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PubMed1990

Fatty acid lessens halothane's inhibition of energy metabolism in isolated hepatocytes.

This study has examined whether adverse halothane effects on liver-cell energy metabolism are influenced by the availability of alternate substrates for energy-generating reactions. Halogenated volatile anesthetics affect both energy supply and energy demand in tissues, and cellular energy deficits have been implicated in anesthetic hepatotoxicity. Using hepatocytes isolated from fed rats either pretreated with phenobarbital or not treated (+PB or -PB cells, respectively), we studied the cellular energetic effects of providing fatty acid (oleic acid) along with glucose as substrate(s) for energy metabolism, while exposing the cells to 0%-2% halothane. In -PB cells incubated with glucose alone, there were halothane dose-related decreases in the oxygen (O2) consumption rate (VO2) and in the balance between adenosine triphosphate (ATP) supply and demand (ATP/ADP ratio), but no effect on lactate metabolism (lactate consumption or production) over the 10-min incubation period. Adding oleate along with glucose (a) raised VO2 but lowered ATP/ADP in the absence of halothane; (b) eliminated the decreases in VO2 and ATP/ADP seen when halothane was introduced; and (c) increased lactate consumption in both the presence and absence of halothane. In +PB cells, VO2 was higher, ATP/ADP lower, and lactate consumption also lower than in -PB cells under comparable conditions. Halothane or oleate effects, or both, on energy metabolism were thus qualitatively similar in +PB and -PB cells, except that in +PB cells incubated without oleate, lactate formation developed as halothane was increased from 0% to 2%, reflecting activation of glycolysis due to insufficient mitochondrial ATP production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1974

Inhibition of ileal water absorption by intraluminal fatty acids. Influence of chain length, hydroxylation, and conjugation of fatty acids.

The influence of fatty acids on ileal absorption of water, electrolytes, glucose, and taurocholate was examined in Thirty-Vella fistulas in five mongrel dogs. Fatty acid absorption also was measured. Segments of terminal ileum were perfused at steady state with isotonic electrolyte solutions containing 11.2 mM glucose, 4.5 mM taurocholate, and 0.1-5.0 mM fatty acid. Three C(18) fatty acids, oleic acid, 10(9)-hydroxystearic acid, and ricinoleic acid, completely inhibited water absorption at 5 mM. Sodium, chloride, and potassium absorptions were inhibited in parallel with absorption of water. Differences between the potencies of C(18) fatty acids were apparent when lesser concentrations were perfused. Dodecanoic and decanoic acids were as effective as C(18) fatty acids at 5 mM but octanoic and hexanoic acids were ineffective. The polar group of C(18) fatty acids was modified by conjugating oleic and ricinoleic acids with taurine. When these compounds and a substituted C(18) fatty acid, p-n-decylbenzenesulfonate, were perfused, water absorption was also inhibited. Short-chain fatty acids (C(3) and C(4)) and their hydroxylated derivatives were ineffective at 5 mM. When water absorption was inhibited, absorption of glucose and taurocholate was decreased. We speculate that the phenomenon of inhibition of water and electrolyte absorption by fatty acids may be relevant to steatorrhea and diarrhea in man.

Animals↗
PubMed2004

Histological alterations in the liver of sea bream, Sparus aurata L., caused by short- or long-term feeding with vegetable oils. Recovery of normal morphology after feeding fish oil as the sole lipid source.

This study evaluated the effects of fish oil (FO) replacement by vegetable oils [soybean oil (SO), rapeseed oil (RO), linseed oil (LO)] and subsequent feeding with FO on the liver morphology of sea bream. A short-term trial (3 months) and long-term trial (6 months) were carried out feeding sea bream with the following experimental diets: FO100%; SO60% + FO40%; RO60% +FO40%; LO60% + FO40%; SO + RO +LO60% + FO40%. Finally, all groups from the long-term trial were fed with FO100% for 95 days (washout period). Liver samples were taken for histological and biochemical studies. In both the short- and long-term trials, livers of sea bream fed LO60% and SO + RO + LO60% showed a similar hepatic morphology to that observed in fish fed FO100%. In contrast, sea bream fed SO60% showed an intense steatosis, with foci of swollen hepatocytes containing numerous lipid vacuoles. After the washout period, a considerable reduction of the cytoplasmic vacuolation and the lipid vacuole accumulation were observed in the livers of fish fed the different experimental diets. The results of this study suggested that the type of non-essential fatty acid, characteristic of vegetable oils, induces the appearance of steatosis in the following order: linoleic acid > linolenic acid > oleic acid. However, the liver alterations found during the experimental periods with vegetable oils are reversible when the fish are re-fed with a balanced diet (FO100%), indicating the non-pathological character of these histological changes.

