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PubMed1971

Effect of hemoglobin concentration on the oxidation of linoleic acid.

The inhibitory effect of high concentrations of hemoglobin on the oxidation of linoleic acid was related to the ability of hemoglobin to associate with the fatty acid. Ultracentrifugation of the mixture of hemoglobin and potassium linoleate revealed that approximately 880 moles of linoleic acid could associate with 1 mole of hemoglobin. High concentrations of hemoglobin apparently reduced the amount of free linoleic acid accessible to the heme group, thus preventing the oxidation of the fatty acid. With low hemoglobin concentrations, at which the oxidation began immediately after the addition of the catalyst, the amount of free linoleic acid was considerably greater than that of bound linoleic acid.

Chemical Phenomena↗
PubMedDate not supplied

Oxidation of linoleic acid encapsulated with gum arabic or maltodextrin by spray-drying.

Linoleic acid was emulsified with gum arabic or maltodextrin at various weight ratios of the acid to the polysaccharide in the presence or absence of a small-molecule emulsifier. The emulsions were spray-dried to produce microcapsules. Emulsions prepared with gum arabic were smaller in droplet size and more stable than those prepared with maltodextrin, and linoleic acid in a gum arabic-based microcapsule was also most resistant to oxidation than that in a maltodextrin-based microcapsule. Although the oil droplet size in the emulsion with maltodextrin decreased and the emulsion stability was improved by addition of a small-molecule emulsifier to linoleic acid, the oxidative stability of the encapsulated linoleic acid was not significantly improved. Encapsulated linoleic acid of small droplet size oxidized more slowly than that of large droplet size.

Drug Compounding↗
PubMed2002

Effects of epidermal growth factor and linoleic acid on lipid contents in human intestinal C2BBe1 cells.

Epidermal growth factor (EGF) was reported to regulate triacyl glycerol synthesis in various cells. Linoleic acid and its metabolites were thought to modulate the signal transduction of growth factors. This study determined whether linoleic acid regulated the effect of EGF on lipid contents in human intestinal C2BBe1 cells. Confluent cells were incubated with serum-free medium (control), EGF (45 ng/mL), linoleic acid (42 microg/mL), or combined EGF (45 ng/mL) and linoleic acid (42 microg/mL) for 48 h. The results showed EGF and linoleic acid significantly increased intracellular cholesterol and triglyceride levels compared with the control and combined groups. EGF was a more potent stimulator for triacyl glycerol synthesis in C2BBe1 cells than linoleic acid. However, intracellular cholesterol and triglyceride levels did not differ between the control and combined groups. The secretion of cholesterol and triglyceride into the medium by C2BBe1 cells did not differ among four groups. Both EGF and linoleic acid strongly stimulated the expression of EGF receptor mRNA in C2BBe1 cells at 48 h compared with the control and combined groups. Therefore, EGF and linoleic acid increased triacyl glycerol synthesis in C2BBe1 cells through stimulating the expression of EGF receptor mRNA. The effect of EGF and linoleic acid on this lipogenesis was reversed in the presence of both EGF and linoleic acid by downregulating the expression of EGF receptor mRNA.

Cell Line↗
PubMed2004

Enrichment of conjugated linoleic acid in oats (Avena sativa L.) by microbial isomerization.

A method for microbial isomerization of oat linoleic acid to conjugated linoleic acid (CLA) was developed. The method includes hydrolysis of oat lipids in aqueous flour slurries by the endogenous oat lipase. Then, the flour slurry containing free linoleic acid is utilized as a substrate for the isomerization reaction carried out by resting cells of Propionibacterium freudenreichii ssp. shermanii. The isomerization reaction progressed most effectively when, after the lipid hydrolysis period, the pH of the slightly acidic oat slurry was elevated to 8.0-8.5 and maintained at this range. With slurries containing 5% (w/v) oat flour, the amounts of CLA formed per dry matter were up to 10.1 mg/g corresponding to 102 mg/g lipids or 0.44 mg/mL slurry. Increments in the flour content up to 15% increased the volumetric production of CLA to 0.85 mg/mL. The proportion of the cis-9,trans-11 isomer was 80% of the total CLA formed. CLA could be concentrated into the solid material of the oat slurry by acidification.

