Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LINOLEIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources

Interleukin-1 enhances the ability of cultured human umbilical vein endothelial cells to oxidize linoleic acid.

Human umbilical vein endothelial cells (HUVEC) were treated with recombinant interleukin (IL)-1 beta, and the metabolism of exogenous linoleic acid was studied. High performance liquid chromatography, gas chromatography-mass spectrometry, and chiral analysis revealed that HUVEC enzymatically convert linoleic acid mainly into 13-(S)hydroxy-9(Z),11(E)-octadecadienoic (13-HODE) and 9-(R)hydroxy-10(E),12(Z)-octadecadienoic acids, which may isomerize toward all-trans compounds. IL-1 beta increased the formation of all octadecanoids in a time- and dose-dependent manner with similar EC50 (approximately 1 unit/ml). The apparent Km values of linoleic acid were 15.59 +/- 8.39 and 152.9 +/- 84 microM (p < 0.05) in IL-1 beta-treated cells and controls, respectively, indicating a higher substrate affinity in cells stimulated with IL-1 beta. Ratios of S/R enantiomers for the hydroxyoctadecanoids produced by untreated and IL-1 beta-treated cells were similar to those from isolated cyclooxygenases (COXs), whereas isolated 15-lipoxygenase yielded 13-HODE with a strict S configuration. The formation of octadecanoids was inhibited in a dose-dependent manner by several COX inhibitors in both controls and IL-1 beta-treated cells, COX2 selective inhibitors being more effective on IL-1 beta-treated cells than on controls. COX1 and COX2 protein levels increased less than 2-fold and 8-fold, respectively, after IL-1 beta treatment. The specificity of COX inhibitors was proven since they did not inhibit 13-HODE formation by human polymorphonuclear leukocytes. Overall, these results indicate that COXs are responsible for the oxidative metabolism of linoleic acid in HUVEC, and IL-1 beta increases it by inducing the expression of new enzyme, mainly COX2.

Cells, Cultured↗

Linoleic acid increases monocyte deformation and adhesion to endothelium.

Fatty acids have been implicated in having both anti- or pro-inflammatory actions, which may contribute to the progression and severity of atherosclerosis. Linoleic acid has been shown by others to decrease CD18 expression and leukocyte adhesion under static conditions. We investigated the effect of steric acid (18:0), oleic acid (18:1), and linoleic acid (18:2) on the cortical tension (a measure of cell membrane deformability) and adhesion characteristics of the monocytic cell line Mono Mac 6 (MM6) cells to TNF-alpha activated HUVEC under fluid flow. Linoleic acid concentrations up to 23 microM decreased cortical tension and increased adhesion frequencies. Increased adhesion was not due to altered cell morphology or adhesion kinetics and occurred despite decreases in receptor expression (CD18 and CD11a). At higher levels of linoleic acid (> or = 46 microM), cell dissociation constants significantly increased. Results show that decreasing cortical tension increased the probability that contact between MM6 cells and endothelium would produce an adhesive interaction, possibly due to increased deformation of the microvilli and the cell membrane cortex. However, more deformable cells rolled more erratically at low shear rates. The different behavior during initial contact and rolling suggest that adhesion is influenced by two force-dependent mechanisms, deformation of microvilli and a steric barrier. Incubation of MM6 with 23 microM steric or oleic acid did not significantly affect cortical tension. However, cells incubated with steric acid greatly increased their adherence to HUVEC and cells incubated with oleic acid showed no significant effect, indicating factors other than deformability may dominate.

Annexin A5↗

The linoleic acid and trans fatty acids of margarines.

Fifty brands of margarine were analysed for cis-polyunsaturated acids by lipoxidase, for trans fatty acid by infared spectroscopy, and for fatty acid composition by gas-liquid chromatography. High concentrations of trans fatty acids tended to be associated with low concentrations of linoleic acid. Later analyses on eight of the brands, respresenting various proportions of linoleic to trans fatty acids, indicated that two of them contained still higher levels of trans fatty acids (greater than 60%) and negligible amounts of linoleic acid. It is proposed that margarine could be a vehicle for the distribution of some dietary linoleic acid and that the level of linoleic acid and the summation of the saturated plus trans fatty acids be known to ascertain nutritional characteristics.

