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It has been shown on the model of thermic oxidation of oleic acid methyl ether that addition of phosphatidylethanolamine and lisophosphatidylcholine into a developed reaction brings about some regularities which can be accounted for as oxidation of two-substances. It is suggested that phospholipids can be the substrate of radical oxidation of substances in oxidative transformations of lipids in the cell. In this case according to oxidation conditions the same phospholipids can appear either as prooxidants or as antioxidants.
A chloroform membrane system containing a given mixture of ketoconazole and oleic acid was applied for the uphill transport of Cd2+ ions as CdI42-. In an HCl medium the ligand could form a stable ion-pair with CdI4(2-), which was readily extractable in the membrane phase. A weak basic solution (pH 8) was used as a suitable stripping medium for the quantitative transport of cadmium across the liquid membrane after 120 min. The selectivity and efficiency of Cd2+ transport from an aqueous solution containing other cations, such as Co2+, Cr3+, Ni2+, Fe2+, Mn2+, Pd2+ and Zn2+ ions, were investigated. It was found that none of these cations interfered with Cd2+ transport.
Several studies have explained the influence of clofibrate on lipid metabolism, and the depressive effect of this drug on blood triglyceride and cholesterol levels is now well-known. Inhibition of triglyceride formation in the liver, and thus a reduced release of newly synthesized triglycerides coupled with increased fatty acid catabolism, might partially explain the lipid-lowering effect of clofibrate. These in vitro studies were designed to determine the effects of a new normolipemic product, procetofen, on hepatic microsomal synthesis of triglycerides and mitochondrial catabolism of oleic acid. These subcellular particles were isolated from normal rats or those treated for 8 days with clofibrate (250 mg/kg/day) or procetofen (100 mg/kg/day). Microsomal triglyceride synthesis from 3H oleate was not significantly changed in the clofibrate-treated group, while it decreased by 25 p. 100 in the procetofen-treated group. In the mitochondrial system, 14CO2 production from 10-14C oleate was small and unaffected by either drug. Therefore, the radioactivity of acid-soluble products was enhanced by 40 or 130 p. 100 when mitochondria were isolated from the livers of rats treated with clofibrate or procetofen, respectively. These data support the hypothesis that the plasma lipid-lowering effect of procetofen in vivo could be explained by increased hepatic fatty acid degradation which probably induced a reduction of triglyceride synthesis.
Group A streptococcal strains of some serotypes can be cultured repeatedly from normal human skin for days or weeks and subsequently produce pyoderma, but strains of other serotypes that cause pharyngitis are rarely recovered from normal human skin or skin lesions. In an attempt to understand the biological differences between "skin" and "throat" strains of group A streptococci, we studied their susceptibility to two bactericidal agents operative at the skin surface--oleic acid and UV light. No consistent differences were found between skin and throat strains; all streptococcal strains were exquisitely sensitive to both oleic acid (10 microgram/ml) and UV light (60 microW/cm2).
Computerized gamma scintigraphy revealed a significant (p less than 0.001) rising lung:heart radioactivity ratio, which has been called "slope of injury" or "slope index", with both 99mTechnetium-tagged human serum albumin (99mTc-HSA) and 99mTechnetium-tagged red blood cells (99Tc-RBC) after 0.05 or 0.2 ml/kg iv oleic acid administration to dogs. This slope index was significantly greater with 99mTc-HSA than 99mTc-RBC (p less than 0.001). These findings verify that the scintigraphic 99mTc-HSA slope of injury is a result of a pulmonary capillary protein leak and not oleic acid induced changes in pulmonary blood or air volume. The leak of red blood cells noted with scintigraphy was confirmed by light microscopy and examination of the tracheal edema fluid. The leak of albumin, however, was much greater than the leak of red blood cells by microscopy and tracheal fluid examination, confirming the scintigraphic data. This study provides further evidence that computerized gamma scintigraphy will be of value for the diagnosis of permeability pulmonary edema and its response to treatment.
