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Reduction in the stearic to oleic acid ratio in the circulating red blood cells: a possible tumour marker in solid human neoplasms.

Gas liquid chromatography study of the 18 carbon chain length fatty acids (C18FA) of the human red blood cells (RBCs) was performed on 65 patients with various clinical disorders. It was found that the stearic to oleic acid ratio (SI) of the RBCs was significantly lower (P less than 0.001) in patients with malignant conditions (n = 20, SI = 0.62 +/- 0.16) compared with pathological non-malignant diseases (n = 10, SI = 1.19 +/- 0.2) and the normal control group (n = 35, SI = 1.57 +/- 0.5). Our early results suggest that the increased unsaturation (oleic acid) in the circulating RBCs could be used as a chemical marker in various solid neoplasms.

Chromatography, Gas↗

Cholesteryl ester transfer protein promotes the association of HDL apolipoproteins A-I and A-II with LDL: potentiation by oleic acid.

The association of apolipoprotein (apo) A-I and apo A-II with apo-B-containing particles was measured after incubation at 37 degrees C of either total plasma or low-density lipoproteins (LDL) and high-density lipoproteins-3 (HDL3) in the presence of partially purified cholesteryl ester transfer protein (CETP). At the end of the incubation, apo-B-containing lipoproteins were separated by immunoprecipitation with an anti-apo B gamma-globulin fraction. In mixtures containing LDL and HDL3, either maintained at 4 degrees C or incubated at 37 degrees C, optimal concentrations of anti-apo B antibodies induced the precipitation of more than 95% of apo B without precipitation of apo A-I and apo A-II. When total plasma was incubated at 37 degrees C for 24 h, a significant proportion of apo A-I and apo A-II became associated with apo-B-containing lipoproteins. The fraction of HDL apoproteins associated with apo-B-containing lipoproteins was significantly reduced when plasma was supplemented with TP2 anti-CETP monoclonal antibodies, which are known to inhibit CETP activity. Incubation of LDL and HDL3 for 24 h at 37 degrees C in the presence of purified CETP also induced the association of a significant proportion of apo A-I and apo A-II with apo-B-containing particles. This effect was dependent on CETP concentration in the incubation mixtures and could be suppressed by the addition of anti-CETP monoclonal antibodies. While oleic acid alone, at a final concentration of 0.2 mmol/l, did not promote any association of HDL-apolipoproteins with LDL, it was able, at this concentration, to greatly enhance the CETP-mediated association of apo A-I and apo A-II with apo-B-containing particles. In the presence of both CETP and oleic acid, the association of apo A-I and apo A-II with apo-B-containing particles was apparent within 3 h of commencing the incubation. Approximately 3 mol of apo A-I and 1 mol of apo A-II co-precipitated with each mol of apo B after a 24 h incubation of LDL, HDL3 and CETP. When oleic acid was added to the incubation mixture in addition to CETP, up to 5.5 mol of apo A-I and 2.3 mol of apo A-II were associated with each mol of apo B.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗

Pulmonary vascular pressure-flow relationship in canine oleic acid pulmonary edema.

We tested the hypothesis that the increased impedance to flow in canine oleic acid (OA) lung injury is predominantly due to an increase in effective downstream pressure (EDP), obtained by extrapolating to zero flow the linear portion of the pulmonary artery pressure (PAP)/flow (Q) relationship. PAP-Q coordinates were obtained in eight anesthetized, O2-ventilated dogs by varying Q through systemic arteriovenous fistulae. PAP-Q lines were obtained before and approximately 5 h after injection of OA. A second group of six dogs served as a time control (TC) group. There was a linear relationship between PAP and Q in both experimental and control groups (mean r value 0.948). The presence of pulmonary edema in the OA group caused the EDP to almost double, from 7 to 12 mmHg (P less than 0.01). In contrast, EDP remained constant in TCs. Incremental vascular conductance (IVC), slope of the PAP/Q line, decreased (P less than 0.05) a similar amount in both groups. The above findings are consistent with the modeling of the pulmonary circulation according to a Starling resistor in that large amounts of edema changed EDP but not incremental conductance.