Chromatography, Gas↗

Fish oil and extruded soybeans fed in combination increase conjugated linoleic acids in milk of dairy cows more than when fed separately.

Eight multiparous Holstein and four multiparous Brown Swiss (78 +/- 43 DIM) cows were used in a 4 x 4 Latin square with 28-d periods to evaluate if feeding fish oil with a source of linoleic acid (extruded soybeans) would stimulate additional amounts of conjugated linoleic acid in milk. Four treatments consisted of a control diet with a 50:50 ratio of forage to concentrate (DM basis), a control diet with 2% added fat from either menhaden fish oil or extruded soybeans, or a combination of fish oil and extruded soybeans each adding 1% fat. DM intake (24.3, 21.6, 24.5, and 22.5 kg/d, for control, fish oil, extruded soybeans, and combination diets, respectively), milk production (32.1, 29.1,34.6, and 31.1 kg/d), and milk fat content (3.51, 2.79, 3.27, and 3.14%) were lower for cows that consumed either fish oil-containing diet, especially the 2% fish oil diet. The proportion of n-3 fatty acids in milk fat increased similarly among all three fat-supplemented diets. Concentrations of transvaccenic acid (1.00, 4.16, 2.17, and 3.51 g/100 g of fatty acids) and cis-9, trans-11 conjugated linoleic acid (0.60, 2.03, 1.16, and 1.82 g/100 g of fatty acids) in milk fat increased more with fish oil than with extruded soybeans. When fed the combination diet, these fatty acids were approximately 50% higher than expected for Holsteins, whereas concentrations were similar for Brown Swiss compared with feeding each fat source separately. These data indicated that fish oil modifies ruminal or systemic functions, stimulating increased conversion of linoleic acid into transvaccenic and conjugated linoleic acids.

Animal Feed↗

Linoleic acid hydroperoxide increases the transfer of albumin across cultured endothelial monolayers.

Exposure to albumin-bound linoleic acid (60 to 150 microM) for 24 h significantly increased the rate of albumin transfer across cultured endothelial monolayers. The increase was dependent on the linoleic acid (18:2) concentration to which the cultures were exposed. Linoleic acid hydroperoxide (18:2-OOH) further accelerated the rate of albumin transfer over that of 18:2. A near maximum albumin transfer was observed after a 2-h incubation with 90 microM 18:2-OOH. Cells exposed to 18:2-OOH caused a marked release of lactate dehydrogenase into the media. On the other hand, 18:2 at concentrations as high as 150 microM, did not significantly affect lactate dehydrogenase release. These results suggest that exposure to 18:2, and in particular to 18:2-OOH, reduces the ability of the endothelium to act as a selective permeability barrier to plasma components.

Animals↗

Inhibition of stearoyl-CoA desaturase activity by the cis-9,trans-11 isomer and the trans-10,cis-12 isomer of conjugated linoleic acid in MDA-MB-231 and MCF-7 human breast cancer cells.

Conjugated linoleic acid (CLA) is a collective term for a group of positional and geometric conjugated dienoic isomers of linoleic acid. CLA has been shown to have strong inhibitory effects on mammary carcinogenesis both in vitro and in vivo. In this study, we investigated the regulation of human stearoyl-CoA desaturase (SCD, EC 1.14.99.5) expression by CLA in human breast cancer cell lines, MDA-MB-231 and MCF-7. Treatment of the cells with the cis-9,trans-11 and trans-10,cis-12 CLA isomers (45 microM) did not repress SCD mRNA in both MDA-MB-231 and MCF-7 cells. However, the cis-9,trans-11 and trans-10,cis-12 CLA isomers significantly decreased SCD protein levels and SCD activity in MDA-MB-231 cells. In MCF-7 cells, both isomers did not affect protein levels, but they inhibited SCD activity. These results suggest that in MDA-MB-231 cells the cis-9,trans-11 and trans-10,cis-12 CLA isomers regulate human SCD by reducing SCD protein levels, while in MCF-7 cells both isomers have a direct inhibitory effect on SCD enzyme activity.

Anticarcinogenic Agents↗

Increasing homicide rates and linoleic acid consumption among five Western countries, 1961-2000.

