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PubMed1990

Dietary linoleic acid prevents the development of deoxycorticosterone acetate-salt hypertension.

The aim of this study was to elucidate the effect of dietary variations of linoleic acid on the development of deoxycorticosterone acetate (DOCA)-salt hypertension in rats. All rats were divided into three groups and fed one of the following isocaloric diets with 8% NaCl: a high linoleic acid (HLA) (20% sunflower oil), a moderate linoleic acid (5% lard oil + 15% sunflower oil), or a low linoleic acid (DLA) (20% lard oil). After 4 weeks of feeding, we determined intraerythrocyte sodium, potassium, and magnesium concentrations, intra-aortic and lymphocyte magnesium content, and erythrocyte ouabain-sensitive 22Na efflux rate constant. Cytoplasmic free calcium concentration of lymphocytes from thymus was also determined with quin-2 as a fluorescent indicator. In the HLA group, the elevation of systolic blood pressure was significantly attenuated, and intraerythrocyte sodium concentration was significantly lower than in the DLA group. There were greater intraerythrocyte potassium and magnesium concentrations, intra-aortic and lymphocyte magnesium contents, and erythrocyte ouabain-sensitive 22Na efflux rate constant in the HLA group as compared with other groups. Cytoplasmic free calcium concentration in the HLA group was significantly lower than in other groups. Systolic blood pressure significantly correlated negatively with intraerythrocyte and intra-aortic magnesium concentrations and intraerythrocyte potassium concentration, and correlated positively with cytoplasmic free calcium concentration. Erythrocyte ouabain-sensitive 22Na efflux rate constant significantly correlated positively with intraerythrocyte magnesium concentration. These findings suggest that dietary linoleic acid can attenuate the development of DOCA-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

[Platelet aggregation and prostaglandin turnover in man during defined linoleic acid supply with formula diets (author's transl)].

A report is given on changes of platelet aggregation and prostaglandin turnover during a cross-over experiment with six female volunteers being given a linoleic acid supply with formula diets of 0 g or 50 g daily. Collagen- and ADP-induced platelet aggregation was determined with a Borne-type aggregometer. Prostaglandin turnover was measured by analyzing the excretion of a joint derivative of prostaglandin metabolites, tetranorprostanedioic acid, in urine. With a linoleic acid supply of 50 g daily we found an increase of tetranorprostanedioic acid in urine, while platelet aggregation decreased. When the experimental subjects came from a conventional diet (linoleic acid intake 20 g daily) these changes were seen later than after a linoleic acid free formula diet. A linoleic acid-deficient formula diet caused a fall in prostaglandin turnover within 24 hr. ADP-induced platelet aggregation was unchanged after 1 week, while collagen-induced platelet aggregation was increased after 1 and 3 weeks of linoleic acid-deficient diet. These results clearly demonstrate the influence of nutrition on platelet aggregation.

Adult↗
PubMed1985

Linoleic acid treatment in inflammatory arthritis.

Ten patients with chronic rheumatic diseases were treated either with sunflower oil (linoleic acid 66%; n = 6) or with olive oil (linoleic acid 4%; n = 4) for 21 days. Sunflower oil but not olive oil increased the serum concentrations of linoleic acid in all fractions studied. In cholesteryl esters, both arachidonic acid and dihomo-gamma-linolenic acid concentrations were slightly diminished. The changes in all these fatty acids were already seen on the first days of treatment. Plasma arachidonic acid metabolites showed no uniform changes during the treatment. Excretions of the main metabolite of prostacyclin (6-keto-PGF1 alpha) and thromboxane B2 into urine were slightly increased in most patients on sunflower oil. No marked improvement was seen in the clinical or conventional laboratory parameters in either treatment.

Arachidonic Acids↗
PubMed2003

Dose response of milk fat to intravenous administration of the trans-10, cis-12 isomer of conjugated linoleic acid.