Animals↗

Small, but not large, unilamellar liposomes composed of dioleoylphosphatidylethanolamine and oleic acid can be stabilized by human plasma.

Small unilamellar liposomes, composed of dioleoylphosphatidylethanolamine (DOPE) and oleic acid (OA), prepared by sonication, were incubated in the presence of human plasma at 37 degrees C. The release of entrapped calcein after 8-h incubation was about 15% in plasma, compared with about 70% in phosphate-buffered saline under the same conditions. In contrast, dioleoylphosphatidylcholine (DOPC)/OA liposomes under the same conditions release about 70% in plasma and only 10% in PBS. Total release of calcein from the DOPE/OA liposomes was observed in a PBS solution containing bovine serum albumin, and the release was completely blocked by preincubation of the liposomes with plasma. These results indicate that the unstable DOPE/OA liposomes are stabilized by incubation with plasma. The stabilization process was very fast, being completed within 1 min. Only relatively small liposomes (d less than or equal to 200 nm) were completely stabilized by plasma; larger liposomes were progressively less stabilizable. SDS-polyacrylamide gel electrophoresis of liposomes which had been incubated with plasma and then washed indicated that several proteins were tightly associated with liposomes. Using liposomes containing [14C]OA, it was found that about 70% of the original OA was extracted after 1-h incubation with human plasma at 37 degrees C. Thin-layer chromatographic analysis of the plasma-treated liposomes showed the presence of the plasma lipids in the liposomes. These results suggest that liposomes composed of DOPE/OA are stabilized by protein and/or lipid components from human plasma and that the composition of the liposomes is altered. The mechanism of stabilization is discussed in terms of the surface pressure of small vesicles with a high degree of curvature.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

Increased production of apolipoprotein B and its lipoproteins by oleic acid in Caco-2 cells.

The production of lipids, apolipoproteins (apo), and lipoproteins induced by oleic acid has been examined in Caco-2 cells. The rates of accumulation in the control medium of 15-day-old Caco-2 cells of triglycerides, unesterified cholesterol, and cholesteryl esters were 102 +/- 8, 73 +/- 5, and 11 +/- 1 ng/mg cell protein/h, respectively; the accumulation rates for apolipoproteins A-I, B, C-III, and E were 111 +/- 9, 53 +/- 4, 13 +/- 1, and 63 +/- 4 ng/mg cell protein/h, respectively. Whereas apolipoproteins A-IV and C-II were detected by immunoblotting, apoA-II was absent in most culture media. In contrast to an early production of apolipoproteins A-I and E occurring 2 days after plating, the apoB expression appeared to be differentiation-dependent and was not measurable in the medium until the sixth day post-confluency. In the control medium, very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL), and lipid-poor very high density lipoproteins (VHDL) accounted for 12%, 46%, 18%, and 24% of the total lipid and apolipoprotein contents, respectively. The triglyceride-rich VLDL contained mainly apoE (75%) and apoB (23%), while the protein moiety of LDL was composed of apoB (59%), apoE (20%), apoA-I (15%), and apoC-III (6%). The cholesterol-rich HDL contained mainly apoA-I (69%) and apoE (27%). In the control medium, major portions of apolipoproteins B and C-III (93-97%) were present in LDL, whereas the main parts of apoA-I (92%) and apoE (76%) were associated with HDL and VHDL. Oleate increased the production of triglycerides 10-fold, cholesteryl esters 7-fold, and apoB 2- to 4-fold. There was also a moderate increase (39%) in the production of apoC-III but no significant changes in those of apolipoproteins A-I and E. These increases were reflected mainly in a 55-fold elevation in the concentration of VLDL, and a 2-fold increase in the level of LDL; there were no significant changes in HDL and VHDL. VLDL contained the major parts of total neutral lipids (74-86%), apoB (65%), apoC-III (81%) and apoE (58%). In the presence of oleate, the VLDL, LDL, HDL, and VHDL accounted for 76%, 15%, 3%, and 6% of the total lipoproteins, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Apolipoproteins↗

[Experimental study on effect of altitude xishi capsule in treating oleic acid induced lung injury in acute hypoxia rats].

