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PubMed1990

Proton and divalent cations induce synergistic but mechanistically different destabilizations of pH-sensitive liposomes composed of dioleoyl phosphatidylethanolamine and oleic acid.

Protons and divalent cations show synergistic effects on the destabilization of liposomes composed of unsaturated phosphatidylethanolamine and oleic acid (Düzgünes et al., Biochemistry (1985) 24, 3091). We have extended these observations and investigated the effects of Ca2+ and Mg2+ on the proton-induced destabilization of dioleoyl phosphatidylethanolamine/oleic acid (DOPE/OA) (4:1 molar ratio) liposomes. Temperature-induced aggregation was measured by 90 degrees light scattering. Lipid mixing was used to monitor vesicle destabilization and freeze-fracture electron microscopy was used to examine the structures formed from DOPE/OA vesicles in the presence of Ca2+ and/or protons. Both Mg2+ and Ca2+ shift the pH required for 50% lipid mixing to higher values. Temperature-induced vesicle aggregation occurs at lower temperatures in the presence of divalent cations and/or protons, indicating that intervesicular repulsions are decreased. Freeze-fracture electron micrographs show that the structures formed from DOPE/OA in the presence of Ca2+ differ significantly from those found in the presence of protons. In general, protons induce the formation of hexagonal phase, while the presence of Ca2+ leads to the formation of extensive regions of lamellar sheets with numerous lipidic particles. The synergistic effect of divalent cations and proton may be important for the maximal biological activity of DOPE/OA liposomes.

Calcium↗
PubMed1993

Oleic acid differentially affects gap junction-mediated communication in heart and vascular smooth muscle cells.

The effects of oleic acid (OA) on gap junction-mediated intercellular communication between A7r5 cells and neonatal rat cardiac myocytes were determined. In A7r5 cells the extent of dye coupling was influenced in a biphasic manner by increasing concentrations of OA. Low concentrations of OA (0.1-1 microM) reduced the incidence of dye coupling from 90% (in control cells) to approximately 50%. Further increases in OA concentration, up to 100 microM, had no further effect on extent of dye coupling. In contrast, dye coupling between cardiac myocytes was reduced to near zero levels in a linear fashion by 1-25 microM OA. Whereas high OA concentrations reduce junctional conductance (gj) between heart cells to zero [J. M. Burt, K. D. Massey, and B. N. Minnich. Am. J. Physiol. 260 (Cell Physiol. 29): C439-C448, 1991], gj between A7r5 cells was decreased by a maximum of 45% by OA. These differences in OA sensitivity between the two cell types were not explained by differences in the rate or magnitude of OA uptake by the cells or by differences in the fraction of incorporated OA accessible to albumin washout, i.e., the plasma membrane fraction. Instead, the activity of the individual channel types exhibited different sensitivities to OA. In the presence of increasing concentrations of OA, the activities of first the 70-pS channel population [composed of connexin40 (Cx40)] and then the 108-pS channel population (composed of Cx43) were diminished, leaving predominantly the 140-pS channels (composed of Cx43) at high OA concentrations. The uncoupling effects of OA in both cell types could be reversed by washout with albumin-containing solution; however, higher concentrations of albumin and more vigorous wash conditions were required for full recovery in the A7r5 cells. In addition, albumin also reversed the effects of OA on channel activity. These data suggest that OA binds with greater affinity to the 70- vs. 108- or 140-pS channels and associated with binding is reduced channel activity.

Animals↗
PubMed1996

Lipoprotein composition in NIDDM: effects of dietary oleic acid on the composition, oxidisability and function of low and high density lipoproteins.