Intravenous infusion of conjugated linoleic acid (CLA) was evaluated as a simpler method than abomasal infusion and the feeding of calcium salts to examine milk fat depression. The objectives were to determine the dose-dependent response of milk fat and plasma metabolites to intravenous administration of the trans-10, cis-12 isomer of CLA, an isomer identified to possess an inhibitory effect on milk fat synthesis. Four multiparous Holstein cows averaging 123 +/- 30 d in milk were randomly assigned to treatments in a 4 x 4 Latin square design. Catheters were inserted into the jugular vein for infusions and blood sampling. Treatments consisted of intravenous infusions of 0, 2, 4, and 6 g/d CLA (> 95% trans-10, cis-12 CLA). Infusates contained 72 g/d of a parenteral solution, saline, and CLA to 90 ml. Periods were of 5 d duration with a 7 d wash out. Milk was sampled at each milking and analyzed for fat, protein, and fatty acids. Blood samples were obtained on the last day of each period. Dry matter intake (22.4 +/- 2.4 kg/d), milk yield (28.5 +/- 3.3 kg/d), and protein percent (3.26 +/- 0.08%) of cows were not affected by treatment. However, milk fat percentage was reduced linearly with increasing doses of CLA. Milk fat percentage was 4.17, 3.53, 3.29, and 2.92% on d 5 for treatments 0, 2, 4, and 6 g/d CLA, respectively. Concentrations (4.2 mg/g of fat) of cis-9, trans-11 CLA in milk fat were not affected by treatment. However, an increase in the trans-10, cis-12 CLA content of milk fat was observed. Milk fat contained 0.00, 0.02, 0.06, and 0.10 mg of trans-10, cis-12 CLA per g of fat (SEM = 0.065) for treatments 0, 2, 4, and 6 g/d CLA, respectively. Plasma NEFA concentration increased linearly with the dose of the trans-10, cis-12 CLA. Intravenous infusion of the trans-10, cis-12 isomer of CLA depressed milk fat in a linear manner over the range of infusion studied and, therefore, is an alternative to abomasal infusion.

Abomasum↗
PubMed1987

Metabolism in humans of cis-12,trans-15-octadecadienoic acid relative to palmitic, stearic, oleic and linoleic acids.

Mixtures of triglycerides containing deuterium-labeled hexadecanoic acid (16:0), octadecanoic acid (18:0), cis-9-octadecenoic acid (9c-18:1), cis-9,cis-12-octadecadienoic acid (9c, 12c-18:2) and cis-12,trans-15-octadecadienoic acid (12c,15t-18:2) were fed to two young-adult males. Plasma lipid classes were isolated from samples collected periodically over 48 hr. Incorporation and turnover of the deuterium-labeled fats in plasma lipids were followed by gas chromatography-mass spectrometry (GC-MS) analysis of the methyl ester derivatives. Absorption of the deuterated fats was followed by GC-MS analysis of chylomicron triglycerides isolated by ultracentrifugation. Results were the following: (i) endogenous fat contributed about 40% of the total fat incorporated into chylomicron triglycerides; (ii) elongation, desaturation and chain-shortened products from the deuterated fats were not detected; (iii) the polyunsaturated isomer 12c,15t-18:2 was metabolically more similar to saturated and 9c-18:1 fatty acids than to 9c,12c-18:2; (iv) relative incorporation of 9c,12c-18:2 into phospholipids did not increase proportionally with an increase of 9c,12c-18:2 in the mixture of deuterated fats fed; (v) absorption of 16:0, 18:0, 9c-18:1, 9c,12c-18:2 and 12c,15t-18:2 were similar; and (vi) data for the 1- and 2-acyl positions of phosphatidylcholine and for cholesteryl ester fractions reflected the known high specificity of phosphatidylcholine acyltransferase and lecithin:cholesteryl acyltransferase for 9c,12c-18:2. These results illustrate that incorporation of dietary fatty acids into human plasma lipid classes is selectively controlled and that incorporation of dietary 9c,12c-18:2 is limited. These results suggest that nutritional benefits of diets high in 9c,12c-18:2 may be of little value to normal subjects and that the 12c,15t-18:2 isomer in hydrogenated fat is not a nutritional liability at the present dietary level.

Adult↗
PubMed2000

Linoleic acid metabolism in the spontaneously diabetic rat: delta6-desaturase activity vs. product/precursor ratios.

