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PubMed2002

Treatment of Shwachman syndrome by Japanese herbal medicine (Juzen-taiho-to): stimulatory effects of its fatty acids on hemopoiesis in patients.

Juzen-taiho-to (a Japanese herbal medicine) has been traditionally administered to patients with anemia, neutropenia, or wasting syndrome. We previously attempted to isolate and purify the hemopoiesis-stimulatory components in Juzen-taiho-to extracts using an in vitro hemopoietic stem cell (HSC) assay method in which mouse HSCs can proliferate on a stromal cell line (MS-5). We have found that fatty acids (particularly oleic acid and linolenic acid) actively promote the proliferation of HSCs, and that the effect is mediated by stromal cells, rather than by any direct action on the HSCs. In the present study, we show, using human normal bone marrow cells (BMCs) and umbilical cord blood cells, that similar stimulatory effects are due to the presence of oleic acid and linolenic acid, which stimulate the proliferation of HSCs in stroma-based culture systems. Furthermore, a marked stimulatory effect was noted on BMCs from patients with Shwachman syndrome, which shows pancreatic and bone marrow dysfunctions. We also show the data on hemopoietic recovery after the administration of Juzen-taiho-to to a patient with Shwachman syndrome. These findings suggest that decreased fatty acid levels in the blood, caused by exocrine pancreatic insufficiency, induce bone marrow dysfunction in Shwachman syndrome.

Bone Marrow Diseases↗
PubMed1998

Differential regulation of neurofibromin and p120 GTPase-activating protein by nutritionally relevant fatty acids.

Arachidonic acid, phosphatidic acid, and other lipids inhibit the catalytic fragment of neurofibromin more potently than that of p120 guanosine triphosphatase-activating protein (GAP). The effects of fatty acids other than arachidonic acid on full-length neurofibromin and p120 GAP, to our knowledge, have not been studied. In this study, we analyzed the effects of eight nutritionally relevant fatty acids on guanosine triphosphatase (GTPase) stimulatory activity of full-length neurofibromin and p120 GAP. The fatty acids tested were saturated stearic acid, monounsaturated oleic acid, and three n-6 and three n-3 polyunsaturated fatty acids. Analysis was performed by Ras immunoprecipitation GTPase assay. The full-length p120 GAP expressed in insect Sf9 cells and immunoaffinity-purified full-length neurofibromin were used. In contrast to neurofibromin, which was readily inhibited by stearic and oleic acid, p120 GAP was only weakly inhibited even at high concentrations (> 80 microM). Neurofibromin was also two- to threefold more sensitive to inhibition by other fatty acids tested. A chimeric protein in which the neurofibromin catalytic domain was fused to the NH2-terminal sequences of p120 GAP was used to determine that differential sensitivity to fatty acid inhibition maps to the catalytic domain of the proteins. These results indicate that nutritionally relevant fatty acids can modulate the GTPase function of c-Ha-Ras protein by inhibiting GTPase stimulatory activity of two Ras regulators, full-length neurofibromin and p120 GAP, at physiologically relevant concentrations in vitro.

Animals↗
PubMed1999

Delta 9-fatty acid desaturase from arachidonic acid-producing fungus. Unique gene sequence and its heterologous expression in a fungus, Aspergillus.

Based on the sequence information for delta 9-desaturase genes (from rat, mouse and yeast), which are involved in the desaturation of palmitic acid and stearic acid to palmitoleic acid and oleic acid, respectively, the corresponding cDNA and genomic gene were cloned from the fungal strain, Mortierella alpina 1S-4, which industrially produces arachidonic acid. There was a cytochrome b5-like domain linked to the carboxyl terminus of this Mortierella desaturase, as also seen in the yeast delta 9-desaturase. The Mortierella delta 9-desaturase genomic gene had only one intron, in which a novel phenomenon was observed: there was a GC-end at the 5'-terminus instead of a GT-end that is, in general, found in introns of eukaryotic genes. The full-length cDNA clone was expressed under the control of an amyB promoter in a filamentous fungus, Aspergillus oryzae, resulting in drastic changes in the fatty acid composition in the transformant cells; the contents of palmitoleic acid (16:1) and oleic acid (18:1) increased significantly, with accompanying decreases in palmitic acid (16:0) and stearic acid (18:0). These changes were controlled by the addition of maltose as a carbon source to the medium. Also, the expression of the gene caused a significant change in the lipid composition in the Aspergillus transformant. Genomic Southern blot analysis of the transformant with the Mortierella delta 9-desaturase gene as a probe confirmed the integration of this gene into the genome of A. oryzae.