Oxidation of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis and is related to the fatty acid composition which is altered in diabetes mellitus. This study examines the relationship between the fatty acid composition of LDL and high density lipoprotein (HDL) and lipoprotein oxidation. A group of nine non-insulin-dependent diabetic (NIDDM) patients were compared to seven healthy control subjects before and after a high monounsaturated diet. Lipoproteins were isolated and oxidisability was measured by conjugated diene formation and lipid peroxide analysis. Serum HDL cholesterol was significantly lower in the diabetic patients. LDL cholesteryl ester linoleic acid in the diabetic patients was significantly higher at baseline and decreased after diet (p < 0.05) while oleic acid increased in both diabetic and non-diabetic subjects (p < 0.05). HDL cholesteryl ester oleic acid was lower in the diabetic patients compared with control subjects (p < 0.05) before diet and it increased significantly after diet (p < 0.05). LDL lipid peroxides and conjugated diene formation were related to LDL glycation (r = 0.46, p < 0.05 and r = 0.49, p < 0.05, respectively). Both decreased following diet (lipid peroxides for diabetic patients from 476 +/- 30 to 390 +/- 20 nmol/mg protein p < 0.05 and for control subjects from 350 +/- 36 to 198 +/- 30 nmol/mg protein p < 0.05). HDL conjugated diene formation decreased in both groups after diet but only significantly in the control group (55.4 +/- 7.5 to 53.2 +/- 6.7 nmol/mg protein for diabetic patients and 45.8 +/- 6.4 to 31.6 +/- 4.8 nmol/mg protein p < 0.05 for control subjects). There was a positive correlation between LDL lipid peroxide formation and percentage of cholesteryl ester linoleic acid in LDL from diabetic patients (r = 0.61, p < 0.05) and control subjects (r = 0.91, p < 0.01). Fatty acid composition of LDL was reflected in the composition of HDL. In the presence of HDL lipoprotein peroxidation decreased. This decrease in lipoprotein peroxidation was positively related to the percentage of linoleic acid in LDL (r = 0.71, p < 0.05). This study confirms the close relationship between the fatty acid composition of LDL and HDL and demonstrates the importance of the fatty acid composition of the cholesteryl ester fraction in relation to LDL oxidation in diabetes. Linoleic acid in HDL appears to be a protecting factor against oxidation.

Adult↗
PubMed1996

EITS changes following oleic acid induced lung water.

We present the results of using electrical impedance tomographic spectroscopy (EITS) to follow the changes in lung water induced by oleic acid. Measurements were made on three goats before and after the injection of oleic acid. In addition to the EITs measurements, lung water was also measured using a double-indicator technique. Large falls in lung electrical impedance were seen as a result of the increase in lung water but the size of the fall was a function of the frequency at which the measurements were made. These changes have been modelled using the Cole equation. Four-electrode measurements were also made on two extracted porcine lungs and Cole equation modelling carried out following the introduction of saline into the lungs. Results were similar in the two sets of animal experiments.

Animals↗
PubMed1995

Effects of inhaled prostacyclin as compared with inhaled nitric oxide in a canine model of pulmonary microembolism and oleic acid edema.

OBJECTIVE: Recently, it has been shown that the inhalation of nitric oxide (NO) and of prostacyclin (PGI2) elicits selective pulmonary vasodilation in a canine model of pulmonary hypertension induced by hypoxic pulmonary vasoconstriction. The present study was designed to investigate whether inhaled NO or PGI2-aerosol, respectively, is also effective in decreasing pulmonary artery pressure in a canine model of acute pulmonary microembolism and oleic acid edema. DESIGN: Prospective, randomized, cross-over design. SETTING: University animal research laboratory. PARTICIPANTS: Eight anesthetized, mechanically ventilated dogs (28 +/- 1 kg). INTERVENTIONS: Acute pulmonary microembolization (PME) was induced using glass microbeads (mean diameter: 100 microns) and 0.01 mL/kg of oleic acid. Subsequently, inhaled PGI2 (concentration: 10 micrograms/mL) or NO (50 ppm), respectively, was randomly administered for 15 minutes each and then withdrawn. MEASUREMENTS AND MAIN RESULTS: Central hemodynamics (heart rate [HR], cardiac output [CO], stroke volume [SV], mean arterial pressure [MAP], systemic vascular resistance [SVR], mean pulmonary artery pressure [PAP], pulmonary vascular resistance [PVR]) and gas exchange (PaO2/FIO2 ratio, intrapulmonary shunt [Qs/Qt], alveolar-arterial oxygen difference, [AaDO2]) were assessed. Measurements were performed at control, after PME, and during administration of PGI2 and NO, respectively. PME induced a significant increase (p < 0.001) of MAP (+9%), PAP (+68%), and PVR (+163%), whereas HR, CO, and SV remained unchanged and lung function deteriorated. Inhalation of NO slightly decreased PAP (-10%; p < 0.05) and PVR (-26%; p < 0.01) and improved AaDO2 and PaO2/FIO2. In contrast, inhalation of PGI2 had no consistent effect on pulmonary vascular tone or gas exchange. CONCLUSION: The data demonstrate that inhaled NO may elicit selective pulmonary vasodilation and improve gas exchange in a canine model of pulmonary microembolism and respiratory insufficiency. However, the degree of these effects was relatively small. The aerosolization of PGI2 under conditions of positive-pressure ventilation did not exert a significant vasodilatory effect on pulmonary vessels and did not improve pulmonary gas exchange in this model.