OBJECTIVE: In acute respiratory failure, increased cardiac output (Qt) increases shunt (Qs/Qt). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region. DESIGN: Oleic acid edema was induced in the left lower lobe (LLL) of 11 pigs. Qt was varied with bleeding and infusion of blood and dextran. Blood flow to the LLL was measured at low and high Qt with electromagnetic low probes in 6 animals and with a gamma camera in 5. In the gamma camera pigs regional ventilation was also measured. MEASUREMENTS AND RESULTS: Qt was increased by 45% (electromagnetic flow probes) and 73% (gamma camera). Qs/Qt increased from 24.9-31.3% (p < 0.05) and from 17.6-28.8% (p < 0.001) respectively. No change in fractional perfusion of LLL could be seen, neither with flow probes nor with gamma camera. A decrease in ventilation of LLL, 2.6%, was observed when Qt was increased (p < 0.05). CONCLUSION: Theoretically a small decrease in ventilation can explain the increase in shunt, if regions with low ventilation/perfusion (VA/Q) ratio are transformed to shunt. This is, however, unlikely since earlier studies have shown that blood flow is distributed either to regions with normal VA/Q ratio or to shunt regions. We conclude that the cardiac output dependent shunt is not caused by redistribution of blood flow between lobes or by decreased ventilation in the edematous region. We cannot exclude that blood flow is redistributed within the edematous lobe.
To study the value of indexes of endothelial cell function in experimentally induced pulmonary microvascular injury, lung damage was produced in anesthetized dogs by intravenous injection of oleic acid (OA; n = 6), alpha-naphthylthiourea (ANTU; n = 5), or phorbol myristate acetate (PMA; n = 6). Angiotensin-converting enzyme (ACE) activity in serum and simultaneous measurements of serotonin (SER) and propranolol (PROP) pulmonary extraction along with several physiologic parameters were determined and compared with those obtained in a control group (n = 5) before and then at 2-h intervals for 8 h after administration of the toxic agent. ACE activity in serum showed a sustained and significant increase in the PMA and OA groups throughout the whole study period, whereas it decreased significantly at 4 h in the ANTU group. SER pulmonary uptake decreased significantly, but slightly, only in the PMA group at 8 h (-5%). At 6 and 8 h respectively, PROP extraction dropped significantly in the PMA (-11 and -13%) and OA (-13 and -19%) groups. This decrease in PROP extraction was likely to result from physiologic changes due to the development of pulmonary edema as suggested by the correlation between the changes in amine uptake and those affecting pulmonary artery pressure and total static respiratory compliance. The lack of effects on SER uptake by the lungs under these experimental conditions indicate that dissociation exists between metabolic dysfunction of pulmonary endothelial cells and fluid leakage.
The metabolism of oleoyl coenzyme A (CoA) was examined in developing seed from two soybean (Glycine max [L.] Merr.) genotypes: Williams, a standard cultivar and A5, a mutant containing nearly twice the oleic acid (18:1) content of Williams. The in vitro rates of esterification of oleoyl-CoA to lysophosphatides by acyl-CoA: lysophosphatidylcholine acyltransferase was similar in both genotypes and lysophosphatidyl-ethanolamine was a poor substrate. Crude extracts desaturated exogenous [1-(14)C]dioleoyl phosphatidylcholine at 14% of the rate achieved with [1-(14)C]oleoyl-CoA, and 50 micromolar lysophosphatidylcholine. The desaturase enzyme also required NADH for full activity. Extracts from Williams contained 1.5-fold more oleoyl phosphatidylcholine desaturase activity, on a fresh weight basis, than did A5 and appeared to have a similar affinity for oleoyl-CoA. There was 1.2- to 1.9-fold more linoleic acid (18:2) in phosphatidylcholine from Williams than from A5, measured at two stages of development, but both genotypes had a similar distribution of fatty acids in the one and two positions. Phosphatidylethanolamine in A5 contained relatively more linoleic acid (18:2) in the one position than did Williams. The increased oleic acid (18:1) content in A5 appeared to be a result of decreased rates of 18:1 desaturation of oleoyl-phosphatidylcholine in this genotype.