Avena↗
PubMed1985

Identification, isolation and characterization of epidermal lipids containing linoleic acid.

Three specific linoleate-rich lipids have been identified in pig epidermis and are referred to as O-acylglucosyl ceramide, O-acyl ceramide, and O-acyl acid. The acid moiety is up to 70% linoleic acid and linked via the hydroxyl group of a omega-OH long-chain fatty acid, which itself is linked to sphingosine or glucosyl sphingosine. The identification of O-acyl ceramide confirmed the findings of another group, whereas the structural configuration of the O-acylglucosyl ceramide is different to previous reports. The identification of an O-acyl acid in epidermis is novel. Our evidence allows us to speculate that a hydroxylated derivative of the O-acyl ceramide may be intimately involved in the permeability barrier of skin, perhaps providing sufficient polarity to maintain a lamellar phase in the intercellular space of the lower stratum corneum region, and that it is specifically in this form that linoleic acid is involved in skin barrier function. Alternatively, or concurrently, this species may act as a signal for late keratinisation events.

Animals↗
PubMed2000

Changes in conjugated linoleic acid and its metabolites in patients with chronic renal failure.

BACKGROUND: Conjugated linoleic acid (CLA) is a mixture of isomers of linoleic acid with conjugated double bonds that constitutes the most abundant fatty acid with conjugated dienes (CDs) in humans. CLA, erroneously considered in the past as a product of lipoperoxidation, has a dietary origin and has shown to possess anticarcinogenic and anti-atherogenic activity, mainly in animal studies. CLA can be metabolized to conjugated linolenic acid (CD18:3) and to conjugated eicosatrienoic acid (CD20:3) and these metabolites may be implicated in CLA activity. Because of the presence of dyslipidemia and the high incidence of cardiovascular and neoplastic diseases in uremic patients, we evaluated CLA and its metabolites in these patients in order to evaluate their metabolism and site distribution. METHODS: We measured CLA, CD18:3, CD20:3, CD fatty acid hydroperoxides (lipoperoxidation products), and linoleic acid in the plasma, adipose tissue, and red blood cell (RBC) membranes by using high-pressure liquid chromatography in the following groups: (1) 23 chronic renal failure (CRF) patients with creatine clearance (CCr)> 10 mL/min (26.2 +/- 16.7); (2) 21 end-stage CRF patients in conservative treatment with CCr <10 mL/min (6.8 +/- 1.8); (3) 30 hemodialysis (HD) patients; and (4) 30 healthy controls. RESULTS: The incorporation of CLA, CD18:3, and CD20:3 in RBC membranes was significantly reduced in group 1 and was even more reduced in groups 2 and 3. CLA significantly increased both in the plasma and adipose tissue of end-stage CRF patients only. CD18:3 and CD20:3 did not change in the plasma and adipose tissue of any group. No significant changes in linoleic acid and CD fatty acid hydroperoxides were found. CONCLUSIONS: The alterations of CD in CRF patients are not due to lipoperoxidation. The increased levels of CLA in plasma and adipose tissue of end-stage CRF patients may be due either to a reduced metabolization of CLA to CD18:3 and CD20:3, or to an altered site distribution with reduced incorporation in cellular membranes and accumulation in the plasma and adipose tissue. The clinical significance of these changes remains to be investigated.

Adipose Tissue↗
PubMed1987

Capacity of the European eel (Anguilla anguilla) to elongate and desaturate dietary linoleic acid.