Administration, Inhalation↗
PubMed1985

Albumin attenuation of oleic acid edema in dog lung depleted of blood components.

Circulating fatty acids are normally transported principally bound to serum albumin. We examined whether administering oleic acid (OA) in a concentrated albumin solution would attenuate its edemogenic potential in the isolated dog lung lobe perfused with a solution nearly depleted of blood cellular and protein components. The isolated ventilated lower left lobe (LLL) was perfused (7.3 +/- 0.6 ml X min-1 X g LLL-1) with a balanced salt solution containing 6% dextran and approximately 10% serum (vol/vol). Hourly weight gain, net LLL weight gain, and wet-to-dry weight ratio (W/D) were used as indices of extravascular lung fluid changes. Group I lobes (n = 5) were given saline, whereas both group II (n = 5) and III (n = 5) lobes were administered 1 microliter OA/kg body wt. The OA was incubated with 5 ml of albumin solution containing approximately 640 mg of bovine fatty acid-free albumin before infusion into group III lobes. Group I gained weight at rate of 10.8 +/- 0.5 g X h-1 X 100 g LLL-1 after saline, whereas group II exhibited a greater (P less than 0.005) rate of weight gain of 42 +/- 13 after OA. Group III weight gain of 8.4 +/- 0.5 g X h-1 X 100 g LLL-1 was not different (P greater than 0.05) from group I but was lower (P less than 0.005) than group II.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[The beta-adrenoceptor and pathophysiological study on acute lung injury induced by oleic acid in rats].

Sixty male Wistar rats were randomized into six groups. In the control and injury group normal saline and oleic acid were injected in tail veins respectively. Dexamethasone, Salviae mitiorrhizae, Ligustrazini and phenobarbitalum natrium were intraperitoneally for the other four groups 15 minutes before the intravenous injection of oleic acid separately. The results showed that the Bmax of beta-adrenoceptor in injury group were decreased markedly and there was correlation between the decreasing of beta-adrenoceptor numbers and pathologic damage in acute lung injury rat. The Bmax of beta-adrenoceptor in cortisone group were similar to control group, which indicated that cortisone is effective to prevent pathologic damage from lung injury by maintenance of the activity of beta-adrenoceptor.

Animals↗
PubMed1987

The prone position improves arterial oxygenation and reduces shunt in oleic-acid-induced acute lung injury.