The activity of delta6-desaturase of linoleic acid, a rate-limiting step in the formation of arachidonic acid, is decreased in animal models of severe, uncontrolled diabetes. The aim of the study was to measure the activity of liver microsomal delta6-desaturase of spontaneously diabetic BioBreeding/Edinburgh rats receiving subcutaneous insulin daily and of genetically related nondiabetic animals. The activity of delta6-desaturase was then compared with indices of activity (plasma lipid fatty acid product/precursor ratios) frequently used in human studies. Diabetic rats treated with insulin had 75 +/- 8% of the activity of microsomal delta6-desaturase of nondiabetic controls (P < 0.05). Insulin withdrawal tended to reduce the activity further (61% of control), although the activity did not differ from insulin-treated diabetic rats. The ratio of plasma phospholipid or cholesteryl ester gamma-linolenic over linoleic acid was not decreased in insulin-treated diabetic rats. By contrast, the ratio of gamma-linolenic over linoleic acid of microsomes was almost three-fold higher in insulin-treated diabetic rats (P < 0.05). The gamma-linolenic over linoleic acid ratio as an index of activity gave inconsistent results in insulin-deprived rats. The ratio of gamma-linolenic over linoleic acid of cholesteryl esters did not differ between control and diabetic rats, nor did it correlate with microsomal delta6-desaturase activity. Furthermore, the index of delta6-desaturase activity, derived from the fatty acid composition of microsomal phospholipids, did not correlate with microsomal delta6-desaturase activity. Diabetes, even when controlled by regular insulin injections, reduces the metabolism of linoleic acid, but the effect is less than previously published. The fatty acid compositions of plasma and liver microsomal lipids are not reliable indices of delta6-desaturase activity in diabetes.

Animals↗
PubMed1992

A spectrophotometric microtiter-based assay for the detection of hydroperoxy derivatives of linoleic acid.

An assay for the detection of hydroperoxy derivatives of linoleic acid formed by the action of 15-lipoxygenase is described. The assay developed is based on a method first reported by Ohishi et al. (1985) Biochem. Int. 10, 205-211) with some important modifications. The assay described herein takes advantage of the ability of (9Z,11E)-13-hydroperoxyoctadecadienoic acid (13-HPODE), the product of the action of 15-lipoxygenase on linoleic acid, to oxidize N-benzoyl leucomethylene blue to methylene blue in the presence of hemoglobin. The resultant blue color is stable to light and air and can be quantified spectrophometrically at 660 nm. The linear range of the assay is 1.6-32 nmol (0.5-10 micrograms) of 13-HPODE. The utility of the assay can be extended to detect other peroxides as well as inhibitors of 15-lipoxygenase. The assay is a rapid, reliable method for the detection of lipid hydroperoxide production.

Animals↗
PubMed1990

Absorption and metabolism of [3H]arachidonic and [14C]linoleic acid in essential fatty acid-deficient rats.

[3H]arachidonic acid (20:4) and [14C]linoleic acid (18:2) were fed in a triolein emulsion to essential fatty acid-deficient (EFAD) rats and to age-matched controls. Tissues were analyzed for radioactivity of different lipid classes after 1, 2, and 4 h. As in earlier studies [Nilsson and Melin. Am. J. Physiol. 255 (Gastrointest. Liver Physiol. 19): G612-G618, 1988], control rats retained more [3H]20:4 than [14C]18:2 in all organs except adipose tissue. In EFAD rats, recovery of [14C]18:2 was increased in small intestine, liver, heart, and kidneys. In comparison to controls, EFAD rats retained much more [14C]18:2 in phospholipids of these organs. The increase in the incorporation of both 3H and 14C into phosphatidylethanolamine was particularly pronounced. Another striking feature was the drastic increase in the retention after 4 h of 14C in cardiolipin, which is specifically located in the inner mitochondrial membrane. In contrast, incorporation of both 3H and 14C into phosphatidylinositol was decreased or unchanged in EFAD rats. Although fecal fat excretion was increased there was no evidence for a malabsorption or an increased retention in intestinal triacyglycerol of the radioactive fatty acids in EFAD rats. The proportion of [14C]18:2 that had been converted to [14C]20:4 was generally low but increased significantly with time in the liver and intestine of EFAD rats.

Aging↗
PubMed1990

Epithelium-derived linoleic acid metabolites modulate airway smooth muscle function.

Cultured epithelial cells obtained from guinea pig tracheal preparations metabolized arachidonic acid into 5- and 15-hydroxy-eicosatetraenoic acid and into the prostaglandins E2 and F2 alpha. Linoleic acid was converted by the epithelial cells into 9-hydroxy-octadecadienoic acid (9-HODE) and smaller amounts of 13-HODE. It was further investigated whether linoleic acid metabolites are of importance for the regulation of airway smooth muscle function. 13-HODE caused an increase of maximal contraction of tracheal rings to histamine, while 9-HODE had no effect.