OBJECTIVE: To explore the effect and pathophysiological mechanism of Altitude Xishi Capsule (XSC) on lung injury during acute hypoxia. METHODS: A new model of acute lung injury was established by administering oleic acid into superior vena cava in experimental rat during acute hypoxia, which was formed by putting the animal in a hypobaric room, and reduced the pressure gradually in uniform speed till a simulated environment of 6000 m above sea level was formed and lasted for 12 hours. XSC was given orally to the rat before oleic acid administration. The effect of XSC on the model was observed by determination of PaO2, wet/dry ratio of lung and pathologic examination at 1, 2, 3 and 4 hours separately. RESULTS: The respiratory frequency of model animal increased markedly, with the water content of lung reduced and aggravated as the hypoxia prolonged. XSC could obviously improve the pulmonary edema and inflammatory cell infiltration in lung. CONCLUSIONS: The aforesaid acute lung injury model with successful rate of 100%, it resembles the clinical acute lung injury and was useful for research on pathophysiology and treatment of ARDS or acute lung injury, XSC could improve the oleic acid induced lung injury in hypoxia rats by reducing the pulmonary edema and inflammatory cell infiltration.

Animals↗

Response of three enzymes to oleic acid, trypsin, and calmodulin chemically modified with a reactive phenothiazine.

Calmodulin was covalently modified with 10-(1-propionyloxysuccinimide)-2-trifluoromethylphenothiazine++ + to stoichiometries between 0 and 2 mol/mol in the presence of Ca2+. The modified calmodulins, oleic acid, and trypsin were assayed for their ability to activate pea plant NAD kinase, bovine brain 3',5'-cAMP phosphodiesterase, and human erythrocyte Ca2+-ATPase. All modified calmodulins activated both phosphodiesterase and Ca2+-ATPase; at the highest concentration assayed, calmodulin modified with 2 mol of reagent/mol activated phosphodiesterase and Ca2+-ATPase to 53% and 100%, respectively, of the activation obtained with unmodified calmodulin. However, higher concentrations of the modified calmodulins were required to observe the same activation; at least 900-fold and 100-fold higher concentrations were required for the two enzymes, respectively. NAD kinase was not activated by any calmodulin labeled to a stoichiometry greater than 1 mol/mol even when a concentration equal to 17,000 times the apparent dissociation constant of calmodulin for NAD kinase was assayed. Therefore, the modified protein (and not some fraction resistant to labeling) is active toward the mammalian enzymes but inactive toward plant NAD kinase. The different response of the three enzymes to the chemical modification suggests that the enzymes may utilize different binding domains on calmodulin. NAD kinase also was not activated by other known activators of the two mammalian enzymes, namely lipids and limited proteolysis. In parallel experiments using the same agents on each enzyme, NAD kinase was the only enzyme of the three that was not activated by oleic acid and several other lipids or by limited trypsin digestion. These results show that NAD kinase possesses several attributes which would not be predicted by current models of the mechanism of activation of enzymes by calmodulin.

3',5'-Cyclic-AMP Phosphodiesterases↗

Effect of feeding high-oleic-acid peanuts to growing-finishing swine on resulting carcass fatty acid profile and on carcass and meat quality characteristics.