The ability of eels (Anguilla anguilla) to further desaturate and chain elongate linoleic acid, 18:2n-6, was studied by feeding diets containing either corn oil or a fish oil to groups of elvers for 12 wk and analyzing proportions of fatty acids in tissue lipids. Over the 12-wk period elvers given both dietary treatments increased in weight by fourfold. The proportion of arachidonic acid, 20:4n-6, present in polar lipids of elvers fed the diet containing corn oil increased from an initial value of 5% by weight to 12% by weight; the corresponding value for elvers given a diet containing fish oil, with little linoleic acid in it, was less than 4% by weight. The capacity of this fish to modify dietary linoleic acid metabolically was confirmed by examining the metabolic fate of radioactive carbon after giving [1-14C]linoleic acid orally to eels. Seven days after administration of the linoleic acid approximately 10% of the radioactivity recovered in liver fatty acids was present in trienes and tetraenes with about 4% occurring in arachidonic acid. Compositional analyses from the feeding experiment also indicated that dietary docosaenoic acid, 22:1n-11, is preferentially oxidized by eels.

Anguilla↗
PubMed2006

Conjugated linoleic acid, unlike other unsaturated fatty acids, strongly induces glutathione synthesis without any lipoperoxidation.

Enhancement of the redox status of cells is a cytoprotective strategy against oxidative damage. We recently showed that DHA upregulates glutathione (GSH) content via an induction of its related enzymes gamma-glutamylcysteine ligase and glutathione reductase. In the present study, we investigated the effects of eight other fatty acids on the redox status and lipid peroxidation of human fibroblasts. After 48 h, only arachidonic acid and conjugated linoleic acid (CLA) enhanced GSH content through an induction of gamma-glutamylcysteine ligase. CLA was more potent than arachidonic acid in inducing GSH synthesis. For all the fatty acids tested, lipoperoxidation, estimated by cell malondialdehyde measurement, did not differ from that of controls at 48 h but dramatically increased at 7 d, except for CLA. Lipoperoxidation is associated at 7 d with a high level of reactive oxygen species and with increased haemoxygenase-1 and cyclooxygenase-2 mRNA expression. As demonstrated by a tert-butylhydroperoxide cytotoxicity test, the GSH synthesis obtained with arachidonic acid is not sufficient to protect the cells, whereas this protective effect was obvious with CLA at 48 h as well as at 7 d. The present results show that CLA is the only PUFA able to induce GSH synthesis without any change in oxidative balance, whereas an upregulation of cyclooxygenase-2 by other PUFA is concomitant with an overproduction of malondialdehyde and reactive oxygen species. The particular hairpin conformation obtained for CLA by molecular modelling could account for this specific biological effect.

Arachidonic Acid↗
PubMed2003

Glucuronidation of arachidonic and linoleic acid metabolites by human UDP-glucuronosyltransferases.

Arachidonic acids (AA) and linoleic acids (LAs) are metabolized, in several tissues, to hydroxylated metabolites that are important mediators of many physiological and pathophysiological processes. The conjugation of leukotriene B4 (LTB4), 5-hydroxyeicosatetraenoic acid (HETE), 12-HETE, 15-HETE, and 13-hydroxyoctadecadienoic acid (HODE) by the human UDP-glucuronosyltransferase (UGT) enzymes was investigated. All substrates tested were efficiently conjugated by human liver microsomes to polar derivatives containing the glucuronyl moiety as assessed by mass spectrometry. The screening analyses with stably expressed UGT enzymes in HK293 showed that glucuronidation of LTB4 was observed with UGT1A1, UGT1A3, UGT1A8, and UGT2B7, whereas UGT1A1, UGT1A3, UGT1A4, and UGT1A9 also conjugated most of the HETEs and 13-HODE. LA and AA metabolites also appear to be good substrates for the UGT2B subfamily members, especially for UGT2B4 and UGT2B7 that conjugate all HETE and 13-HODE. Interestingly, UGT2B10 and UGT2B11, which are considered as orphan enzymes since no conjugation activity has so far been demonstrated with these enzymes, conjugated 12-HETE, 15-HETE, and 13-HODE. In summary, our data showed that several members of UGT1A and UGT2B families are capable of converting LA and AA metabolites into glucuronide derivatives, which is considered an irreversible step to inactivation and elimination of endogenous substances from the body.

Androsterone↗
PubMed1994

Enhancement effects of BSA and linoleic acid on hybridoma cell growth and antibody production.

