesis in the two species and their hybrid. With GC and GC-MS analyses using single gland extracts, the ratio of (Z)-9-hexadecenal to (Z)-11-hexadecenal was determined as 2.1:100 in H. armigera, and 1739:100 in H. assulta. The hybrid has a ratio of 4.0: 100, which is closer to that of H. armigera, but significantly different from H. armigera. We investigated pheromone biosynthesis with labeling experiments, using various fatty acid precursors in H. armigera, H. assulta and the hybrid. In H. armigera, (Z)-11-hexadecenal is produced by delta11 desaturation of palmitic acid, followed by reduction and terminal oxidation; (Z)-9-hexadecenal results from delta11 desaturation of stearic acid, followed by one cycle of chain shortening, reduction and terminal oxidation. delta11 desaturase is the unique desaturase for the production of the two pheromone components. In our Chinese strain of H. assulta, palmitic acid is used as the substrate to form both the major pheromone component, (Z)-9-hexadecenal and the minor one, (Z)-11-hexadecenal. Our data suggest that delta9 desaturase is the major desaturase, and delta11 desaturase is responsible for the minor component in H. assulta, which is consistent with previous work. However, the weak chain shortening acting on (Z)-9 and (Z)-11-octadecenoic acid, which is present in the pheromone glands, does occur in this species to produce (Z)-7 and (Z)-9-hexadecenoic acid. In the hybrid, the major pheromone component, (Z)-11-hexadecenal is produced by delta11 desaturation of palmitic acid, followed by reduction and terminal oxidation. The direct fatty acid precursor of the minor component, (Z)-9-hexadecenoic acid is mainly produced by delta9 desaturation of palmitic acid, but also by delta11 desaturation of stearic acid and one cycle of chain shortening. The greater relative amounts of (Z)-9-hexadecenal in the hybrid are due to the fact that both palmitic and stearic acids are used as substrates, whereas only stearic acid is used as substrate in H. armigera. The evolutionary relationships between the desaturases in several Helicoverpa species are also discussed in this paper.

Aldehydes↗

PubMed1984

Stereochemistry of the reactions catalyzed by chicken liver fatty acid synthase.

The stereochemistry of the four partial reactions catalyzed by chicken liver fatty acid synthase that lead to the synthesis of palmitic acid has been determined. The reduction of acetoacetyl-CoA to 3-hydroxybutyryl-CoA by NADPH proceeds with the transfer of the pro-4S hydrogen of NADPH to form D-3-hydroxybutyryl-CoA. During the subsequent dehydration of D-3-hydroxybutyryl-CoA the pro-2S hydrogen and the 3-hydroxyl group are removed in a syn elimination to form crotonyl-CoA. Crotonyl-CoA is reduced to butyryl-CoA by NADPH, with the transfer of the pro-4R hydrogen of NADPH to the pro-3R position in butyryl-CoA and the transfer of a solvent hydrogen to the pro-2S position. The occurrence of the syn dehydration, when combined with the results of a previous study [ Sedgwick , B., & Cornforth , J. W. (1977) Eur. J. Biochem. 75, 465-479], implies that the condensation of the enzyme-bound malonyl moiety with the enzyme-bound saturated fatty acid to form a 3-keto intermediate proceeds with inversion at C-2 of the malonyl. The stereochemistry of the hydration was derived from an analysis of the spin-spin coupling constant of 3-hydroxy[2-2H]butyric acid benzylamides obtained from 3-hydroxy[2-2H]butyryl-CoA synthesized by fatty acid synthase. The elucidation of the stereochemistry of the reduction of crotonyl-CoA relied on the previously established stereochemistry of pork liver acyl-CoA dehydrogenase. The source of all 28 prochiral hydrogens of the palmitic acid synthesized by chicken liver fatty acid synthase was inferred from the results of this work.

Acyl Coenzyme A↗

PubMed1981

Activation of the metabolism of the fatty acyl group in granulocyte phospholipids by phorbol myristate acetate.

Phorbol myristate acetate is known to reproduce the stimulated oxidative activities characteristic of phagocytosis and its initial action is on the cell membrane. In the present study the effect of phorbol myristate acetate on the metabolism of the fatty acyl groups of granulocyte phospholipids was examined and compared with that of phagocytic stimuli. Phorbol myristate acetate stimulated the labeling of phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol by [1-14C]palmitic acid but not by [U-14C]glycerol, whereas starch granules selectively increased the labeling of phosphatidylinositol by both radioactive tracers. Labeled palmitic acid was found at both sn-1- and sn-2-positions of phospholipids and more radioactivity was recovered from the 2-position. The radioactivity at both positions was enhanced in stimulated cells. These data suggest that phorbol myristate acetate increased palmitic acid incorporation into glycerophospholipids by increasing the acylation of the lyso derivatives and that starch granules enhanced the formation of phosphatidylinositol via de novo synthesis and acylation of the lyso derivative as well. Both phorbol myristate acetate and starch granules selectively augmented the incorporation of [1-14C]arachidonic acid into phosphatidylinositol which exhibited the highest specific radioactivity among the phospholipids in control and in stimulated cells. The possible significance of the increased incorporation of arachidonic acid into phosphatidylinositol is discussed.