Animals↗
PubMed2002

An enriched mixture of trans-10,cis-12-CLA inhibits linoleic acid metabolism and PGE2 synthesis in MDA-MB-231 cells.

Conjugated linoleic acid (CLA) isomers are potent inhibitors of mammary tumor cell growth. Evidence suggests that CLA modulates essential fatty acid (EFA) metabolism; however, it is not clear which parts of this pathway are important regulatory points modulated by CLA. Enriched mixtures of D9-cis,11-trans (D9c,11t)- and D10-trans,12-cis (D10t,12c)-18:2 were used to assess outcome measures of EFA metabolism pertaining to membrane phospholipid incorporation, tumor cell growth, and prostaglandin E2 (PGE2) synthesis in the MDA-MB-231 mammary tumor cell line. Tumor cells were treated with linoleic acid (LA), an equal mixture (Mix), or enriched preparations of D9c,11t- or D10t,12c-18:2. Treatment with Mix or the enriched mixture of D10t,12c-18:2 significantly inhibited the synthesis of arachidonic acid (AA) from LA, resulting in increased levels of LA and decreased levels of AA in membrane phosphatidylcholine and phosphatidylethanolamine (P < 0.05). LA and AA levels were not altered in cells treated with enriched D9c,11t-18:2 and were similar to those in LA control treated cells. All CLA treatments reduced [3H]thymidine uptake, an indicator of tumor cell growth, by more than one-half relative to LA controls. MDA-MB-231 cells challenged with AA in the presence of all CLA mixtures resulted in significantly reduced PGE2 synthesis relative to controls treated with LA (P < 0.05). It is evident that individual isomers exert inhibitory effects at specific steps of EFA metabolism, which correspondingly leads to a reduction in PGE2 synthesis and, ultimately, tumor growth.

Analysis of Variance↗
PubMed1998

Effect of intake of pasture on concentrations of conjugated linoleic acid in milk of lactating cows.

We examined the effect of intake of fresh pasture on concentrations of conjugated linoleic acid in milk fat. Sixteen Holstein cows were paired and divided into either the control group or the grazing group. The study involved initial, transition, and final periods. During the initial period, all cows consumed a total mixed diet. Cows in the control group were fed the total mixed diet throughout the study, and cows in the grazing group were gradually adjusted to a diet consisting of intensively managed pasture. Performance of cows in the grazing group was significantly reduced from that of cows in the control group during the final period (dry matter intake, 19% less; milk yield, 29.6 vs. 44.1 kg/d; and live weight, 40 kg less). During the initial period, when both groups were consuming a total mixed diet, concentrations of conjugated linoleic acid in milk fat were similar (X = 5.1 mg/g of milk fat). As the grazing group was gradually adjusted to pasture, concentrations of conjugated linoleic acid in milk gradually increased. During the final period, when cows in the grazing group were consuming a diet consisting of pasture only, conjugated linoleic acid concentrations in the milk fat were doubled (10.9 vs. 4.6 mg/g of milk fat). Furthermore, results showed the individual consistency of the milk fat content of conjugated linoleic acid over time but also demonstrated substantial variation among individual cows within treatment groups. Overall, this study indicated that the concentration of conjugated linoleic acid in milk fat is enhanced by dietary intake of fresh pasture.

Animal Feed↗
PubMed2006

Nutritional supplementation with trans-10, cis-12-conjugated linoleic acid induces inflammation of white adipose tissue.

Conjugated linoleic acids (CLAs) are conjugated dienoic isomers of linoleic acid. Many people supplement their diets with CLAs to attempt weight loss, and the trans-10,cis-12 isomer (t10,c12-CLA) of CLA reduces adiposity in animal models and humans. However, CLA treatment in mice causes insulin resistance that has been attributed to the lipoatrophic state, which is associated with hyperinsulinemia and hepatic steatosis. Here, we investigated the effect of t10,c12-CLA on adipose tissue inflammation, another factor promoting insulin resistance. We confirmed that t10,c12-CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes hyperinsulinemia. In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such as tumor necrosis factor-alpha and interleukin-6 gene expression in WAT without affecting their serum levels. In vitro, t10,c12-CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an nuclear factor-kappaB-dependent mechanism. In vivo, however, the lipoatrophic adipose tissue of CLA-treated mice was notable for a dramatic increase in macrophage infiltration and gene expression. Thus, CLA supplementation directly induces inflammatory gene expression in adipocytes and also promotes macrophage infiltration into adipose tissue to a local inflammatory state that contributes to insulin resistance.