Lipid and lipoprotein concentrations and apolipoprotein profile were investigated in canine pancreatitis induced by infusion with oleic acid (OA) into the accessory pancreatic duct. Pancreatitis was diagnosed by physical, hematological, biochemical and pathological examinations. In OA-treated dogs, serum triglyceride (TG) concentration was increased; however, there were no changes in serum total cholesterol (TC) and phospholipid (PL) concentrations. Serum concentrations of TG, TC, PL and total lipids (TL) in beta lipoprotein and those of TC, PL and TL in pre-beta lipoprotein were increased and those of TC, PL and TL in alpha, lipoprotein were decreased. In apolipoprotein profile, the proportions of apolipoprotein B100 in low density lipoprotein fraction and apolipoprotein A-IV in high density lipoprotein fraction were increased. In addition, decreased proportion of apolipoprotein A-I and the appearance of serum amyloid A protein in high density lipoprotein fraction were observed. These results suggest that lipoprotein profiles observed in canine acute pancreatitis are attributed to the alterations in apolipoprotein compositions.
AIMS: To investigate how linoleic acid affects conidial production and sclerotial development in a strictly mitotic Aspergillus parasiticus field isolate as related to improving biocompetitivity of atoxigenic Aspergillus species. METHODS AND RESULTS: We disrupted A. parasiticusDelta12-oleic acid desaturase gene (odeA) responsible for the conversion of oleic acid to linoleic acid. We examined conidiation and sclerotial development of SRRC 2043 and three isogenic mutant strains deleted for the odeA gene (DeltaodeA), either with or without supplementing linoleic acid, on one complex potato dextrose agar (PDA) medium and on two defined media: nitrate-containing Czapek agar (CZ) and Cove's ammonium medium (CVN). The DeltaodeA mutants produced less conidia than the parental strain on all media. Linoleic acid supplementation (as sodium linoleate at 0.3 and 1.2 mg ml(-1)) restored the DeltaodeA conidial production comparable to or exceeding the unsupplemented parental level, and the effect was medium dependent, with the highest increase on CVN and the least on PDA. SRRC 2043 and the DeltaodeA mutants were unable to produce sclerotia on CVN. On unsupplemented PDA and CZ, DeltaodeA sclerotial mass was comparable to that of SRRC 2043, but sclerotial number increased significantly to two- to threefold. Supplementing linoleic acid to media, in general, tended to decrease wild type and DeltaodeA sclerotial mass and sclerotial number. CONCLUSIONS: Linoleic acid stimulates conidial production but has an inhibitory effect on sclerotial development. The relationship between the two processes in A. parasiticus is complex and affected by multiple factors, such as fatty acid composition and nitrogen source. SIGNIFICANCE AND IMPACT OF STUDY: Conditions that promote sclerotial development differ from those required to promote maximum conidial production. Manipulation of content and availability of linoleic acid at different fungal growth phases might optimize conidial and sclerotial production hence increasing the efficacy of biocompetitive Aspergillus species.
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Hepatic PPARgamma expression is increased in several animal models of diabetes and obesity, and liver-specific overexpression of PPARgamma induces liver steatosis. The aim of this study was to investigate the regulation of PPARgamma expression in primary mouse hepatocytes. PPARgamma2, but not PPARgamma1, was up-regulated by insulin and to a lesser extent by oleic acid. Insulin increased transcription of the PPARgamma2 gene via phosphatidylinositol 3-kinase activation. The PPARgamma agonist, rosiglitazone, increased PPARgamma2 expression, but not PPARgamma1, only in the presence of insulin. Also aP2 mRNA expression was induced by rosiglitazone to a higher degree in the presence of insulin, while acyl-CoA oxidase was increased independently of insulin. In summary, PPARgamma2 is increased in hepatocytes by oleic acid and insulin. These results may help to understand the regulation of PPARgamma expression in liver, which possibly plays a role in the development of liver steatosis.