Clinical intervention trials and animal studies indicate that increasing dietary intakes of long chain n-3 FA or reducing linoleic acid intake may reduce aggressive and violent behaviors. Here we examine if economic measures of greater n-6 consumption across time and countries correlate with greater risk of homicide. Linoleic acid available for human consumption was calculated from World Health Organization disappearance data for 12 major seed oils in the food supply for the years 1961 to 2000 in Argentina, Australia, Canada, the United Kingdom, and the United States (US). Homicide mortality rates, adjusted for age, were obtained from the central judicial authority of each country. Apparent linoleic acid intake from seed oil sources ranged from 0.29 en% (percentage of daily food energy) (Australia 1962) to 8.3 en% (US 1990s). Greater apparent consumption of linoleic acid correlated with higher rates of homicide mortality over a 20-fold range (0.51-10.2/100,000) across countries and time in an exponential growth regression model (r = 0.94, F = 567, P < 0.00001). Within each country, correlations between greater linoleic acid disappearance and homicide mortality over time were significant in linear regression models. Randomized controlled trials are needed to determine if reducing high intakes of linoleic acid by seed oils with alternative compositions can reduce the risk of violent behaviors. These dietary interventions merit exploration as relatively cost-effective measures for reducing the pandemic of violence in Western societies, just as dietary interventions are reducing cardiovascular mortality. Low linoleate diets may prevent behavioral maladies that correctional institutions, social service programs, and mental health providers intend to treat.

Homicide↗

[Role of cyclooxygenase-2 in inhibition of human gastric adenocarcinoma cell line SGC-7901 by c9, t11-conjugated linoleic acid].

OBJECTIVE: To study the effects of c9, t11-conjugated linoleic acid (c9, t11-CLA) on the critical enzyme (COX-2) and its product - prostaglandin E2 (PGE2) of linoleic acid metabolism path in human gastric adenocarcinoma cell line (SGC-7901). METHODS: Expression of COX-2 mRNA and protein were measured by reverse transcription polymerase chain reaction (RT-PCR) and Western blot, PGE2 was determined by radioimmunoassay (RIA). RESULTS: At the concentrations of 25, 50, 100, 200 pmol/L, c9, t11-CLA suppressed the expression of COX-2 mRNA, protein and PGE. CONCLUSION: COX-2 is involved anti-cancer action of c9, t11-CLA and is likely to act as an important target.

Adenocarcinoma↗

Increased saturated phospholipid in cultured cells grown with linoleic acid.

We found that fetal bovine serum supplementation of culture medium provided limited quantities of linoleic acid, an essential fatty acid, to cells grown in culture (2.8 +/- 0.3% of total fatty acids in 12 lots). Supplementation of the medium with additional linoleic acid resulted in altered phospholipid acyl composition in cells of two established lines, A549, a putative model of the pulmonary Type II epithelial cell, and SIRC, a line derived from rabbit corneal epithelium. In particular, linoleic acid supplementation induced a relative increase in disaturated choline phosphoglycerides of 33 and 36%, respectively, in cells of the two lines. This observation may be relevant to design of media for primary culture of Type II cells, in which disaturated phospholipid synthesis used as an index of differentiated function (surfactant production). Linoleate supplementation did not alter growth or size (protein content) of cells of either line and caused a slight increase in accumulation of neutral lipid, in the form of cytoplasmic droplets, in A549 cells. Supplementation of cell cultures with equivalent concentrations of the nonessential fatty acids palmitic and oleic acid did not significantly alter the growth, morphologic appearance, or lipid composition of the cells. However, it was demonstrated in cells of one line that palmitic acid supplementation temporarily stimulated synthesis of disaturated choline phosphoglyceride from radiolabeled choline.

Animals↗

Protection of coumarins against linoleic acid hydroperoxide-induced cytotoxicity.