A high-oleic-acid peanut breeding line was used in a study designed to determine the effects of feeding swine diets containing elevated levels of monounsaturated fatty acids as a means to increase the level of monounsaturates and total unsaturates in the resulting carcass fat. Forty-eight pigs were allotted to four treatments that consisted of corn-soybean meal diets that contained 1) high-oleic peanuts (HOP), 2) regular commercial peanuts (RP), or 3) canola oil (CO), each added at a dietary level to provide 10% added fat/oil, and 4) a control diet with no added fat/oil. The oil of HOP averaged 75% oleic acid vs 60% for CO and 53% for RP. The pigs were fed the experimental diets from 33 to 102 kg BW, after which all pigs were slaughtered. All three dietary oil sources resulted in increases (P < .01) of monounsaturates in the backfat; the HOP diet resulted in the greatest increase (32% greater than control). Both CO and RP increased (P < .01) the level of polyunsaturates by nearly twofold; HOP resulted in a small decrease. Total unsaturates increased (P < .01) by 24, 24, and 27% for HOP, RP, and CO treatments, respectively, over that obtained from the control treatment. Carcass fat was softer/oilier (P < .05) from pigs fed CO and RP diets, but not from those fed HOP diets, compared with carcass fat of pigs fed the control diet. Dietary fat/oil source had no effect (P > .05) on other carcass compositional traits and various meat quality attributes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Incorporation of oleic acid and eicosapentaenoic acid into glycerolipids of cultured normal human fibroblasts.

Confluent skin fibroblasts from normal humans were incubated in serum free medium with up to 100 nmole/mL eicosapentaenoic acid (EPA; bound to albumin in a 4.6:1 ratio) and compared with cells incubated with oleic acid (OA) at similar concentrations. The rate of [14C]OA incorporation into triacylglycerol (TG) (nmol/mg/h) was approximately 5-fold greater than that of [14C]EPA. The mass of TG formed after incubation of fibroblasts with EPA was also significantly lower than that formed with OA (43.2 +/- 9.3 vs. 59.5 +/- 6.6 micrograms/mg cell protein, respectively, P = 0.006). The addition of excess, unlabeled EPA reduced the rate of incorporation of [14C]OA into TG whereas unlabeled OA stimulated incorporation of [14C]EPA into TG. When the cells were preincubated with human serum basic proteins (BP I, II and III), the mass of TG formed (compared to baseline) was significantly higher with the basic proteins whether OA or EPA was studied. Only BP I significantly stimulated the mass of cell phospholipids, an effect that occurred with either OA or EPA in the medium. The results suggest that in cultured normal human fibroblasts, OA is a better substrate for TG synthesis than EPA and that this effect may be accentuated by the presence of the basis proteins.

Binding, Competitive↗

Rat intestinal lymph osmolarity during glucose and oleic acid absorption.

The two major purposes of this study were to determine 1) how glucose and oleic acid absorption by the intestinal villi influenced the osmotic composition of lymph as it exited the villus base and 2) what if any changes in lymph osmolarity occurred as the lymph traversed through the bowel wall. The rat jejunum was used in all studies and lymph was collected from individual lymphatics at 0.5-1 nl/min during control states and luminal exposure to 35-550 mg% glucose solutions (isotonic in saline) and 5 and 20 mM oleic acidtaurocholate solutions. Lymph collected from the base of villi during vigorous motility had an osmolarity of 403 +/- 15 mosM at rest and was only increased 30-50 mosM more except during exposure to 550 mg% glucose, where osmolarity increased over 100 mosM. Under comparable conditions, the submucosal lymph osmolarity at rest was 302 +/- 3.5 mosM and increased to 330-350 mosM during exposure to all of the solutions tested. When intestinal motility was virtually stopped, the submucosal lymph osmolarity was isotonic for all solutions tested. These observations indicate that absorption of glucose and oleic acid increased the osmolarity of lymph, leaving the villus only 30-50 mosM unless a glucose concentration of 550 mg% was present. Furthermore, the increased flow of villus lymph during absorption raised the osmolarity of the submucosal lymph when bowel motility assisted the lymph propulsion. This movement of materials from the villus to the submucosa by venular blood and lymph flow provides an opportunity for the villus tissue to influence the composition of the submucosal interstitial environment.