Analysis of Variance↗
PubMed1989

Essential fatty acid-deficient rats are resistant to oleic acid-induced pulmonary injury.

Because leukotrienes and prostaglandins are inflammatory mediators derived from arachidonic acid, their potential role in oleic acid-induced lung injury was evaluated in control and in essential fatty acid-deficient (EFAD) rats depleted of arachidonic acid substrate. In control rats, oleic acid (0.06 ml/kg iv) increased the pulmonary permeability index (measured by scintigraphy) from -10 +/- 13 x 10(-6) s-1 to 217 +/- 20 x 10(-6) s-1 and 118 +/- 13 x 10(-6) s-1 at 5 and 50 min (P less than 0.05), respectively. It also caused arterial hypoxemia at 30 min (P less than 0.05). Compared with saline controls, oleic acid increased bronchoalveolar lavage fluid levels of immunoreactive (i) LTC4/D4, iLTB4, (P less than 0.01), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) (P less than 0.05). In EFAD rats, oleic acid failed to significantly increase the lung permeability index at 5 and 50 min. In contrast to control rats, oleic acid failed to cause hypoxemia in the EFAD rats. Bronchoalveolar lavage levels of iLTB4 and i6-keto-PGF1 alpha after oleic acid in EFAD rats were lower compared with oleic acid controls, whereas iLTC4/D4 in the oleic acid EFAD group was not decreased. Treatment with intraperitoneal ethyl arachidonate (400 mg over 2 wk) reversed the resistance of EFAD rats such that the pulmonary edema (P less than 0.05) was evident after oleic acid. This latter group also manifested a significant (P less than 0.05) rise in the bronchoalveolar lavage levels of iLTB4 and i6-keto-PGF1 alpha. These results suggest that arachidonic acid metabolites contribute to oleic acid-induced pulmonary permeability.

Animals↗
PubMed2004

Effect of fatty acids on the membrane potential of an alkaliphilic bacillus.

Effect of various fatty acids on the membrane potential of an alkaliphilic Bacillus, YN-2000, was examined. Addition of unsaturated fatty acids such as palmitoleic acid, oleic acid, linoleic acid, and linolenic acid at 30 microM caused the instantaneous depolarization of the membrane potential of the bacterium, which appears to result in the drastic decrease of viability. On the other hand, no depolarization was detected by the addition of saturated acids such as palmitic acid, stearic acid, and 12-hydroxystearic acid even at 1 mM.

Bacillus↗
PubMed1996

Products of aniline and triglycerides in oil samples associated with the toxic oil syndrome.

The toxic oil syndrome (TOS) was a devastating disease that occurred in Spain in 1981. The disease was associated with the consumption of aniline-denatured and refined rapeseed oil that had been illegally sold as olive oil. Many aniline-derived oil components have been identified in the oils; however, no etiological agent has ever been identified for this disease. We have continued the study of the TOS problem by applying new technology in the form of liquid chromatography interfaced via atmospheric pressure ionization with tandem mass spectrometry. Using liquid chromatography tandem mass spectrometry, we studied diluted TOS-associated oils by direct analysis without prior sample treatment. Using this technology, we found new classes of compounds that are associated with disease-related oils. The compounds that have been identified are esters and ester amides of 3-(N-phenylamino)-1,2-propanediol and are products of aniline and triglycerides. Because of the varied fatty acid (oleic acid, etc.) content of the oils, many variations of the above compounds are possible. We now report the identities of more than 20 compounds not previously identified. These compounds are strongly associated with oils that caused the toxic oil syndrome. We believe these compounds should be considered for future animal studies.