Coumarins comprise a group of natural phenolic compounds found in a variety of plant sources. Protective effects of coumarins against cytotoxicity induced by linoleic acid hydroperoxide were examined in cultured human umbilical vein endothelial cells. When the cells were incubated in medium supplemented with linoleic acid hydroperoxide and coumarins, esculetin (6,7-dihydroxycoumarin) and 4-methylesculetin protected cells from injury by linoleic acid hydroperoxide. Fraxetin and caffeic acid showed weak, but significant, protection. Esculin as well as esculetin and 4-methylesculetin were effective for protecting cells against linoleic acid hydroperoxide-induced cytotoxicity in the case of pretreatment for 24 h, however fraxetin and caffeic acid showed no protection. Since esculetin was detected after 24 h treatment with esculin, a sugar moiety in the esculin molecule appears to be hydrolyzed during pretreatment. Coumarins such as umbelliferone containing only one hydroxyl group showed no protective effect in pretreatment or concurrent treatment. Esculetin and 4-methylesculetin provided synergistic protection against cytotoxicity induced by linoleic acid hydroperoxide with alpha-tocopherol. Furthermore, the radical-scavenging ability of coumarins was examined in electron spin resonance spectrometry. Esucletin, 4-methylesculetin, fraxetin, and caffeic acid showed the quenching effect on the 1,1-diphenyl-2-picrylhydrazyl radical. These results indicate that the presence of an ortho catechol moiety in the coumarin molecules plays an important role in the protective activities against linoleic acid hydroperoixde-induced cytotoxicity.

Cell Survival↗

Studies on linoleic acid 8R-dioxygenase and hydroperoxide isomerase of the fungus Gaeumannomyces graminis.

Linoleic acid is sequentially converted to 7S,8S-dihydroxy-9Z,12Z-octadecadienoic acid by the 8R-dioxygenase and hydroperoxide isomerase of the fungus Gaeumannomyces graminis, which is a common pathogen of wheat. The objective of this study was to separate and characterize the two enzyme activities. The isomerase activity was found mainly in the microsomal fraction of the mycelia and the 8R-dioxygenase in the cytosol. The 8R-dioxygenase could be partially purified by ammonium sulfate precipitation, gel filtration, ion exchange chromatography or isoelectric focusing. The 8R-dioxygenase was unstable during purification, but it could be stabilized by glutathione, glutathione peroxidase and ethylenediaminetetraacetic acid. Several protease inhibitors reduced the enzyme activity. Gel filtration with Sephacryl S-300 showed that most 8R-dioxygenase activity was eluted with the front with little retention. Isoelectric focusing in the presence of ethylene glycol (20%) indicated an isoelectric point of pl 6.1-6.3. The enzyme was retained on strong anion exchange columns at pH 7.4 and could be eluted with 0.3-0.5 M NaCl. Incubation of the enzyme with 0.1 mM linoleic acid led to partial inactivation, which may indicate product inhibition. Paracetamol and the lipoxygenase inhibitor ICI 230,487 at 30 microM inhibited the 8R-dioxygenase by 44 and 58%, respectively. 8R-hydroperoxy-9Z,12Z-octadecadienoic acid was isolated from incubations of linoleic acid with the partially purified enzyme or with the cytosol in the presence of p-hydroxymercuribenzoate. The hydroperoxide was rapidly converted by the hydroperoxide isomerase in the microsomal fractions to 7S,8S-dihydroxy-9Z,12Z-octadecadienoic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Formation of acyl radical in lipid peroxidation of linoleic acid by manganese-dependent peroxidase from Ceriporiopsis subvermispora and Bjerkandera adusta.

Lipid peroxidation by managanese peroxidase (MnP) is reported to decompose recalcitrant polycyclic aromatic hydrocabon (PAH) and nonphenolic lignin models. To elucidate the oxidative process, linoleic acid and 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid [13(S)-HPODE] were reacted with MnPs from Ceriporiopsis subvermispora and Bjerkandera adusta and the free radicals produced were analyzed by ESR. When the MnPs were reacted with 13(S)-HPODE in the presence of Mn(II), H2O2 and tert-nitrosobutane (t-NB), the ESR spectrum contained a sharp triplet of acyl radical (aN = 0.81 mT). Formation of acyl radical was also observed in the reactions of Mn(III)-tartrate with 13(S)-HPODE and with linoleic acid, but the latter reaction occurred explosively after an induction period of around 30 min. Reactions of MnP with linoleic acid in the presence of Mn(II), H2O2 and t-NB gave no spin adducts while addition of t-NB after preincubation of linoleic acid with MnP/Mn(II)/H2O2 for 2 h gave spin adducts of carbon-centered (aN = 1.53 mT, aH = 0.21 mT) and acyl (aN = 0.81 mT) radicals. In contrast to linoleic acid, methyl linoleate and oleic acid were not peroxidized by MnP and chelated Mn(III) within a few hours, indicating that structures containing both the 1,4-pentadienyl moiety and a free carboxyl group are necessary for inducing the peroxidation in a short reaction time. These results indicate that MnP-dependent lipid peroxidation is not initiated by direct abstraction of hydrogen from the bis-allylic position during turnover but proceeds by a Mn(III)-dependent hydrogen abstraction from enols and subsequent propagation reactions involving the formation of acyl radical from lipid hydroperoxide. This finding expands the role of chelated Mn(III) from a phenol oxidant to a strong generator of free radicals from lipids and lipid hydroperoxides in lignin biodegradation.