The arterial oxygen tension (PaO2) may increase when patients with the adult respiratory distress syndrome are turned from supine to prone. We sought to reproduce this observation in dogs with acute lung injury to study the physiologic mechanism by which the improvement in oxygenation might occur. Twenty anesthetized dogs were ventilated with a constant tidal volume (20 ml/kg) of 100% oxygen. Oleic acid (0.09 ml/kg) was injected into the right atrium while rotating the animals through 360 degrees in 4 stages. Animals in Group I (n = 5) remained supine for 10 to 120 min until the supine PaO2 fell below 200 mm Hg. Those in Group II (n = 4) were kept prone during this period. Dogs in Groups I and II were then turned supine or prone every 30 min 5 times. Cardiac output and pulmonary vascular pressures, functional residual capacity (helium dilution), and regional diaphragmatic motion (determined by dorsal and ventral diaphragmatic markers relative to markers on the chest wall seen on lateral chest radiographs taken at FRC and at end-inspiration) were obtained in each position. Eleven dogs were kept supine (Group III, n = 6) or prone (Group IV, n = 5) for 2 h after oleic acid infusion, after which intrapulmonary shunt (Qs/QT) and ventilation-perfusion heterogeneity were measured in the supine and prone positions using the multiple inert gas elimination technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2004

Isolation and characterization of a lipoxygenase from Pseudomonas 42A2 responsible for the biotransformation of oleic acid into ( S )-( E )-10-hydroxy-8-octadecenoic acid.

The isolation of a new lipoxygenase-like (LOX-like) enzyme from Pseudomonas 42A2 and its characterization is described. The enzyme, located in the periplasm of the cell, which contained 0.55 mol of Fe2+ per mol of protein, is monomeric and has a molecular mass of 45 kDa. In the presence of oxygen, the enzyme converts oleic acid into (E)-10-hydroperoxy-8-octadecenoic acid (HPOD), which decomposes to the corresponding (E)-10-hydroxy-8-octadecenoic acid (HOD). The absolute configuration of this acid was determined as S on the basis of exciton-coupled CD data, and specific rotation and NMR analysis of the corresponding p -bromobenzoate derivative. The reaction in vivo leads to the dihydroxy derivative (E)-7,10-dihydroxy-8-octadecenoic acid (DHOD), so that the three hydroxy-fatty acids can be isolated from the culture medium. The activity of the enzyme was optimal between 25 and 30 degrees C and 44% of its activity still remained at 55 degrees C. Its optimal pH is 8.5-9; and the presence of magnesium ions increased LOX activity by 1.5. The activity of the LOX is highest in unsaturated fatty acids containing double bonds in position 9 (oleic, linoleic and linolenic acids), linoleic acid being preferred (100% activity) over linolenic (60.4%) and oleic acids (46%). However, kinetic studies showed that the affinity of the enzyme is similar for the three substrates.

Biotransformation↗
PubMed2001

In vitro visualization and quantification of oleic acid induced changes in transdermal transport using two-photon fluorescence microscopy.

In a novel application of two-photon scanning fluorescence microscopy, three-dimensional spatial distributions of the hydrophilic and hydrophobic fluorescent probes, sulforhodamine B and rhodamine B hexyl ester, in excised full-thickness human cadaver skin were visualized and quantified. Both sulforhodamine B and rhodamine B hexyl ester were observed to lie primarily in the lipid multilamellae region surrounding the corneocytes within the stratum corneum. From the two-photon scanning fluorescence microscopy scans, the changes in the concentration gradient and the vehicle to skin partition coefficient of each probe induced by the oleic acid enhancer action were calculated relative to the control sample (not exposed to oleic acid), and subsequently applied to theoretically derived mathematical expressions of transdermal transport to quantitatively characterize the oleic acid-induced relative changes in the skin diffusion coefficient and the skin barrier diffusion length of the permeant. For the hydrophobic probe rhodamine B hexyl ester, the permeability enhancement was primarily driven by an increase in the vehicle to skin partition coefficient, leading to an increase in the steepness of the concentration gradient across the skin. The primary oleic acid-induced changes in the transport properties of the hydrophilic probe sulforhodamine B included increases in the vehicle to skin partition coefficient and the skin diffusion coefficient. These findings utilizing the two-photon scanning fluorescence microscopy methodology and data analysis described here demonstrate that, in addition to providing three-dimensional images that clearly delineate probe distributions in the direction of increasing skin depth, the subsequent quantification of these images provides additional important insight into the mechanistic changes in transdermal transport underlying the visualized changes in probe distributions across the skin.