Animals↗

PubMed1991

Inhibition by salicylic acid of the activation and thus oxidation of long chain fatty acids. Possible role in the development of Reye's syndrome.

Administration of either aspirin or salicylic acid (3 mmol.kg-1 b.wt. i.p.) decreased by 50 and 65%, respectively, the in vivo oxidation of [U-14C]palmitic acid to [14C]CO2 in mice; after salicylic acid administration, exhalation of [14C]CO2 from [1-14C]palmitic acid, [1-14C]octanoic acid or [1-14C]butyric acid was decreased by 87, 33 and 38%, respectively. Inhibition lasted 9 hr. It was associated with markedly decreased blood glucose concentrations and increased plasma ketone bodies. Repeated administration of salicylic acid (2 mmol.kg-1 i.p. every 8 hr) tripled hepatic triglycerides and produced mild microvesicular steatosis of the liver at 22 hr in fasted mice. In vitro, salicylic acid (1.5 mM) had no or little effect on the formation of beta-oxidation products from [1-14C]octanoic or [1-14C]palmitoyl-L-carnitine, in the presence of ATP, carnitine (40 microM) and coenzyme A (40 microM), but decreased by 51% that from [1-14C]palmitic acid. In the latter system, increasing the concentrations of coenzyme A and carnitine to 200 microM suppressed the inhibitory effect of salicylic acid. Salicylic acid (1.5 mM) decreased by 80% the in vitro mitochondrial formation of palmitoyl-coenzyme A from [1-14C]palmitic acid and 10 microM coenzyme A; again, increasing the concentration of coenzyme A prevented inhibition. We conclude that salicylic acid decreases the mitochondrial activation and thus beta-oxidation of long chain fatty acids, presumably by sequestering extramitochondrial coenzyme A and possibly carnitine.

Adenosine Triphosphate↗

PubMed1996

Palmitoylation of the murine leukemia virus envelope glycoprotein transmembrane subunits.

The envelope protein of Friend murine leukemia virus is modified by fatty acylation of the transmembrane (TM) protein subunit. The labeling by [3H]palmitic acid was found to be sensitive to treatment with the reducing reagents 2-mercaptoethanol and hydroxylamine, indicating the presence of a thioester linkage. Pulse-chase experiments showed that the precursor protein can be labeled by [3H]palmitic acid prior to its cleavage into the surface and TM subunits. By using site-directed mutagenesis, we determined that palmitoylation occurs on a cysteine residue, Cys 606, located in the transmembrane domain. A thin-layer chromatography assay after acid hydrolysis showed that incorporated label comigrated with palmitic acid. When another cysteine residue was introduced into the cytoplasmic tail 22 amino acids from the transmembrane domain, no palmitoylation was observed to occur on this cysteine residue, demonstrating the importance of the position of the cysteine residue for palmitoylation. Sequence comparison revealed that most retrovirus envelope proteins have one or two conserved cysteine residues in their transmembrane domain. Mutations that change the palmitoylation state of the murine leukemia virus envelope protein did not affect its transport, processing, surface expression, or cell fusion activity. The palmitate-deficient viral envelope proteins were incorporated into virus particles, and replication of the virus in vitro was not affected significantly by the mutation of the palmitoylation site.

3T3 Cells↗

PubMed1999

Inhibition and stimulation of long-chain fatty acid oxidation by chloroacetaldehyde and methylene blue in rats.

The effects of chloroacetaldehyde (CAA) and methylene blue, both alone and together, on mitochondrial metabolism, hepatic glutathione content, and bile flow were investigated in rats. Oxidation of [1-14C]palmitic acid, [1-14C]octanoic acid, and [1,4-14C]succinic acid allowed for the differentiation between carnitine-dependent long-chain fatty acid metabolism, medium chain fatty acid oxidation, and citric acid cycle activity, respectively. CAA, a metabolite of the anticancer drug ifosfamide, which may be responsible for ifosfamide-induced encephalopathy, inhibited palmitic acid metabolism but not octanoic or succinic acid oxidation, depleted hepatic glutathione, and stimulated bile flow. Methylene blue, which is clinically used to either prevent or reverse ifosfamide-associated encephalopathy, markedly stimulated palmitic acid oxidation either in the presence or absence of CAA, but did not affect the oxidation of octanoic and succinic acid or hepatic glutathione. Taken together, this study demonstrates that CAA inhibits palmitic acid metabolism. Methylene blue stimulates long-chain fatty acid oxidation, most likely by facilitating the translocation of fatty acids into mitochondria, and compensates for the CAA effect in vivo.

Acetaldehyde↗