Anilides↗
PubMed1968

The characterization and distribution of hexahydropolyprenyl esters in cultures of Aspergillus fumigatus Fresenius.

The total mycelial lipid of Aspergillus fumigatus was analysed and over half of its hexahydropolyprenol was shown to be esterified with fatty acids. Comparison of the fatty acid content of the prenyl esters with the sterol ester and the total lipid indicated a marked predominance of saturated fatty acids in the polyprenyl esters. The predominant acids esterified to the prenols were palmitic acid, linoleic acid, oleic acid, lignoceric acid, stearic acid and palmitoleic acid. Most of the unesterified polyprenol was found in the mitochondrial fraction, but the esterified prenol was equally distributed throughout the cell fractions. This distribution was unlike that found for ergosteryl ester in the same tissue.

Alcohols↗
PubMed1998

Skin penetration enhancing action of cis-unsaturated fatty acids with omega-9, and omega-12-chain lengths.

The skin penetrative action of high purity cis-omega-12-octadecenoic acid (petroselinic acid, HP-PSA) on rat skin was compared with that of high purity cis-omega-9-octadecenoic acid (oleic acid, HP-OA), following treatment of rat intact skin surface with either 0.05 M HP-PSA or HP-OA in propylene glycol (PG), using Fourier transform/attenuated total reflection (FT-IR/ATR) analysis. Both HP-PSA and HP-OA disordered the lipid structures of the stratum corneum region to a similar extent. Removal of the extractable lipids of the stratum corneum region was marked with HP-PSA/PG but was very slight upon HP-OA/PG treatment. The spectra of the amide II region which originated from proteins suggests that HP-PSA/PG more rapidly disordered the protein structures of both the stratum corneum and the dermis than HP-OA/PG. However, the extent of disordering of the protein structures was presumed to be similar between these two skin penetration enhancers at the maximum level. Enhancement of PG flux in the dermis showed strong positive correlation with the degree of dermis-disordering action of HP-PSA/PG and HP-OA/PG. These results demonstrate that HP-PSA, which has a double bond at an even numbered position (omega-12), more rapidly affects the perturbation of the structures of both the stratum corneum and the dermis than HP-OA, which has the double bond at an odd numbered position (omega-9). Differences in the physicochemical properties of HP-PSA and HP-OA which originate from differences in the double bond position most likely determine the efficacy of these compounds as skin penetration enhancers.

Animals↗
PubMed2005

[Study on the encapsulation technique of high purity gamma-linolenic acid, part 1--saponification reaction and saponification value].

OBJECTIVE: To measure the saponification value and fatty acid formation of evening primrose oil, to study the effects of pH value on production yield and fatty acid formation during the saponification reaction, and to provide rationales for the selection of raw material, the enhancement of production yield of saponification, and the encapsulation of gamma-linolenic acid with urea. METHOD: To measure fatty acid's formation with gas chromatographic method and to measure the saponification value. RESULT: The content of gamma-linolenic acid is 7%-10% in evening primrose oil. The content of gamma-linolenic acid is inversely correlated with that of unsaturated fatty acid. The saponification value, the amount of KOH for saponification of evening primrose oil, and the pH value for subsequent isolations of oils are determined. From the measurement of fatty acids of evening primrose oil in two different cultivation locations, the content of gamma-linolenic acid is determined to be 7%-10%, unsaturated oils account for 90%. CONCLUSION: The saponification value of evening primrose oil is between 180-200, pH value of isolated oil is 1.5-2.0 after saponification reaction. Fatty acids mainly include palmitic acid, stearic acid, oleic acid, linolic acid and gamma-linolenic acid.

Fatty Acids, Essential↗
PubMed1969

The effects of unsaturated fatty acids on hepatic microsomal drug metabolism and cytochrome P-450.