Biological Transport↗
PubMed1975

Effect of non-ionic detergents on the absorption of oleic acid in the anaesthetised rat.

The effects of bile salts and of the non-ionic detergents Tween 80 and Pluronic F68 on the absorption and esterification of oleic acid (in presence of monoglyceride) by loops of rat intestine "in vivo" were studied. Absorption of oleic acid was highest from 10mM taurocholate, but was also substantial from the non-ionic detergents. Tween 80 acted synergistically with low concentrations of bile salts. Most of the absorbed fatty acid recovered in the intestinal wall was esterified, the proportion found as triglyceride being greater when a non-ionic detergent had been present. Under the conditions of these experiments a much smaller proportion of radio-active label left the intestine after absorption from 10mM taurocholate than from 2mM taurocholate or from the non-ionic detergents. The detergents Tween 80 and Pluronic F68 in low concentrations may improve absorption of fatty acids where this is impaired due to bile salt deficiency.

Animals↗
PubMed2006

Prediction of oil and oleic acid concentrations in individual corn (Zea mays L.) kernels using near-infrared reflectance hyperspectral imaging and multivariate analysis.

Due to their heterogeneous structure and variability in form, individual corn (Zea mays L.) kernels present an optical challenge for nondestructive spectroscopic determination of their chemical composition. Increasing demand in agricultural science for knowledge of specific traits in kernels is driving the need to find high-throughput methods of examination. In this study macroscopic near-infrared (NIR) reflectance hyperspectral imaging was used to measure small sets of kernels in the spectroscopic range of 950 nm to 1700 nm. Image analysis and principal component analysis (PCA) were used to determine kernel germ from endosperm regions as well as to define individual kernels as objects out of sets of kernels. Partial least squares (PLS) analysis was used to predict oil or oleic acid concentrations derived from germ or full kernel spectra. The relative precision of the minimum cross-validated root mean square error (RMSECV) and root mean square error of prediction (RMSEP) for oil and oleic acid concentration were compared for two sets of two hundred kernels. An optimal statistical prediction method was determined using a limited set of wavelengths selected by a genetic algorithm. Given these parameters, oil content was predicted with an RMSEP of 0.7% and oleic acid content with an RMSEP of 14% for a given corn kernel.

Agriculture↗
PubMed2006

The Arabidopsis stearoyl-acyl carrier protein-desaturase family and the contribution of leaf isoforms to oleic acid synthesis.

In plants, changes in the levels of oleic acid (18:1), a major monounsaturated fatty acid (FA), results in the alteration of salicylic acid (SA)- and jasmonic acid (JA)-mediated defense responses. This is evident in the Arabidopsis ssi2/fab2 mutant, which encodes a defective stearoyl-acyl carrier protein-desaturase (S-ACP-DES) and consequently accumulates high levels of stearic acid (18:0) and low levels of 18:1. In addition to SSI2, the Arabidopsis genome encodes six S-ACP-DES-like enzymes, the native expression levels of which are unable to compensate for a loss-of-function mutation in ssi2. The presence of low levels of 18:1 in the fab2 null mutant indicates that one or more S-ACP-DES isozymes contribute to the 18:1 pool. Biochemical assays show that in addition to SSI2, four other isozymes are capable of desaturating 18:0-ACP but with greatly reduced specific activities, which likely explains the inability of these SSI2 isozymes to substitute for a defective ssi2. Lines containing T-DNA insertions in S-ACP-DES1 and S-ACP-DES4 show that they are altered in their lipid profile but contain normal 18:1 levels. However, overexpression of the S-ACP-DES1 isoform in ssi2 plants results in restoration of 18:1 levels and thereby rescues all ssi2-associated phenotypes. Thus, high expression of a low specific activity S-ACP-DES is required to compensate for a mutation in ssi2. Transcript level of S-ACP-DES isoforms is reduced in high 18:1-containing plants. Enzyme activities of the desaturase isoforms in a 5-fold excess of 18:1-ACP show product inhibition of up to 73%. Together these data indicate that 18:1 levels are regulated at both transcriptional and post-translational levels.