The effects of linoleic acid and bovine serum albumin on hybridoma cell growth and antibody production were investigated. In dish cultivation, linoleic acid on its own promoted cell growth when used at concentrations below 50 mg L-1, but strongly inhibited growth at a concentration of 100 mg L-1 on more. However, linoleic acid bound to bovine serum albumin did not inhibit cell growth, even at a concentration as high as 100 mg L-1. Also, linoleic acid did not affect the specific antibody production rate, with or without bovine serum albumin. In order to elucidate the enhancement of antibody production by bovine serum albumin, fractions were prepared by ultrafiltration (98% molecular weight cut-offs, 50,000 and 17,000) and the effects of the fractionation on antibody production were studied in batch cultivation. The high-molecular-weight fraction (> or = 50,000) promoted antibody production whereas the low-molecular-weight fraction (< or = 17,000) inhibited it. In continuous cultivation, the high-molecular-weight fraction was also found to enhance antibody production.

Animals↗
PubMed1990

Production of arachidonic and linoleic acid metabolites by guinea pig tracheal epithelial cells.

Pulmonary epithelial cells may be responsible for regulating airway smooth muscle function, in part by release of fatty acid-derived mediators. Incubation of isolated guinea pig tracheal epithelial cells with radiolabeled arachidonic acid (AA) leads to the production of 5- and 15-hydroxyeicosatetraenoic acid (5- and 15-HETE) and smaller amounts of leukotriene (LT) B4 and C4 and 12-hydroxyheptadecatrienoic acid (HHT). Epithelial cells also are able to release linoleic acid (LA) metabolites. Incubation with radiolabeled linoleic acid leads to the formation of 9- and 13-hydroxyoctadecadienoic acid (9- and 13-HODE). The biological significance of these mediators produced by epithelial cells is discussed.

Animals↗
PubMed1982

Interaction between Mitochondrial Cytochromes and Linoleic Acid Hydroperoxide: POSSIBLE CONFUSION WITH LIPOXYGENASE AND ALTERNATIVE PATHWAY.

O(2) uptake by tissue extracts in the presence of linoleic acid is generally ascribed to lipoxygenase. Such an O(2) uptake can be observed not only with mitochondria of Solanum tuberosum L. and Arum maculatum L. and pure lipoxygenase but also with cytochrome c. However, the rate of oxidation is highly dependent on the procedure used to prepare the solutions of linoleic acid. Unless special care is taken to prevent contact between linoleic acid and O(2), it appears that linoleic acid hydroperoxide is readily formed. This derivative can be readily oxidized by mitochondria or cytochrome c. On the other hand, the use of a rapid and specific enzymic procedure to estimate the disappearance of linoleic acid demonstrates that linoleic acid itself is not consumed at any appreciable rate by mitochondria or cytochrome c, the true substrate being linoleic acid hydroperoxide. During the reaction, the heme nucleus of added cytochrome c or of mitochondrial cytochromes undergoes deep alterations. Therefore, caution should be exerted when equating an O(2) uptake observed in the presence of linoleic acid to a lipoxygenase activity. The same holds true for the similarity of reaction towards specific inhibitors between lipoxygenase and the cyanide-insensitive pathway oxidase.

Journal Article↗
PubMed1988

Modulation of rat gastric mucosal prostaglandin E2 release by dietary linoleic acid: effects on gastric acid secretion and stress-induced mucosal damage.

We studied chronic intake of diets deficient in or supplemented with linoleic acid to determine whether it affects gastric acid secretion, release of prostaglandin E2, and stress-induced lesions. For 8-10 wk rats were fed three dietary regimens supplying 3.5% (control group), 0.3%, and 10% of total calories as linoleic acid. We found that diets deficient in linoleic acid (0.3%) reduced release of prostaglandin E2 into the gastric lumen (-77%) and increased basal (+133%) and pentagastrin-stimulated acid secretion (+93%) and the area of cold restraint-induced gastric mucosal lesions (+280%), when compared with the control group. Diets supplemented with linoleic acid (10%) increased prostaglandin E2 release into the gastric lumen (+106%) and reduced basal (-44%) and pentagastrin-stimulated acid secretion (-78%) and the area of cold restraint-induced mucosal.lesions (-80%). Prevention of these lesions by the 10% linoleic acid diet was confirmed by quantitative histology. Pretreatment with indomethacin (8 mg/kg intraperitoneally) abolished the effects of the 10% linoleic acid diet on prostaglandin formation, acid secretion, and mucosal injury. We conclude that in rats chronic intake of dietary linoleic acid reduces acid secretion and prevents cold restraint-induced mucosal lesions, possibly because of augmented synthesis of endogenous prostaglandins in the gastric mucosa.