STUDY OBJECTIVE: To compare volume-controlled inverse ratio ventilation (VCIRV) with volume-controlled ventilation with conventional inspiratory to expiratory (I:E) ratio (VCV PEEP) at equal levels of end-expiratory pressure. DESIGN: Animal study using an oleic acid lung injury model with random application of VCV PEEP and VCIRV. SETTING: Experimental investigation at the Department of Clinical Physiology at Uppsala University. ANIMALS: Seven pigs. INTERVENTIONS: VCV PEEP, VCIRV at an end-expiratory pressure level of 10 cm H2O. MEASUREMENTS AND RESULTS: Lung mechanics, hemodynamics, gas exchange, and functional residual capacity. Recruitment of lung tissue, regional lung density, and distribution of inspired gas by computed tomography. Mean and peak airway pressures were 22 +/- 4 and 41 +/- 8 cm H2O with VCIRV and 18 +/- 2 and 45 +/- 7 cm H2O with VCV PEEP. Cardiac output and arterial oxygen tension were equal with VCV PEEP and VCIRV as were static compliance, physiologic dead space, and functional residual capacity. End-expiratory, end-inspiratory, and CT densities during a full ventilatory cycle were not statistically different and the amounts of nonaerated and poorly aerated lung areas were of equal size with VCV PEEP and VCIRV. CONCLUSIONS: VCIRV was comparable to VCV PEEP at similar PEEP levels in alveolar recruitment, aeration of the lung tissues, and in oxygenating the blood. Since cardiac output also remained unchanged, oxygen delivery to peripheral tissues did not differ significantly between the two modes. Neither method has thus proved superior to the other one.
Previous studies established that low in vitro temperatures (27 degrees C, termed nonpermissive) suppressed murine primary thymus-dependent (TD), but not primary thymus-independent (TI) or secondary TD, antibody responses. Suppression was rescued by the addition of oleic acid (18:1), recombinant interleukin (rIL)-2 and/or rIL-4, but not rIL-1. These observations suggested that low temperatures suppress the functions of virgin T cells (Tv) but not those of memory T cells (Tm), B cells, or accessory cells and that hypothetically 18:1 may rescue suppressed responses by altering the membranes of Tv cells, allowing them to proliferate and subsequently secrete interleukins. In this study negatively selected Tm and Tv cells were stimulated with various mitogens at 37 or 27 degrees C. The results indicated that proliferation was suppressed at 27 degrees C to all mitogens tested. The subsequent addition of 18:1 induced proliferative responses at 27 degrees C to both concanavalin A (Con A) and a combination of 12-O-tetradecanoylphorbol 13-acetate (TPA) and calcium ionophore (A23187), but not to phytohemagglutinin-P (PHA). Both Tm and Tv cells showed significant secretion of IL-2 and expression of IL-2 receptor (IL-2R) at 27 degrees C in response to all mitogens, irrespective of proliferation, and the subsequent addition of 18:1 caused little or no change in the levels of IL-2 secretion or IL-2R expression. These findings indicate that suppression of Tm and Tv cell proliferative responses occurs irrespective of IL-2R expression and, unlike antibody production, of IL-2 secretion. Furthermore, it appears that 18:1 can synergistically act with Con A or TPA/A23187, but not PHA, in activating Tm and Tv cells to induce proliferation at 27 degrees C. These findings suggest differences in signal transduction mechanisms between these various mitogens.
Growth on Dubos oleic acid agar plates, incubated for 48 hr at 37 C in candle jars, provides a method for differentiating meningococci from gonococci. All of our 54 strains of meningococci, but none of the 49 strains of gonococci, grew on this medium.
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Small unilamellar vesicles (SUV) formed by egg yolk phosphatidylcholine (PC) and free oleic acid (OA) undergo aggregation induced by Ca2+ at pH greater than 7.0. The rate of the process, as monitored by turbidity changes, presents a linear dependence on phospholipid concentration and a hyperbolic dependence on Ca2+ concentration. The aggregation curves show a lag period which is tentatively attributed to an activation step induced by Ca2+. The incorporation of either cholesterol, alpha-tocopherol or egg yolk phosphatidylethanolamine (PE) produced a decrease in the aggregation rate and an increase in the lag period. Fusion was not detected in any of the different experiments, either by the assay of mixing the membrane phospholipids or by the assay of mixing the aqueous contents. A possible mechanism, explaining the aggregation process is proposed.