1. The effects of unsaturated fatty acids on drug-metabolizing enzymes in vitro were measured by using rat and rabbit hepatic 9000g supernatant fractions. 2. Unsaturated fatty acids inhibited the hepatic microsomal metabolism of ;type I' drugs with inhibition increasing with unsaturation: arachidonic acid>linolenic acid>linoleic acid>oleic acid. Inhibition was independent of lipid peroxidation. Linoleic acid competitively inhibited the microsomal O-demethylation of p-nitroanisole and the N-demethylation of (+)-benzphetamine. 3. The hepatic microsomal metabolism of ;type II' substrates, aniline and (-)-amphetamine, was not affected by unsaturated fatty acids. 4. The rate of reduction of p-nitrobenzoic acid and Neoprontosil was accelerated by unsaturated fatty acids. 5. Linoleic acid up to 3.5mm did not decelerate the generation of NADPH by rat liver soluble fraction, nor the activity of NADPH-cytochrome c reductase of rat liver microsomes. Hepatic microsomal NADPH oxidase activity was slightly enhanced by added linoleic acid. 6. No measurable disappearance of exogenously added linoleic acid occurred when this fatty acid was incubated with rat liver microsomes and an NADPH source. 7. The unsaturated fatty acids used in this study produced type I spectra when added to rat liver microsomes, and affected several microsomal enzyme activities in a manner characteristic of type I ligands.

Amphetamine↗
PubMed2002

Bile acid binding to sevelamer HCl.

BACKGROUND: Clinical studies have shown sevelamer HCl (Renagel) to be effective for the reduction of serum phosphate in hemodialysis patients. These studies also consistently have demonstrated a significant reduction of low-density lipoprotein (LDL) cholesterol following treatment with sevelamer. METHODS: Equilibrium binding of bile acids and oleic acid was determined by incubating sevelamer with ligand containing buffer. Aliquots of the solution were filtered and the free ligand concentrations quantitated by high-pressure liquid chromatography (HPLC). Flow kinetics were determined using a cylindrical flow cell containing trapped sevelamer. Bile acid and oleic acid were pumped through the stirred cell in a manner designed to mimic the in vivo situation. Binding was monitored by HPLC. RESULTS: Sevelamer binds bile acids cooperatively and with high capacity. At low binding densities, the presence of the more hydrophobic bile acids enhances the binding of the less hydrophobic bile acids, and the presence of oleic acid enhances the binding of all bile acids. At saturating oleic acid concentrations, the bile acid binding capacity of sevelamer is reduced by only a factor of two. Moreover, the presence of oleic acid dramatically diminishes the release rate of bile acids from sevelamer. CONCLUSIONS: The favorable bile acid binding characteristics of sevelamer provide a compelling explanation for its ability to lower LDL cholesterol in hemodialysis patients and in healthy volunteers.

Bile Acids and Salts↗
PubMed1991

Inactivation of T5 phage by cis-vaccenic acid, an antivirus substance from Rhodopseudomonas capsulata, and by unsaturated fatty acids and related alcohols.

The antiviral extract from Rhodopseudomonas capsulata was purified and the predominant active component was defined as cis-vaccenic acid (Cl-8:1 delta 11) by gas-liquid chromatography and gas chromatography-mass spectrometry analyses. Antiviral activities of unsaturated fatty acids and related alcohols against T5 phage were also tested. Among them, linoelaidic acid, oleic acid, and petroselenyl alcohol inactivated 98%, 53%, 67% of T5 phage at the concentration of 50 micrograms/ml, respectively.

Alcohols↗
PubMed1976

Galactolipid Synthesis in Vicia faba Leaves: II. Formation and Desaturation of Long Chain Fatty Acids in Phosphatidylcholine, Phosphatidylglycerol, and the Galactolipids.

The labeling kinetics of the fatty acids of phosphatidylcholine (PC), phosphatidylglycerol (PG), monogalactosyldiglyceride (MGDG), and digalactosyldiglyceride (DGDG) were examined after (14)CO(2) feeding and incubation of leaf discs of Vicia faba over 72 hours in continuous light. The results indicate a rapid accumulation and turnover of radioactivity into PC and PG fatty acids (oleic acid in PC and oleic and palmitic acids in PG). Radioactivity accumulates in MGDG and DGDG fatty acids much more slowly and continuously over 72 hours. Most of this activity is found in linoleic and linolenic acids; very little activity is found in the more saturated fatty acids. Little or no desaturation occurs in situ in conjunction with the galactolipids. The results suggest that PC and PG may act as "carriers" for MGDG and DGDG fatty acid synthesis. Analyses of the labeling patterns of the molecular species of MGDG after (14)CO(2) and (14)C-acetate feeding confirm that MGDG is formed by galactosylation of a preformed diglyceride containing predominantly unsaturated fatty acids.