Animals↗
PubMed1990

Caecal and colonic uptake of both linoleic acid and cholesterol in rats following intestinal resection.

Caecal and colonic uptake of both linoleic acid and cholesterol were studied in rats after distal small bowel resection (DSBR). The results showed that the surgical operation increased the caecal and colonic uptake of linoleic acid. Supplementation with linolenic acid inhibited caecal and colonic uptake of linoleic acid. Experiments carried out in the presence of rotenone and ouabain suggest that facilitated diffusion is the predominant mechanism of caecal and colonic linoleic acid absorption, at least at low concentrations. An increase in caecal and colonic uptake of cholesterol was observed after the surgical operation. The study showed that facilitated diffusion seems to be the mechanism of linoleic acid absorption in the caecum and colon, and that both organ growth and changes in transport function of the epithelial cells of caecum and colon appear to be involved in the adaptive response of the bowel to intestinal resection.

Adenosine Triphosphate↗
PubMed2000

Conjugated linoleic acid (CLA) content of milk from cows offered diets rich in linoleic and linolenic acid.

Two experiments were conducted to determine the conjugated linoleic acid (CLA) content of milk from cows offered diets rich in linoleic and linolenic acid. In experiment 1, 36 cows were assigned to a control and five treatment groups. Cows in the control group received a diet containing 51% forage and 49% grain on a dry matter basis. In the treatment group, grain was partly replaced by either 18% raw cracked soybeans, 18% roasted cracked soybeans, 3.6% soybean oil, 2.2% linseed oil, or 4.4% linseed oil. Experimental diets were fed for 5 wk. Average CLA contents in milk fat from wk 2 through 5 were 0.39% in control and 0.37, 0.77, 2.10, 1.58, and 1.63% of total fatty acids in the raw soybean, roasted soybeans, soybean oil, 2.2% linseed oil, and 4.4% linseed oil treatments, respectively. In experiment 2, 36 cows were assigned to a control and 5 treatment groups. Cows in the control group received a diet containing 55% forage and 45% grain. In the treatment groups, grain was partly replaced by soybean oil at 0.5, 1.0, 2.0, 4.0, or by linseed oil at 1.0% of the dietary dry matter. Experimental diets were fed for 5 wk. Average CLA contents in milk fat from wk 2 through 5 were 0.50% in control and 0.75, 0.76, 1.45, 2.08, and 0.73% of total fatty acids in 0.5, 1.0, 2.0, 4.0 soybean oil and 1.0% linseed oil treatments, respectively. Diets rich in linoleic or linolenic acid can increase CLA content of milk when dietary oil is accessible to the rumen microorganisms.

Animals↗
PubMed2001

Incorporation of 1-(14)C linoleic acid in rat liver nuclei and chromatin fractions.