Adsorption↗

Percutaneous absorption of indomethacin from mixtures of fatty alcohol and propylene glycol (FAPG bases) through rat skin: effects of oleic acid added to FAPG base.

The effects of oleic acid (OA) added to mixtures of fatty alcohol and propylene glycol (FAPG bases) on the percutaneous absorption of indomethacin (ID) were investigated by using the abdominal skin of rats in vivo. The percutaneous absorption of propylene glycol (PG) from FAPG base was simultaneously examined. The percutaneous absorption of ID from FAPG bases in the absence of OA was poor as compared with that from FAPG bases containing OA. It was observed that when OA was added to the vehicles in the range of 5 to 30%, the percutaneous absorption of ID from the vehicles was increased. In particular, the maximal enhancement of percutaneous absorption of ID was achieved at 5% OA. However, the enhancing effect of percutaneous absorption of ID diminished when the OA content in the vehicle exceeded 50%. PG was readily absorbed through the rat skin from FAPG bases and its percutaneous absorption profiles were similar to those of ID. It can be presumed that PG and ID penetrate together through the skin. In addition, it was confirmed that the percutaneous absorption of ID and PG from FAPG bases was not affected by the viscosity of the vehicle. If FAPG base is to be used as a vehicle for the purpose of percutaneous absorption of ID, OA is considered to be a useful additive.

Animals↗

Long term incubation of cardiac myocytes with oleic acid and very-low density lipoprotein reduces heparin-releasable lipoprotein lipase activity.

An exogenous [3H]triolein emulsion was hydrolyzed by intact cardiac myocytes with functional LPL located on the cell surface. This surface-bound LPL could be released into the medium when cardiac myocytes were incubated with heparin. Incubation of cardiac myocytes with VLDL, or the products of TG breakdown, oleic acid or 2-monoolein, did not increase LPL activity in the medium. However, incubation of cardiac myocytes with either VLDL or oleic acid for > 60 min did reduce heparin-releasable LPL activity. In the heart, this inhibitory effect of FFA could regulate the translocation of LPL from its site of synthesis in the cardiac myocyte to its functional site at the capillary endothelium.

Animals↗

Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.

The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange.

Analysis of Variance↗

[Study of photocatalytic performance of TiO2 membrane for oleic acid by FTIR-ATR technique].

The TiO2 membranes were prepared on glass, ceramic tile and aluminum pieces by Sol-Gel and PVD methods. A fast and exact evaluation on the photocatalytic self-cleaning performance of the membrane materials was achieved by FTIR-ATR technique using oleic acid which was laid on the surface of the membrane. The hydrophilic property of the samples was also determined by the contact angle with water. The results showed that both the TiO2 membrane prepared on glass by the Sol-Gel and PVD methods displayed good photo-induced hydrophilic property and degradation activity of oleic acid, and no difference in hydrophilic property, but the former was a little superior to the latter in photocatalytic activity. The photocatalytic conversion of oleic acid on the TiO2/glass, TiO2/ceramic tile and TiO2 aluminum piece were 92%, 85% and 46%, respectively after illumination 3.5 h, showing a distinct effect of support material property on TiO2 photocatalytic performance. The results suggested that the photocatalytic activity of TiO2 membrane coated on insulator support was higher than that coated on conductor support.

Adsorption↗

Effect of corticosteroid therapy on the acute injury and recovery stage of oleic acid induced lung injury in the rat.