Amino Acid Sequence↗
PubMed1988

Comparison of output particle size distributions from pressurized aerosols formulated as solutions or suspensions.

The delivery of particles as small as possible (preferably less than 5 microns) to the respiratory tract should be the aim of those formulating metered dose inhalers (MDIs). This may be facilitated by the formulation of solution, rather than suspension-type, pressurized aerosol units. Two series of MDIs were compared; one contained suspended micronized disodium fluorescein (0.1%, w/v), while the other contained the same concentration of dissolved salicylic acid. Either oleic acid, L-alpha-phosphatidylcholine, or sorbitan trioleate was incorporated at 0.15% (w/v) as suspending agent (disodium fluorescein) or solubilizing agent (salicylic acid). The propellant blend was 70% (w/w) Freon 12 and 30% (w/w) Freon 11 in all cases. This exhibited a vapor pressure of 50.6 psig (444.7 kPa) at 21 degrees C. The output particle size distribution of the aerosol reaching the cascade impactor showed a mass median aerodynamic diameter (MMAD) of approximately 4 and 2 microns for the suspension and solution formulations respectively, regardless of the surfactant used. Larger MMADs were observed for solution aerosols formulated with oleic acid (2.32 microns) compared to those containing L-alpha-phosphatidylcholine (1.93 microns) or sorbitan trioleate (2.07 microns). Possible reasons for these observations are discussed.

Aerosols↗
PubMed1975

13-C nuclear magnetic resonance studies on the lipid organization in enveloped virions (vesicular stomatitis virus).

13-C nuclear magnetic resonance (NMR) studies are described regarding the lipid organization in the envelope of the vesicular stomatitis virion. The fatty acid chains (oleic acid) and the choline moiety of the 3-sn-phosphatidylcholine and spingomyelin have been labeled specifically with 13-C by growing the virions in prelabeled host cells (BHK 21 cells). The results suggest that 130C NMR spectroscopy is a very feasible method for the study of natural membranes provided the isotope is highly enriched in specific positions and incorporated biochemically. Spin-lattice relaxation (T1) measurements of particular C atoms have been carried out with whole virions, with virions deprived of their surface projections by trypsinization but unaltered in their shape and size, and with liposomes prepared from the total lipid mixture of the envelope in order to get insight into the molecular structure of this model membrane. The mobility of the central part of 11-13-C-labeled oleic acid incorporated into the ester and amide lipids and the choline group of 3-sn-phosphatidylcholine and sphingomyelin is very restricted as indicated by their short T1 times. It is concluded from the data presented here that the high cholesterol content (cholesterol/P: 0.7) of the envelope lipid phase is responsible for the rather rigidly packed envelope structure. The mode and extent of the interactions between lipids and glycoprotein surface projections are subjects for further study.

Animals↗
PubMed1992

Eicosanoid balance and perfusion redistribution of oleic acid-induced acute lung injury.

We have proposed that endogenous prostacyclin opposes the vasoconstriction responsible for redistribution of regional pulmonary blood flow (rPBF) away from areas of increased regional lung water concentration (rLWC) in canine oleic acid- (OA) induced acute lung injury (D. P. Schuster and J. Haller. J. Appl. Physiol. 69: 353-361, 1990). To test this hypothesis, we related regional lung tissue concentrations of 6-ketoprostaglandin (PG) F1 alpha and thromboxane (Tx) B2 in tissue samples obtained 2.5 h after administration of OA (0.08 ml/kg iv) to rPBF and rLWC measured by positron emission tomography. After OA only (n = 16), rLWC increased in dependent lung regions. Some animals responded to increased rLWC by redistribution of rPBF away from the most edematous regions (OA-R, n = 6), whereas others did not (OA-NR, n = 10). In another six animals, meclofenamate was administered after OA (OA-meclo). After OA, tissue concentrations of 6-keto-PGF1 alpha were greater than TxB2 in all groups, but concentrations of 6-keto-PGF1 alpha were not different between OA-R and OA-NR animals. TxB2 was increased in the dependent regions of animals in both OA-R and OA-NR groups compared with controls (no OA, n = 4, P < 0.05). The tissue TxB2/6-keto-PGF1 alpha ratio was smaller in controls and OA-NR in which no perfusion redistribution occurred than in OA-R and OA-meclo in which it did occur. This TxB2/6-keto-PGF1 alpha ratio correlated significantly with the magnitude of perfusion redistribution.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Substrate selectivity of various lipases in the esterification of cis- and trans-9-octadecenoic acid.