Arabidopsis↗
PubMed1988

Interactions of oleic acid with liver fatty acid binding protein: a carbon-13 NMR study.

13C NMR spectroscopy was used to probe the structural interactions between carboxyl-13C-enriched oleic acid (18:1) and rat liver fatty acid binding protein (FABP) and the partitioning of 18:1 between FABP and unilamellar phosphatidylcholine (PC) vesicles. Spectra of systems containing 2-8 mol of 18:1/mol of FABP (but no PC) exhibited one carboxyl resonance (182.2 ppm) corresponding to FABP-bound 18:1. At pH values less than 8.0, an additional carboxyl resonance, corresponding to unbound 18:1 in a lamellar phase, was observed. Both resonances exhibited ionization shifts with estimated apparent pKa values of less than 5 (bound 18:1) and greater than 7 (unbound 18:1). The intensity of the resonance corresponding to FABP-bound 18:1 increased with increasing 18:1/FABP mole ratio and at 8/1 mole ratio indicated that at least 2 and 6 mol of 18:1/mol of FABP were FABP-bound at pH 7.4 and 8.6, respectively. NMR spectra of systems containing equal concentrations (w/v) of FABP and PC and from 1 to 4 mol of total fatty acid (FA)/mol of FABP exhibited two 18:1 carboxyl resonances (182.2 and 178.5 ppm, pH 7.4). The downfield resonance corresponded to FABP-bound 18:1 and the upfield resonance to PC vesicle bound 18:1. At 1/1 mole ratio (FA/FABP), the intensities of both resonances were approximately equal, but at 4/1 mole ratio the resonance for PC vesicle bound 18:1 was 3-fold more intense than that for FABP-bound 18:1. The following conclusions are reached: (i) The carboxyl groups of 18:1 bound to liver FABP experience only one type of binding environment (the aqueous milieu adjacent to the protein surface).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Suppression of calcium sparks in rat ventricular myocytes and direct inhibition of sheep cardiac RyR channels by EPA, DHA and oleic acid.

The anti-arrhythmic effects of long-chain polyunsaturated fatty acids (PUFAs) may be related to their ability to alter calcium handling in cardiac myocytes. We investigated the effect of eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) on calcium sparks in rat cardiac myocytes and the effects of these PUFAs and the monounsaturated oleic acid on cardiac calcium release channels (RyRs). Visualization of subcellular calcium concentrations in single rat ventricular myocytes showed that intensity of calcium sparks was reduced in the presence of EPA and DHA (15 micro M). It was also found that calcium sparks decayed more quickly in the presence of EPA but not DHA. Sarcoplasmic vesicles containing RyRs were prepared from sheep hearts and RyR activity was determined by either [(3)H]ryanodine binding or by single-channel recording. Bilayers were formed from phosphatidylethanolamine and phosphatidylcholine dissolved in either n-decane or n-tetradecane. EPA inhibited [(3)H]ryanodine binding to RyRs in SR vesicles with K(I) = 40 micro M. Poly- and mono-unsaturated free fatty acids inhibited RyR activity in lipid bilayers. EPA (cytosolic or luminal) inhibited RyRs with K(I) =32 micro M and Hill coefficient, n(1) = 3.8. Inhibition was independent of the n-alkane solvent and whether RyRs were activated by ATP or Ca(2+). DHA and oleic acid also inhibited RyRs, suggesting that free fatty acids generally inhibit RyRs at micromolar concentrations.

Animals↗
PubMed2004

[Changes of carbon monoxide, nitric oxide levels and heme oxygenase system in acute respiratory distress syndrome induced by oleic acid].