Electron Spin Resonance Spectroscopy↗

Epoxy-keto derivative of linoleic acid stimulates aldosterone secretion.

Plasma levels of aldosterone are not always predictable from the activity of renin and the concentration of potassium. Among the unexplained are elevated levels of aldosterone in some obese humans. Obesity is characterized by increased plasma fatty acids and oxidative stress. We postulated that oxidized fatty acids stimulate aldosteronogenesis. The most readily oxidized fatty acids are the polyunsaturated, and the most abundant of those is linoleic acid. We tested oxidized derivatives of linoleic acid for effects on rat adrenal cells. One derivative, 12,13-epoxy-9-keto-10(trans)-octadecenoic acid (EKODE), was particularly potent. EKODE stimulated aldosteronogenesis at concentrations from 0.5 to 5 micromol/L, and inhibited aldosteronogenesis at higher doses. EKODE's stimulatory effect was most prominent when angiotensin and potassium effects were submaximal. The lipid's mechanism of action was on the early pathway leading to pregnenolone; its action was inhibited by atrial natriuretic peptide. Plasma EKODE was measured by liquid chromatography/mass spectrometry. All human plasmas tested contained EKODE in concentrations ranging from 10(-9) to 5x10(-7) mol/L. In samples from 24 adults, levels of EKODE correlated directly with aldosterone (r=0.53, P=0.007). In the 12 blacks in that cohort, EKODE also correlated with body mass index and systolic pressure. Those other correlations were not seen in white subjects. The results suggest that oxidized derivatives of polyunsaturated fatty acids other than arachidonic are biologically active. Compounds like EKODE, derived from linoleic acid, may affect adrenal steroid production in humans and mediate some of the deleterious effects of obesity and oxidative stress, especially in blacks.

Adult↗

1-14C-linoleic acid distribution in various tissue lipids of guinea pigs following an oral dose.

A recent study on the metabolism of 1-14C-alpha-linolenic acid in the guinea pig revealed that the fur had the highest specific activity of all tissues examined, 48 h after dosing. The present study investigated the pattern of tissue lipid labeling following an oral dose of 1-14C-linoleic acid after the animals had been dosed for the same time as above. Guinea pigs were fed one of two diets with a constant linoleic acid content (18% total fatty acids) and a different content of alpha-linolenic acid (0.3 or 17.3%) from weaning for 3 wk and 1-14C-linoleic acid was given orally to each animal for 48 h prior to sacrifice. The most highly labeled tissues (dpm/mg of linoleic acid) were liver, followed by brain, lung and spleen, heart, kidney and adrenal and intestines, in both diet groups. The liver had almost a three-fold higher specific activity than skin and fur which was more extensively labeled than the adipose and carcass. Approximately two-thirds of the label in skin plus fur was found in the fur which, because of a low lipid mass, would indicate that the fur was highly labeled. All tissues derived from animals on the diet with the low alpha-linolenic acid level were significantly more labeled than the tissues from the animals on the high alpha-linolenic acid diet, by a factor of 1.5 to 3. The phospholipid fraction was the most highly labeled fraction in the liver, free fatty acids were the most labeled fraction in skin & fur, while triacyglycerols were the most labeled in the carcass and adipose tissue. In these tissues, more than 90% of the radioactivity was found in fatty acids with 2-double bonds in the tissue lipids. These data indicate that the majority of label found in guinea pig tissues 48 h after dosing was still associated with a fatty acid fraction with 2-double bonds, which suggests there was little metabolism of linoleic acid to more highly unsaturated fatty acids in this time frame. In this study, the labeling of guinea pig tissues with linoleic acid, 48 h after dosing, was quite different from the labeling with alpha-linolenic acid reported previously. The retention of the administered radioactivity from 14C-linoleic acid in the whole body lipids was 1.6 times higher in the group fed the low alpha-linolenic acid diet (diet contained a total of 1.8 g PUFA/100 g diet) compared with the group fed the high alpha-linolenic acid diet (diet contained 3.6 g PUFA/100 g diet). The lack of retention of 14C-labeled lipids in the whole body would be consistent with an increased rate of beta-oxidation of the labeled fatty acid on the diet rich in PUFA, a result supported by other studies using direct measurement of labeled carbon dioxide.