The incorporation of 1-(14)C linoleic acid in several chromatin fractions of rat liver nuclei was investigated using two different procedures: (1) rat liver nuclei were incubated with ATP, CoASH, Mg(++) and 1-(14)C linoleic acid. After 40 min at 37 degrees C the chromatin obtained by sonication of nuclei suspended in 0.25 M sucrose was fractionated by differential sedimentation; (2) chromatin fractions obtained by differential sedimentation were incubated separately with ATP, CoASH, Mg(++) and 1-(14)C linoleic acid 40 min at 37 degrees C in order to characterize the fatty acid incorporation in isolated chromatin. A comparative study of the incorporation of 1-(14)C linoleic acid in microsomes and nuclei isolated from rat liver is also presented for the purpose of comparison. Linoleic acid was incorporated into nuclear lipids as well as in chromatin fractions. The fatty acid incorporation was stimulated considerably in the acylation system when compared to control, it appears to be highly dependent on the state of condensation of chromatin, being barely detectable in the lowest density fraction. The major proportion of 1-(14)C linoleic acid was found in phospholipids and in a lesser proportion it remained esterified to triglycerides and cholesteryl esters. The distribution of radioactivity in different classes of phospholipids present in microsomes and nuclei isolated from rat liver, showed a similar profile of distribution. The major proportion of radioactivity, approximately 50% was found in phosphatidylcholine and in a lesser proportion in sphingomyelin, phosphatidylserine and phosphatidylethanolamine. When chromatin fractions were incubated separately, it was observed that the major proportion of 1-(14)C linoleic acid in phospholipids was found in heavy chromatin fractions whereas low density chromatin fraction only incorporated in a lesser proportion.

Acylation↗
PubMed2004

Oxidized linoleic acid regulates expression and shedding of syndecan-4.

Syndecan-4, a heparan sulfate proteoglycan that is widely expressed in the vascular wall and as a cell surface receptor, modulates events relevant to acute tissue repair, including cell migration and proliferation, cell-substrate interactions, and matrix remodeling. While syndecan-4 expression is regulated in response to acute vascular wall injury, its regulation under chronic proatherogenic conditions such as those characterized by prolonged exposure to oxidized lipids has not been defined. In this investigation, arterial smooth muscle cells were treated with 13-hydroperoxy-9,11-octadecadienoic acid (HPODE) and 13-hydroperoxy-10,12-octadecadienoic acid, oxidized products of linoleic acid, which is the major oxidizable fatty acid in LDL. Both oxidized fatty acids induced a dose-dependent, rapid upregulation of syndecan-4 mRNA expression that was not attenuated by cycloheximide. This response was inhibited by pretreatment with N-acetylcysteine, catalase, or MEK1/2 inhibitors, but not by curcumin or lactacystin, known inhibitors of NF-kappaB. These data suggest that oxidized linoleic acid induces syndecan-4 mRNA expression through the initial generation of intracellular hydrogen peroxide with subsequent activation of the extracellular signal-regulated kinase signaling pathway via MEK1/2. Notably, the HPODE-induced enhancement of syndecan-4 mRNA was accompanied by accelerated shedding of syndecan-4. In principle, alterations in both the cell surface expression and shedding of syndecan-4 may augment a variety of proatherogenic events that occur in response to oxidized lipids.

Animals↗
PubMed2000

Conjugated linoleic acid reduces body fat mass in overweight and obese humans.

Conjugated linoleic acid (CLA) has been shown to reduce body fat mass (BFM) in animals. To investigate the dose-response relationships of conjugated linoleic acid with regard to BFM in humans, a randomized, double-blind study including 60 overweight or obese volunteers (body mass index 25-35 kg/m(2)) was performed. The subjects were divided into five groups receiving placebo (9 g olive oil), 1.7, 3.4, 5.1 or 6.8 g conjugated linoleic acid per day for 12 wk, respectively. Dual-energy X-ray absorptiometry was used to measure body composition [measurements at wk 0 (baseline), 6 and 12]. Of the 60 subjects, 47 completed the study. Eight subjects withdrew from the study due to adverse events; however, no differences among treatment groups were found regarding adverse events. Repeated-measures analysis showed that a significantly higher reduction in BFM was found in the conjugated linoleic acid groups compared with the placebo group (P: = 0.03). The reduction of body fat within the groups was significant for the 3.4 and 6.8 g CLA groups (P: = 0.05 and P: = 0.02, respectively). No significant differences among the groups were observed in lean body mass, body mass index, blood safety variables or blood lipids. The data suggest that conjugated linoleic acid may reduce BFM in humans and that no additional effect on BFM is achieved with doses > 3.4 g CLA/d.

Absorptiometry, Photon↗