3T3-L1 Cells↗
PubMed2004

Alpha-eleostearic acid (9Z11E13E-18:3) is quickly converted to conjugated linoleic acid (9Z11E-18:2) in rats.

We previously showed that alpha-eleostearic acid (alpha-ESA; 9Z11E13E-18:3) is converted to conjugated linoleic acid (CLA; 9,11-18:2) in the liver and plasma of rats that were given diets including 1% alpha-ESA for 4 wk. In this study, we investigated this phenomenon in detail. First, the chemical structure of CLA produced by alpha-ESA administration was determined. After alpha-ESA was orally administered to rats, CLA in rat liver was isolated by HPLC. The positional and geometric isomerism was determined using GC-EI/MS and (13)C-NMR, respectively, and the CLA generated in rats after alpha-ESA feeding was confirmed to be 9Z11E-CLA. Next, the concentrations of alpha-ESA and CLA were determined 0, 3, 6, and 24 h after oral administration of alpha-ESA to rats. Moreover, we also investigated whether enteric bacteria are involved in the conversion of alpha-ESA to CLA using germ-free rats. alpha-ESA was orally administered to germ-free and normal rats and alpha-ESA and CLA were detected in the organs of both groups. In addition, to confirm that this reaction was enzyme-mediated, alpha-ESA was reacted with tissue homogenates (liver, kidney, and small intestine mucous) and coenzymes (NADH, NAD(+), NADPH, and NADP(+)), and the enzyme activities were estimated from the amount of CLA produced. CLA was detected when alpha-ESA was reacted with liver, kidney, and small intestine mucous homogenates and a coenzyme (NADPH). These results indicated that alpha-ESA is converted to 9Z11E-CLA in rats by a Delta13-saturation reaction carried out by an NADPH-dependent enzyme.

Animals↗
PubMed1991

Metabolism of oxidized linoleic acid: distribution of activity for the enzymatic oxidation of 13-hydroxyoctadecadienoic acid to 13-oxooctadecadienoic acid in rat tissues.

Oxidation products of linoleic acid, including hydroperoxy- and hydroxyoctadecadienoic acids have been shown to possess biological activities in a number of different systems. In this work we describe an enzymatic activity which catalyzes the conversion of 13-hydroxyoctadecadienoic acid to a 2,4-dienone product, 13-oxooctadecadienoic acid. The enzyme activity is widely distributed, with the highest activity in the colon and the liver. The distribution of activity among various tissues is distinct from other dehydrogenases known to use oxygenated unsaturated fatty acids as substrates. This enzyme may play a key role in the metabolism of 13-hydroxyoctadecadienoic acid in epithelial tissues.

Alcohol Oxidoreductases↗
PubMed1997

Cytotoxicity of linoleic acid diols to renal proximal tubular cells.

Monoepoxides of linoleic acid (leukotoxin and isoleukotoxin) have been associated with a variety of pathophysiological diseases in humans including multiple organ failure. They also have been shown to be toxic when injected into experimental animals. Because leukotoxin and isoleukotoxin are excellent substrates for epoxide hydrolases, we tested the hypothesis that the diol metabolites are less toxic than the parent monoepoxides using the rabbit renal proximal tubule (RPT) suspension model. An equimolar mixture of the positional isomers of the methyl esters of leukotoxin and isoleukotoxin did not cause cell death to RPT cells at concentrations up to 1 mm using lactate dehydrogenase release as the endpoint. The corresponding diols, however, caused cell death in a time- and concentration-dependent manner beginning at 4 hr and reaching 42% cell death in 6 hr at 1 mm. Cell death was not due to oxidative stress since malondialdehyde content did not increase and the iron chelator deferoxamine and the antioxidant N,N'-diphenyl-1, 4-phenylenediamine were not cytoprotective. In contrast, cell death was associated with mitochondrial dysfunction with respiration decreasing 54% prior to the onset of cell death. Secondary to the mitochondrial dysfunction, the diols completely inhibited active Na+ transport within 30 min of addition. These results suggest that the in vivo toxicity and pathophysiology previously attributed to the monoepoxides of linoleic acid may be due to the diol metabolites.

Animals↗
PubMed1986

The stoichiometry of oxygen uptake and conjugated diene formation during the dioxygenation of linoleic acid by the pure reticulocyte lipoxygenase. Evidence for aerobic hydroperoxidase activity.