Adrenal Glands↗

Linoleic acid, but not cortisol, stimulates accumulation of casein by mouse mammary epithelial cells in serum-free collagen gel culture.

A two-step culture system has been developed to analyze the role of hormones in casein accumulation by mammary epithelial cells obtained from adrenalectomized and ovariectomized adult virgin mice. In the first step cells are grown inside collagen gel in medium containing insulin, epidermal growth factor (EGF), and linoleic acid for 9 days; these conditions stimulate very little casein accumulation. Following this growth phase the gels are released to float in medium containing insulin, prolactin, and linoleic acid. During this second phase the mammary cells will accumulate large amounts of casein, but only in the simultaneous presence of insulin, prolactin, and linoleic acid; in the absence of linoleic acid casein accumulation is greatly reduced. The casein accumulation is not dependent on the presence of the glucocorticoid cortisol and will occur in spite of the presence of the antiglucocorticoid agent RU 38 486. To determine if the response to cortisol observed in organ culture by other investigators might be mediated by stromal cells, epithelial cells were grown in collagen gel under fatty acid-free conditions and then cocultured with explants of mammary fat pads from adult virgin mice with or without mammary parenchyma. The cocultures were performed in fatty acid-free medium containing insulin and prolactin with or without cortisol. In the majority of experiments the mammary epithelial cells in the collagen gel accumulate more casein in the presence of cortisol than in its absence, irrespective of the presence of mammary parenchyma in the explant. Thus, mammary epithelial cells are directly dependent on insulin and prolactin for casein accumulation and indirectly dependent on cortisol by means of its effect on the stromal cells. This cortisol effect may be to cause release into the medium of linoleic acid or a metabolic product of linoleic acid from the stromal cells.

Animals↗

The effect of linoleic acid and benzyl alcohol on the activity of glycosyltransferases of rat liver Golgi membranes and some soluble glycosyltransferases.

The effects of the membrane perturbing reagents linoleic acid and benzyl alcohol on the activities of four rat liver Golgi membrane enzymes, N-acetylglucosaminyl-, N-acetylgalactosaminyl-, galactosyl-, and sialyltransferases and several soluble glycosyltransferases, bovine milk galactosyl- and N-acetylglucosaminyltransferases and porcine submaxillary N-acetylgalactosaminyltransferases have been studied. In rat liver Golgi membranes, linoleic acid inhibited the activities of N-acetylgalactosaminyl- and galactosyltransferases by 50% or greater, sialyltransferase by 10-15%, and N-acetylglucosaminyltransferase not at all. The isolated bovine milk N-acetylglucosaminyltransferase and porcine submaxillary N-acetylgalactosylaminyltransferase were not inhibited but bovine milk galactosyltransferase was inhibited by 95% or greater. The inhibition by linoleic acid on Golgi membrane galactosyltransferase appears to be a direct effect of the reagent on the enzyme. Incorporation of bovine milk galactosyltransferase into liposomes formed from saturated phospholipids, DMPC, DPPC, and DSPC (dimyristoyl-, dipalmitoyl-, and distearoylphosphatidylcholine) prevented inhibition of the enzyme activity suggesting that the lipid formed a barrier which did not allow linoleic acid access to the enzyme. The water soluble benzyl alcohol was more effective in inhibiting enzymes of the isolated rat liver Golgi complex. All four glycosyltransferases were inhibited, the N-acetylglucosaminyl- and N-acetylgalactosaminyltransferases by more than 95%. A higher concentration of benzyl alcohol was necessary to inhibit the galactosyltransferases than was required for the other Golgi enzymes. Benzyl alcohol also inhibited the isolated bovine milk N-acetylglucosaminyl- and galactosyltransferases 90% to 95%, respectively, but did not affect the isolated porcine submaxillary gland N-acetylgalactosaminyltransferase. Benzyl alcohol did not inhibit the milk galactosyltransferase incorporated into DMPC or DPPC liposomes but showed a complex effect on the activity of the enzyme incorporated into DSPC vesicles, a stimulation of activity at low concentrations followed by an inhibition. A lipid environment consisting of saturated lipids appears to present a barrier to inhibiting substances such as linoleic acid and benzyl alcohol, or lipid may stabilize the active conformation of the enzyme. The different effects of these reagents on four transferases of the Golgi complex suggest that the lipid environment around these enzymes may be different for each transferase.