The substrate selectivity of numerous commercially available lipases from microorganisms, plants and animal tissue towards 9-octadecenoic acids with respect to the cis/trans configuration of the C=C double bond was examined by the esterification of cis- and trans-9-octadecanoic acid (oleic and elaidic acid respectively) with n-butanol in n-hexane. A great number of lipases studied, e.g. those from Pseudomonas sp., porcine pancreas or Carica papaya, were unable to discriminate between the isomeric 9-octadecenoic acids. However, lipases from Candida cylindracea and Mucor miehei catalysed the esterification of oleic acid 3-4 times faster than the corresponding reaction of elaidic acid and therefore have a high preference for the cis isomer. Of all biocatalysts examined, only recombinant lipases from Candida antarctica favoured elaidic acid as substrate. While the preference of Candida antarctica lipase B for the trans isomer was quite low, Candida antarctica lipase A had an extraordinary substrate selectivity and its immobilized enzyme preparation [Chirazyme L-5 (3) from Boehringer] esterified elaidic acid about 15 times faster than oleic acid.

Bacteria↗
PubMed1988

Synthesis of apolar ecdysone esters by ovaries of the cockroach Periplaneta americana.

Ecdysteroid levels detected by RIA in extracts of mature ovaries from Periplaneta americana increased approximately fourfold (53 +/- 10 to 184 +/- 38 ng/g; +/- SEM, n = 3) on treatment with Helix pomatia "sulphatase" enzymes. HPLC analysis showed that this increase in immunoreactivity resulted from the hydrolysis of six apolar compounds that cochromatographed with the ecdysteroid esters previously shown to be present in newly laid oothecae (A1, A2, A3, A4, A5, and A6; A. J. Slinger, L. N. Dinan, and R. E. Isaac (1986). Insect Biochem. 16 (i), 115-119). Intact ovaries cultured in saline were able to take up [3H]ecdysone from the medium and synthesize ecdysone esters, most of which cochromatographed with immunoreactive peaks from ovaries and oothecae. Crude homogenates and membranes prepared from mature ovaries were also able to esterify ecdysone in vitro. The enzyme activity associated with a high-speed pellet was greatly enhanced by the addition of coenzyme A fatty acyl esters, each reaction resulting in the synthesis of a single major metabolite. The three esters formed on incubating ecdysone with coenzyme A-palmitate, -lineate, and -oleate could be characterized by their retention times on HPLC which were identical to compounds A2, A5, and A6, respectively. These compounds were the three quantitatively important immunoreactive esters found in ovaries and newly laid oothecae. The data presented indicates that ovaries can esterify ecdysone with palmitic, linoleic, and oleic acids and that these apolar derivatives are transferred to the egg. The esters appear to be different from the ecdysone 22-fatty acyl esters that have been isolated from ticks and other insects.

Acyl Coenzyme A↗
PubMed1994

The effect of positive end-expiratory pressure on regional pulmonary perfusion during acute lung injury.

PURPOSE: To determine whether positive end-expiratory pressure (PEEP) would change the altered regional pulmonary perfusion pattern caused by oleic acid (OA)-induced acute lung injury was the aim of this study. Our hypothesis was that fixed intravascular obstruction would not be affected by PEEP, leaving the perfusion pattern unchanged if this was the principal cause of perfusion redistribution after lung injury. METHODS: Regional measurements of pulmonary perfusion and lung water concentration (LWC) were obtained both before and after lung injury and before and after PEEP (10 cm H2O) with the nuclear medicine imaging technique of positron emission tomography after injections of H2 15O in 7 supine anesthetized dogs. Four animals were also treated with meclofenamate to enhance perfusion redistribution after acute lung injury. RESULTS: The application of PEEP before lung injury did not significantly affect the regional perfusion pattern. After administration of OA, LWC increased and fractional flow (without PEEP) decreased to the most edematous lung regions, consistent with perfusion redistribution. With the reapplication of PEEP, the perfusion pattern reverted toward the baseline pattern. The magnitude of this effect was roughly proportional to the effect of PEEP on regional inflation (r = .53), as evidenced by changes in LWC. CONCLUSIONS: The reversibility with PEEP of the perfusion pattern caused by acute lung injury suggests that fixed intravascular obstruction is not the principal determinant of perfusion redistribution after OA-induced injury.