In the rat model of lung injury induced by oleic acid (OA), we studied the effect of corticosteroid therapy on pulmonary inflammation and compliance at acute (1 day post OA) and recovery (3 and 7 days post OA) stages. Methylprednisolone (MP) and dexamethasone (DM) were examined for therapeutic benefit in this model. Histologic examination, lung compliance, and analysis of bronchoalveolar lavage (BAL) fluid were used to assess lung injury. Our results demonstrated that, at 1 day post OA, both steroids effectively reduced pulmonary inflammation and restored lung compliance when compared to animals that received only OA. In comparison to DM, MP was more effective in inhibiting the pulmonary inflammation induced by OA, but was less effective in restoring lung compliance. However, at 3 and 7 days post OA, cell and/or protein levels in BAL fluid from both MP- and DM-treated OA animals were significantly higher than levels observed in animals that received only OA. Lung compliance returned to normal by 3 days in animals that received only OA. This effect, however, was blocked in OA animals that were treated with either steroid, MP, or DM. Our data suggest that steroid therapy can be beneficial in the acute stage of OA-induced lung injury, but appears to be detrimental during the early recovery stage, perhaps by inhibiting the repair process.

Animals↗

Increase of oleic acid in erythrocytes associated with malignancies.

Total lipid extracts of erythrocyte cell membranes from 60 patients with documented malignancies, 41 patients with various acute and chronic diseases, and 40 healthy subjects were analysed. The results were expressed as ratios of stearic to oleic acid, reflecting the degree of desaturation of stearic acid. The mean ratios for the healthy subjects and controls without cancer were 1.5 (SD 0.27) and 1.45 (0.28), respectively, whereas the ratios for patients with malignancies were consistently lower than the cut off point of 1.0, with a mean of 0.69 (0.15) (p less than 0.001). The desaturation ratio was also significantly lower (p less than 0.001) in the group with recurrent tumours (mean 0.75 (0.04)) compared with those with no evidence of recurrent tumours (mean 1.55 (0.27)). It is suggested that the increased unsaturation (oleic acid) in the circulating erythrocytes may be useful in the diagnosis and postoperative monitoring of patients with cancer.

Erythrocyte Membrane↗

[Therapeutic effect of anisodamine on acute lung injury induced by oleic acid in dogs].

Acute lung injury was inflicted in 30 dogs with an intravenous injection of oleic acid of the dose 0.06 ml/kg. Half of the animals were treated with anisodamine. Another 5 dogs were injected with saline to serve as control. The dynamic changes of total hemolytic complement activity, neutrophil aggregation rate, platelet aggregation rate, fibrin degradation products, white cell count and platelet count in both the peripheral arterial and venous blood, and blood gas analysis were tested. The pathological and clinical changes were also observed. The results of the study suggest that the pathogenesis of oleic acid-induced acute lung injury was apparently related to the increase of complement activation, neutrophil aggregating activity, and blood coagulation. The therapeutic effect of anisodamine can be enhanced if the complement neutrophil-fibrin degradation products pathway is blocked.

Animals↗

Melittin-mediated release of [3H]-oleic acid from E. coli cells is dependent upon heat- and trypsin-sensitive factor(s) in human serum.

Synthetic melittin mediated the release of [3H]-oleic acid ([3H]-OA) or its acylated lipids from [3H]-OA-labeled E. coli cells exposed to human serum. This phenomenon was not observed in the absence of serum and was calcium independent. The addition of serum was not required for melittin-mediated lysis of erythrocytes, although lysis was greater in the presence of serum than in its absence (P<0.001). Trypsin treatment of human serum reduced the melittin-mediated release of [3H]-OA/acylated lipids, and this effect was more pronounced upon boiling the serum (P<0.01). A kinetic study showed that maximum release of [3H]-OA/acylated lipids occurred within 3-6 min. Thin layer chromatography (TLC) analysis showed the lipids to be phosphatidyl ethanolamine (PE), phosphatidylethanol (PEt) and phosphatidic acid (PA). There was no detectable level of oleic acid (OA), diacylglycerol (DAG), phosphatidyl choline (PC) or phosphatidyl serine (PS). These findings suggested that a trypsin and heat-sensitive enzyme/factor present in the serum had a role in melittin-mediated action. These findings further showed that melittin activated phospholipase D (PLD), without affecting phospholipase A(2) (PLA(2)) or phospholipase C (PLC) activity.

Chromatography, Thin Layer↗