Journal Article↗
PubMed2001

Effects of arachidonic and docosahexaenoic acids on secretion and degradation of bile salt-dependent lipase in AR4-2J cells.

In this study we demonstrated that two polyunsaturated fatty acids, arachidonic acid (AA, n-6) and docosahexaenoic acid (DHA, n-3), modulate the secretion of bile salt-dependent lipase (BSDL) by pancreatic AR4-2J cells. The effects of AA and DHA were also compared with that of the monounsaturated fatty acid, oleic acid (OA). Our results showed that the chronic treatment of cells with AA or DHA, that did not affect the biosynthesis rate of BSDL, similarly decreased the amount of secreted BSDL and perturbed the intracellular partitioning of the enzyme, whereas OA had no effect. Particularly, AA and DHA induced the retention of the enzyme in microsomes and lowered its content in the cell cytosol. We have further shown that AA treatment decreased the ubiquitination of the protein, and consequently diminished its export toward the cytosol, a result that might explain the retention of BSDL in microsomes and correlated with membrane phospholipids alteration. The retained protein was further degraded by a nonproteasomal pathway that likely involves ATP-dependent endoplasmic reticulum proteases. These findings concerning the regulation of the pancreatic BSDL secretion by two polyunsaturated acids, AA and DHA, might be of physiological importance in the plasmatic and cellular cholesterol homeostasis.

Adenosine Triphosphate↗
PubMed1997

Dietary arachidonic acid increases eicosanoid production in the presence of equal amounts of dietary eicosapentaenoic acid.

Previously, we demonstrated that dietary n-3 PUFA (1.5%, w/w) effectively inhibited the production of eicosanoids derived from tissue arachidonic acid (AA) (Whelan et al., 1991). More recently, we also reported that dietary AA (1.0%, w/w) significantly augmented platelet and macrophage eicosanoid production in vitro (Whelan et al., 1993). This present study was designed to investigate the antithetic relationship of dietary AA and EPA on eicosanoid production in vivo. Forty-nine CD-1 male mice were randomly divided into four dietary groups. Identical diets were supplemented with ethyl esters (1.5%, w/w) of the following fatty acids: oleic acid (OA), AA, EPA or AA + EPA (A + E). After four weeks on diet, peritoneal cells were stimulated in vivo with opsonized zymosan and analyzed for eicosanoid production (PGE2, 6-keto-PGF1a, TXB2, LTE4, LTB4, LTE5 and LTB5). The pooled eicosanoid production in the AA group was 41% and 300% higher compared to the OA (control) and EPA groups, respectively. Pooled eicosanoid production in the EPA group was 47% that of the OA group. When equivalent amounts of AA and EPA (AA + EPA) were included in the diet, the pooled eicosanoid production was 29% and 274% higher compared to the OA and EPA groups, respectively. These data demonstrate that dietary AA (1) enhances eicosanoid production in vivo and (2) abrogates virtually all of the effects observed with dietary EPA when both are included in the diet. The clinical implications of dietary AA as modulated by increased eicosanoid production could be significant, particularly when n-3 PUFA are used to reduce eicosanoid-mediated events.

Analysis of Variance↗
PubMed1991

The stimulatory effect of albumin on luteinizing hormone-stimulated Leydig cell steroid production depends on its fatty acid content and correlates with conformational changes.