Acute Disease↗
PubMed1983

The effects of low-density lipoprotein and cholesterol on acyl-coenzyme A: cholesterol acyltransferase activity in membranes from cultured human fibroblasts.

Membranes prepared from cultured fibroblasts were assayed for acyl-coenzyme A: cholesterol acyltransferase (ACAT) by a method that relied exclusively on the cholesterol already present on the membranes as the sterol substrate. Changes in membrane ACAT activity during incubation of fibroblasts under a variety of conditions were similar to the changes in the rate of incorporation of oleic acid into cholesteryl esters by the intact cells. The addition of low-density lipoprotein (LDL) to fibroblasts pre-incubated with lipoprotein-deficient serum led to a transient increase in membrane ACAT activity, which reached its peak after 7h and was related to the receptor-mediated uptake and degradation of the lipoprotein by the cells. However, after incubation of the membranes with a cholesterol-rich donor lipoprotein, which resulted in an equilibration of cholesterol between membranes and donor, each preparation exhibited the same activity. In contrast with these effects of LDL, incubation of the cells with non-esterified cholesterol produced a prolonged increase in ACAT activity and an increase in the activity observed after equilibration. Furthermore, ACAT activity in cells grown with linoleic acid was higher, both before and after the addition of LDL, than that of cells grown in normal medium or with palmitate. The increase in activity produced by LDL was also greater, reflecting the greater rate of degradation of LDL by the cells, and was associated with an increase in the activity observed after equilibration with donor. The results suggest that although fibroblasts can increase the amount of active enzyme on their membranes to accommodate an exceptionally high or prolonged supply of cholesterol, under normal circumstances the increase in membrane ACAT activity produced by LDL can be explained entirely by an increase in the amount of cholesterol in the substrate pool.

Acyltransferases↗
PubMedDate not supplied

Inhibition of hydroxymethylglutaryl coenzyme A reductase activity does not affect the secretion rate of apolipoproteins B and AI by CaCo-2 cells.

It is believed that the major mechanisms by which hydroxymethylglutaryl coenzyme A reductase inhibitors lower plasma cholesterol levels are by inducing hepatic low-density lipoprotein (LDL) receptor activity and by decreasing apolipoprotein B (apoB) secretion by the liver. However, the intestine is also an important cholesterogenic organ and the possibility that this class of drugs may alter lipoprotein secretion by the intestine has not been fully studied. The purpose of the present study was to examine the possible role of cholesterol in regulating apoB secretion by the intestine by testing if the suppression of cholesterol synthesis by the reductase inhibitor lovastatin affected the secretion of apoB by CaCo-2 human intestinal cells. Differentiated post-confluent CaCo-2 cells were incubated for 24-72 h in serum-free medium in the presence or absence of 5 microM lovastatin, and the secretion rate of lipids, as well as apoB and apolipoprotein AI (apoAI) into the medium, was measured. Lovastatin markedly inhibited the incorporation of [1-14C]acetate into cholesterol for at least 48 h, lowered the content of esterified cholesterol in cells, and reduced their rate of cholesterol secretion. However, under basal conditions lovastatin had no effect on the secretion rate of apoB. After stimulation of apoB secretion by addition of 0.8 mM oleic acid to the medium, lovastatin did not alter apoB secretion in the first 2 days of incubation, but reduced the content of apoB in media from the 3rd day by 30%. This could not be explained by an increase in the rate of LDL degradation. Furthermore, supplementation with mevalonic acid only reversed about one-half of the effect of lovastatin, suggesting that this effect was at least parly nonspecific or unrelated to inhibition of cholesterol biosynthesis. There was also no specific effect of lovastatin on apoAI secretion. When cells were cultured with [1-14C]acetate for 24 or 72 h, the specific activity of cholesterol in medium at the end of the incubation was the same as in cells, suggesting that cholesterol used for lipoprotein secretion was in equilibrium with bulk cellular cholesterol and was not from a segregated compartment derived from newly synthesized cholesterol. This may explain why apoB secretion by CaCo-2 cells was unaffected by inhibition of cholesterol synthesis with lovastatin.

Acetates↗
PubMed1993

Thromboxane receptor stimulation/inhibition and perfusion redistribution after acute lung injury.