Simultaneous measurements of oxygen uptake and conjugated diene formation (increase in the absorbance at 234 nm) during the dioxygenation of linoleic acid by the pure reticulocyte lipoxygenase gave a nearly theoretical stoichiometry of 1.1 in a temperature range from 5 to 30 degrees C and a wide range of concentrations of both oxygen and linoleic acid. At low concentrations of either oxygen or linoleic acid or both, secondary processes occurred such as linoleic acid-supported lipohydroperoxidase reactions leading to the disappearance of conjugated dienes and to the formation of oxodienes, linoleic acid dimers and epoxyhydroxy derivatives. Under these conditions marked deviations of the stoichiometry between oxygen uptake and conjugated diene formation appeared. The formation of conjugated oxodienoic fatty acids absorbing at 285 nm occurred only under conditions of high concentrations of linoleic acid and limiting oxygen supply. The results indicate that lipohydroperoxidase reactions catalyzed by the pure reticulocyte lipoxygenase do not only take place under strictly anaerobic conditions but also under conditions of limiting concentrations of either linoleic acid or oxygen or both.

Aerobiosis↗
PubMed2000

Acute reduction of serum leptin level by dietary conjugated linoleic acid in Sprague-Dawley rats.

The purpose of this study was to clarify the effect of conjugated linoleic acid on lipid accumulation in adipose tissue. Sprague-Dawley rats were fed a diet containing 2% conjugated linoleic acid for 1, 3, 6, and 12 weeks. In rats fed 2% conjugated linoleic acid, the weight of perirenal white adipose tissue was comparable with that of rats fed a conjugated linoleic acid-free diet. For fatty acid composition of perirenal white adipose tissue, both 16:1/16:0 and 18:1/18:0 ratios were significantly lower in the conjugated linoleic acid-fed group than the control group. Although there was no remarkable difference in serum triglyceride, total cholesterol, and phospholipid levels between dietary groups, serum leptin level was significantly lower than the control group, and lipid content in the perirenal white adipose tissue exerted a tendency toward low compared to the control value at 1-week feeding. On the other hand, leptin level in perirenal white adipose tissue was significantly lower in the conjugated linoleic acid-fed group than the control group at 12-week feeding. In conclusion, these observations suggest dietary conjugated linoleic acid is an acute reducer of serum leptin level. This may afford an explanation of the mechanism of anti-obesity effect in conjugated linoleic acid.

Journal Article↗
PubMed1994

Linoleic acid transport by human placental syncytiotrophoblast membranes.

The placenta syncytiotrophoblast is the site of exchange of nutrients, lipids and minerals between the mother and the fetus. In order to characterize the transport of fatty acids by the placenta, we purified bipolar syncytiotrophoblast brush border and basal plasma membranes from human placenta. These purified brush border and basal plasma membranes enriched 3-fold and 22-fold, respectively, in sodium/potassium-ATPase and 27-fold and 6-fold in alkaline phosphatase activity, compared with the placental homogenates. Fatty acid transport was performed at different fatty acid/albumin ratios to evaluate the optimal uptake conditions. The maximal transport efficiency, for linoleic acid bound to albumin by sonication, was obtained with a 6:1 fatty acid/albumin ratio in brush border and basal plasma membranes. The linoleic acid transport observed with brush border membranes followed Michaelis-Menten kinetics, with a Michaelis constant of 7.89 +/- 0.01 microM and a maximal incorporation rate of 30.80 +/- 6.39 pmol.mg-1.min-1. Linoleic acid transport was very low in basal plasma membranes and we obtained a Michaelis constant of 0.95 +/- 0.01 microM and a maximal incorporation rate of 1.62 +/- 5.06 pmol.mg-1.min-1. In order to show that linoleic acid accumulated within brush border and plasma membrane vesicles, and to eliminate the possibility of a non-specific binding of fatty acid to these membranes, we demonstrated by an osmolarity experiment, the decrease of the linoleic acid transport in brush border and basal plasma membranes obtained in the presence of 455 microM essential fatty acid at 23 degrees C for 180 min. The results presented in this study suggest that linoleic acid is transported significantly by syncytiotrophoblast brush border membranes and basal plasma membranes. Thus, it may represent a unidirectional transport from mother to fetus through the brush border membranes facing the mother, followed by transport at a slower rate through basal plasma membranes facing the fetus.

Albumins↗