The effects of purified albumin species and albumin fragments (0.2-1% w/v) on short-term (4 h) steroid secretion by immature rat Leydig cells, in the presence of a maximally stimulating dose of luteinizing hormone (LH), were investigated. Human albumin and the peptic fragment (comprising residues 1-387) enhanced pregnenolone production in isolated rat Leydig cells, whereas chicken albumin and the tryptic fragment (comprising residues 198-585) were not active. This stimulatory effect of human albumin and the peptic fragment correlated with the potential of these proteins to undergo a pH-dependent neutral-to-base transition as measured by circular dichroism. The tryptic fragment and chicken albumin did not have the potential to undergo such a transition. The pH-dependent conformational changes of albumin and fragments thereof occurred in parallel with a change in the binding affinity for testosterone and pregnenolone. The fatty acid oleic acid and the drug suramin, only when present in a molar ligand-to-albumin ratio equal to or higher than 2, inhibited the albumin-mediated stimulation of steroid production. These data show that the stimulatory effects of albumin species on LH-induced Leydig cell pregnenolone production depend on their fatty acid content and correlate with the potential of these molecules to undergo conformational changes. It is unknown via which mechanisms albumin exerts its stimulatory effect, but the LH action through the cyclic AMP pathway seems not to be affected.

Animals↗
PubMed1998

Effect of cis-unsaturated fatty acids on Meth-A ascitic tumour cells in vitro and in vivo.

Earlier studies performed both by us and by others have demonstrated that some n-3 and n-6 fatty acids can inhibit the growth of tumour cells in vitro. Though studies done with various types of oils rich in n-3 and n-6 fatty acids did show that the tumour incidence and growth can be modified, there were relatively few studies wherein the anti-tumour effects of individual free fatty acids were studied. Here we present results which suggest that free fatty acids (oleic acid (OA), linoleic acid (LA), alpha-linolenic acid (ALA), gamma-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) can inhibit the growth of methylcholanthrene-induced sarcoma cells (Meth-A cells) in vitro. The order of potency of various fatty acids on the growth of Meth-A cells was DHA > ALA > EPA > AA > GLA > LA > OA and their ID50 values were 10, 20, 35, 45, 68, 73 and 110 microg/ml/1 x 10(4) cells, respectively. These results indicate that the inhibitory action of different types of n-3, n-6 and n-9 fatty acids on Meth-A cells does not depend on their unsaturation. Vitamin E could partially block the cytotoxicity of these fatty acids indicating a possible role for free radicals. GLA, AA and EPA augmented the generation of superoxide anion and lipid peroxidation in Meth-A cells indicating a possible correlation between the ability of fatty acids to augment free radicals and their tumoricidal action. In an in vivo study, it was observed that OA, LA, ALA, GLA and EPA can prolong the survival of Meth-A-bearing mice when given intraperitoneally. Of all the fatty acids tested, surprisingly, LA was found to be the most potent in enhancing the survival of the tumour-bearing animals at all the concentrations tested. Thus, these studies suggest that free fatty acids can inhibit Meth-A tumour cell proliferation both in vitro and in vivo.

Animals↗
PubMed2003

Fatty acid-binding proteins inhibit hydration of epoxyeicosatrienoic acids by soluble epoxide hydrolase.

Epoxyeicosatrienoic acids (EETs) are potent regulators of vascular homeostasis and are bound by cytosolic fatty acid-binding proteins (FABPs) with K(d) values of approximately 0.4 microM. To determine whether FABP binding modulates EET metabolism, we examined the effect of FABPs on the soluble epoxide hydrolase (sEH)-mediated conversion of EETs to dihydroxyeicosatrienoic acids (DHETs). Kinetic analysis of sEH conversion of racemic [(3)H]11,12-EET yielded K(m) = 0.45 +/- 0.08 microM and V(max) = 9.2 +/- 1.4 micromol min(-1) mg(-)(1). Rat heart FABP (H-FABP) and rat liver FABP were potent inhibitors of 11,12-EET and 14,15-EET conversion to DHET. The resultant inhibition curves were best described by a substrate depletion model, with K(d) = 0.17 +/- 0.01 microM for H-FABP binding to 11,12-EET, suggesting that FABP acts by reducing EET availability to sEH. The EET depletion by FABP was antagonized by the co-addition of arachidonic acid, oleic acid, linoleic acid, or 20-hydroxyeicosatetraenoic acid, presumably due to competitive displacement of FABP-bound EET. Collectively, these findings imply that FABP might potentiate the actions of EETs by limiting their conversion to DHET. However, the effectiveness of this process may depend on metabolic conditions that regulate the levels of competing FABP ligands.

8,11,14-Eicosatrienoic Acid↗