Perfusion redistribution (PR) after acute oleic acid (OA) lung injury may be the result of changes in the tissue concentration ratio of thromboxane (Tx) and prostacyclin (A. H. Stephenson et al. J. Appl. Physiol. 73: 2126-2134, 1992). We tested this hypothesis by determining whether the Tx mimetic U-46619 would mimic PR caused by cyclooxygenase inhibition with meclofenamate and whether the Tx receptor antagonist ONO-3708 would inhibit PR even in the presence of meclofenamate. Measurements of regional pulmonary blood flow (PBF) and lung water concentration were made with the nuclear medicine imaging technique of positron emission tomography. Measurements were made at baseline and 2 h after OA. At baseline, the spatial distribution of PBF was similar in all experimental groups. Two hours after OA, fractional PBF was reduced to the edematous lung in all groups given OA, but the magnitude of change was greater in those groups receiving meclofenamate or U-46619 compared with the change in the group given OA only. Thus, although the Tx mimetic produced the same amount of PR as meclofenamate, Tx inhibition did not prevent PR after meclofenamate. Therefore, the ratio of Tx to prostacyclin per se is not the critical determinant of PR.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Effect of fatty acids and their derivatives on mitochondrial structures.

Reye's Syndrome (RS) is characterized by encephalopathy, fatty degeneration of viscera and high levels of free fatty acids which are implicated in cellular toxicity. We have examined the effects of octanoic acid (C8:0), palmitic acid (C16:0) and oleic acid (C18:1) on rat liver mitochondrial swelling by spectroscopic and microscopic techniques. Of the fatty acids tested oleic acid had a greater effect than palmitic acid while octanoic acid had no effect. Acyl-CoA derivatives produced greater mitochondrial swelling than either acyl-carnitine or free fatty acids. However, identical amounts of palmitoyl-CoA and oleoyl-CoA were required to produce the same degree of swelling. Addition of carnitine (2mM) to oleoyl-CoA reduced the mitochondrial swelling significantly thus suggesting that the toxicity of the fatty acids may be reduced by conversion to their carnitine derivatives. Twice the concentration of oleoyl-carnitine was required to produce half the maximum swelling as compared to oleoyl-CoA. Ultrastructural profiles of mitochondria treated with oleic acid, oleoyl-CoA and oleoyl-carnitine demonstrated greater swelling with oleoyl-CoA than with oleic acid or oleoyl-carnitine. These results suggest that carnitine may protect the mitochondria from damage by the fatty acids and their acyl-CoA derivatives in Reye's Syndrome.

Acyl Coenzyme A↗
PubMed2005

Rho-kinase (ROCK-1 and ROCK-2) upregulation in oleic acid-induced lung injury and its restoration by Y-27632.

The possible contribution of Rho/Rho-kinase signalling in oleic acid (100 mg kg-1, i.v., for 4 h)-induced lung injury was investigated in rats. Furthermore, the possible protective effect of the administration of a Rho-kinase inhibitor, (+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride monohydrate (Y-27632, 0.5-5 mg kg-1, i.v., 15 min before the administration of oleic acid), was also examined. Western blot analysis as well as histopathological examination revealed that Rho-kinase (ROCK-1 and ROCK-2) was upregulated in lungs obtained from oleic acid-administrated rats. In addition, the markers of oxidative and nitrosative stress, i.e., malondialdehyde, myeloperoxidase, 3-nitro-L-tyrosine and nitrite/nitrate, in serum and lung tissue were also increased in the injury group. Treatment of rats with 5 mg kg-1 Y-27632 reversed the oleic acid-induced lung damage, which was demonstrated by histopathological assessment and confirmed in Western blot experiments: ROCK-blots were more intense in the oleic acid group than in control and Y-27632 treatment reversed ROCK upregulation. In addition, malondialdehyde, myeloperoxidase, 3-nitro-L-tyrosine and nitrite/nitrate were also normalized after the administration of Y-27632 (0.5 mg kg-1 and 5 mg kg-1). These findings suggest that ROCK-1 and ROCK-2 are involved in oleic acid-induced lung damage in rats, and that inhibition of this enzyme by Y-27632 may have a protective effect against such damage. Consequently, Rho kinase inhibitors may be potential therapeutic agents in the treatment of acute respiratory distress syndrome (ARDS).

Amides↗
PubMed2002

Inhibition of telomerase by linear-chain fatty acids: a structural analysis.