Animals↗

Effect of conjugated linoleic acid isomers on lipoproteins and atherosclerosis in the Syrian Golden hamster.

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of linoleic acid (LA, C18:2 cis-9, cis-12) that are reported to have important biological activities, including protection against atherosclerosis. In this study, the potential role of the individual cis-9, trans-11 and trans-10, cis-12 isomers of CLA in atherogenesis were compared with LA in the Syrian Golden hamster. Supplementation of a high-fat, high-cholesterol diet (HFHC) with 1% (w/w) cis-9, trans-11 CLA or trans-10, cis-12 CLA did not significantly affect plasma cholesterol levels compared to supplementation with 1% (w/w) LA. Very low density lipoprotein cholesterol (VLDL-C) was lower and plasma triglycerides (TG) were higher in diets where C18:2 fatty acid was added to the HFHC diet, but neither the cis-9, trans-11 CLA group nor trans-10, cis-12 CLA group was significantly different from the LA control group. CLA supplementation did not significantly affect low density lipoprotein cholesterol (LDL-C). Trans-10, cis-12 CLA increased high density lipoprotein cholesterol (HDL-C) levels compared to LA or cis-9, trans-11 CLA (P<0.02), and although the ratio of non-HDL-C:HDL-C in the cis-9, trans-11 CLA group (1.11+/-0.54) and the trans-10, cis-12 CLA group (1.11+/-0.21) was lower than the LA group (1.29+/-0.45), the reduction did not reach statistical significance. Atherosclerosis was assessed in the ascending aorta by measuring the number of aortic cross-sections containing Oil Red O-stained intimal lesions. Compared to the LA group (60+/-11%), both the cis-9, trans-11 CLA group (38+/-8%) and the trans-10, cis-12 CLA group (28+/-7%) had fewer sections displaying a fatty streak lesion, although the differences did not reach statistical significance. These results suggest that individual CLA isomers may reduce atherosclerotic lesion development in the hamster, but when compared to LA, the apparent atheroprotective effects do not correlate with beneficial changes in lipoprotein profile.

Animals↗

[Prevention of gestational hypertension with calcium, linoleic acid, mono and polyunsaturated fatty acid supplements].

BACKGROUND: The aim of this study was to evaluate the benefits of calcium, linoleic acid and mono- and polyunsaturated fatty acids in the prevention of gestational hypertension. METHODS: Between January 1999 and June 2000, 65 primagravidas with a risk of gestational hypertension between the 20th and 24th week of pregnancy were recruited using Doppler velocimetry of the uterine arteries and Holter 24-h pressure monitoring. Patients with diabetes, hypertensive gestosis and previous renal pathologies were excluded. The patients were divided into 2 unequal groups: Group A (40 patients) was treated with calcium, linoleic acid, and mono and polyunsaturated fatty acid supplements; Group B (25 patients) received no treatment. The patients in both groups underwent Doppler velocimetry of the uterine arteries and Holter pressure monitoring at 28-30-32-35 weeks of gestation. RESULTS: Calcium linoleic acid and mono and polyunsaturated fatty acid supplements were effective in significantly reducing the incidence of gestational hypertension (p>0.05); in fact 90% of patients in Group A underwent a physiological evolution of pregnancy compared to only 10% affected by gestational hypertension. In the control group the incidence of this pathology was much higher (32%). CONCLUSIONS: The authors conclude that calcium linoleic acid and mono and polyunsaturated fatty acid supplements are useful and effective in the prevention of gestational hypertension in women at risk for this pathology.

Adult↗