OBJECTIVE: To investigate possible role of carbon monoxide (CO) and heme oxygenase (HO) in the pathogenesis of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) and to compared with that induced by nitric oxide (NO). METHODS: ARDS model was established in rats by oleic acid injection and concentrations of CO and NO in pulmonary arterial, carotid jugular blood and bronchoalveolar lavage fluid (BALF) were measured sequentially. Immunohistochemical method was used to determine the expression of HO in the lung. RESULTS: Pulmonary arterial pressure in ARDS rats elevated 10 min after OA injection [(13.80 +/- 1.87) mm Hg to (19.51 +/- 5.02) mm Hg]. At 0.5 h after OA injection, concentration of CO in pulmonary artery began to increase and was markedly higher at 2 h than that in control rats [(0.135 +/- 0.010) g/L versus (0.116 +/- 0.005) g/L] (P < 0.01), also higher than that in carotid artery [(0.117 +/- 0.013) g/L] and in jugular vein [(0.107 +/- 0.018) g/L] in the same group, and maintained at a relatively high level thereafter. Concentration of CO in BALF also increased at 0.5 - 24 h and diminished at 72 h, as compared with that in controls. Concentration of NO in blood of pulmonary and systemic circulation all elevated markedly at 0.5 h and 2 h after OA injection, and then declined to normal at 12 h. Concentration of NO in BALF was significantly higher than that in controls. Arterial blood gas analysis showed that PaO2 markedly decreased in ARDS rats, especially at 2 h after OA injection. HO-2 could be expressed in the lung tissues of normal rats with immunohistochemical method, the strongest in epithelial cells of the bronchi, and HO-1 could only be expressed in pulmonary blood vessel walls, bronchial epithelial cells, alveolar epithelial cells and inflammatory cells of ARDS rats, lasting for 72 h after OA injection, consistent with that of CO level. CONCLUSION: ARDS rats showed a lastecl increase of CO level in pulmonary blood circulation, suggesting CO/HO system might play a more important role in modulation of blood vessel tension than NO might do in pathogenesis of ARDS.

Animals↗
PubMed2005

Addition of oleic acid to delipidated bovine serum albumin aggravates renal damage in experimental protein-overload nephrosis.

BACKGROUND: Non-esterified fatty acids (NEFA) carried on albumin may have a causal role in the development of chronic proteinuria-induced nephropathy. To investigate whether NEFA aggravate renal structural damage, we studied the effects of NEFA addition to delipidated bovine serum albumin (BSA) in protein-overload nephropathy. METHODS: Three groups of Wistar rats received daily intraperitoneal injections (3 weeks) of either 1 g NEFA-free BSA (BSA-0), or NEFA-free BSA with three (BSA-3) or six (BSA-6) molecules oleic acid added per BSA molecule. An additional group received saline injections only (SAL). Renal damage was evaluated by immunohistochemistry and RT-PCR. RESULTS: Interstitial and glomerular alpha-smooth muscle actin (alpha-SMA, marker of myofibroblast transformation) expression were higher in BSA-3/6 than in saline-injected controls (P < 0.001). Glomerular macrophage influx and desmin (marker of glomerular epithelial cell damage) expression were higher in all BSA-injected rats than SAL (P < 0.001). Interstitial macrophage influx was elevated in BSA-0/3 (P < 0.05) and BSA-6 (P < 0.001) compared to SAL. Addition of six molecules of oleic acid to BSA revealed higher interstitial and glomerular alpha-SMA expression (P < 0.001), increased interstitial macrophage numbers (P < 0.001) and enhanced glomerular desmin expression (P < 0.05) compared to BSA-0. RT-PCR revealed higher glomerular alpha-SMA mRNA expression in BSA-3/6 than SAL (P < 0.001 and 0.05, respectively), interstitial alpha-SMA mRNA was elevated in BSA-6 (P < 0.05). Interstitial TGF-beta1 mRNA expression was significantly higher in BSA-3 than SAL (P < 0.05). CONCLUSIONS: These data show that addition of oleic acid to NEFA-free BSA aggravates renal damage, suggesting a role for NEFA in the pathogenesis of proteinuric nephropathies.

Actins↗