In the present study, we have found that mono-unsaturated linear-chain fatty acids in the cis configuration with C(18) hydrocarbon chains (i.e. oleic acid) strongly inhibited the activity of human telomerase in a cell-free enzymic assay, with an IC(50) value of 8.6 microM. Interestingly, fatty acids with hydrocarbon chain lengths below 16 or above 20 carbons substantially decreased the potency of inhibition of telomerase. Moreover, the cis-mono-unsaturated C(18) linear-chain fatty acid oleic acid was the strongest inhibitor of all the fatty acids tested. A kinetic study revealed that oleic acid competitively inhibited the activity of telomerase ( K (i)=3.06 microM) with respect to the telomerase substrate primer. The energy-minimized three-dimensional structure of the linear-chain fatty acid was calculated and modelled. A molecule width of 11.53-14.26 A (where 1 A=0.1 nm) in the C(16) to C(20) fatty acid structure was suggested to be important for telomerase inhibition. The three-dimensional structure of the telomerase active site (i.e. the substrate primer-binding site) appears to have a pocket that could bind oleic acid, with the pocket being 8.50 A long and 12.80 A wide.

Binding Sites↗
PubMed1986

Role of histamine in acute oleic acid-induced lung injury.

The action of histamine in oleic acid (OA)-induced injury was investigated using the isolated guinea pig lung perfused with blood-free media. OA infusion caused a significant increase in pulmonary arterial pressure, airway inspiratory pressure, lung weight, and protein flux across the alveolar-capillary barrier. These changes were dose dependent and caused injury regardless of the chemical form of OA (salt or free acid). Triolein (a neutral fat) infused at comparable emulsion particle size did not alter lung weight or bronchoalveolar lavage protein concentration in the perfused lung, suggesting that mechanical obstruction or emboli per se is not responsible for initiating early events in OA-induced injury. Infusion of OA caused a significant early histamine release into the venous effluent in the presence of aminoguanidine, a histamine catabolism inhibitor. Pretreatment with H1-receptor antagonists significantly attenuated OA-induced increase in lung weight and protein leak. These data support the link between OA-induced mast cell degranulation, histamine release, and OA-induced edema.

Animals↗
PubMed1986

Indomethacin and dexamethasone decrease oleic acid-induced pulmonary protein leak in rabbits.

Similarities between oleic acid (OA)-induced pulmonary injury and clinical adult respiratory distress syndrome (ARDS) have resulted in extensive use of this model. Using technetium 99m (Tc-99m)-labeled human serum albumin (Tc-HSA) we examined the effect of indomethacin (a prostaglandin synthetase inhibitor) and dexamethasone (a corticosteroid) alone and in combination on OA-induced pulmonary protein leak. Computer-acquired dynamic gamma camera imaging before (15 min), during, and after (60 min) OA infusion were used to generate time-activity curves for lung and heart regions. A lung:heart activity ratio curve with a positive slope indicates pulmonary capillary protein leak of the labeled substance. Tc-99m labeling of red blood cells followed by OA injury showed no significant change in slope, indicating that lung hemorrhage was not being measured; however, Tc-HSA showed significant protein leakage following OA injury. Pretreatment with indomethacin or dexamethasone did not significantly alter either the preinsult or the postinsult slope. Combined pretreatment with indomethacin and dexamethasone significantly decreased, but did not eliminate, the pulmonary protein leak produced by OA injury. Our results indicate that multiple factors are involved in the production of the pulmonary capillary leak in OA-induced lung injury. In addition to the possible therapeutic efficacy of combined corticosteroids and nonsteroidal antiinflammatory drugs, our results demonstrate that these substances may be useful in defining the pathophysiology involved in permeability pulmonary edema.

Animals↗
PubMed1980

Effect of acute nitrogen dioxide exposure on the composition of fatty acids in lung and liver phospholipids.

In order to examine the effects of NO2 on the fatty acid content of the lung and liver phospholipids, the phospholipid fractions of rats exposed to 20 ppm NO2 for 20 and 40 h were extracted and analyzed using gas chromatography. Among the ftty acid species in the lung, the relative amount of palmitic acid, palmitoleic acid and linoleic acid increased significantly, whereas myristic acid, stearic acid and oleic acid decresed significantly after exposure to NO2. These changes in the composition of fatty acids are discussed in comparison with the results of acute, subacute and chronic exposure to NO2 reported by other workers. In the case of the fatty acid species in the liver, a significant increase for stearic acid and arachidonic acid and a decrease in oleic acid were observed.

Animals↗