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PubMed1987

Fatty acid binding protein in kidney of normotensive and genetically hypertensive rats.

Fatty acid binding protein was purified from renal medulla, and its binding activity and fatty acid composition were determined in spontaneously hypertensive stroke-prone rats (SHRSP). Wistar-Kyoto rats (WKY) were used as controls. Fatty acid binding activity was higher in 5-week-old prehypertensive SHRSP than in control WKY (0.155 +/- 0.006 vs 0.030 +/- 0.001 mol palmitic acid/mol protein). However, in 40-week-old rats, the activity was decreased only in SHRSP with established hypertension (0.035 +/- 0.002 vs 0.028 +/- 0.003 mol palmitic acid/mol protein WKY). Fatty acid compositions were similar among 5-week-old and 40-week-old control WKY and 5-week-old SHRSP (palmitic acid, 24%; stearic acid, 14%; oleic acid, 30%; linoleic acid, 29%; arachidonic acid, 3%), although the total amount of bound long-chain fatty acids was decreased in 5-week-old SHRSP, explaining the high fatty acid binding activity in this preparation. Fatty acid binding protein from 40-week-old SHRSP had an elevated proportion of endogenous arachidonic acid, with other fatty acids being relatively reduced (palmitic acid, 8%; stearic acid, 2%; oleic acid, 4%; linoleic acid, 10%; arachidonic acid, 76%), indicating increased arachidonic acid transport in the cytosol. These results show that genetically hypertensive rats had an alteration in fatty acid transport mediated by fatty acid binding protein; this alteration may be involved in the pathogenesis of hypertension.

Animals↗
PubMed2001

[Comparative studies on the fatty acids contained in four species of medicinal plants from family Euphorbiaceae and their endophytic fungi].

OBJECTIVE: The relation of four species of medicinal plants from family Euphorbiaceae and their endophytic fungi was studied to find the source of active substances for developing new pharmaceutical resources. METHOD: The main fatty acids contained in Sapium sebiferum, Euphorbia pekinensis, Euphorbia helioscopia, Bischofia polycarpam and their 28 strains of endophytic fungi were compared and analysed by GC. RESULT: The main fatty acids of the plants are: alpha-linolenic acid, palmitic acid, linolenic acid and oleic acid. Linolenic acid, palmitic acid and oleic acid are the main fatty acids of the endophytic fungi. CONCLUSION: The fatty acids could be produced by the endophytic fungi, which could be used as a factor for identification. There are great differences at the contents of alpha-linolenic acid between the plants and their endophytic fungi, which were suggested to be related with the nutrition absorption and the relationship between the endophytes and the host plant.

Euphorbia↗
PubMed1987

[Studies on the function of fatty acid binding protein in hypertensive rat kidney].

Fatty acid binding protein was purified from renal medulla, and its binding activity and fatty acid composition were determined in spontaneously hypertensive stroke-prone rats. Wistar-Kyoto rats were used as controls. Fatty acid binding activity was higher in 5-week-old prehypertensive spontaneously hypertensive stroke-prone rats (0.155 +/- 0.006 mol palmitic acid/mol protein) as compared with control values in Wistar-Kyoto rats (0.030 +/- 0.001). However, in 40-week-old rats, the activity was decreased only in spontaneously hypertensive stroke-prone rats with established hypertension (0.035 +/- 0.002), and it did not decrease in Wistar-Kyoto rats (0.028 +/- 0.003). Fatty acid compositions were similar among 5 and 40-week-old control rats and 5-week-old hypertensive rats (palmitic acid 24%, stearic acid 14%, oleic acid 30%, linoleic acid 29%, arachidonic acid 3%), although the total amount of bound long-chain fatty acids was decreased in 5-week-old hypertensive rats, explaining the high fatty acid binding activity in this preparation. Fatty acid binding protein from 40-week-old hypertensive rats had an elevated proportion of endogenous arachidonic acid, with other fatty acids being relatively reduced (palmitic acid 8%, stearic acid 2%, oleic acid 4%, linoleic acid 10%, arachidonic acid 76%), indicating increased arachidonic acid transport in the cytosol. These results show that genetically hypertensive rats had an alteration in fatty acid transport mediated by fatty acid binding protein; this alteration may be involved in the pathogenesis of hypertension.

Animals↗
PubMed2004

Involvement of thromboxane A2 (TXA2) in the early stages of oleic acid-induced lung injury and the preventive effect of ozagrel, a TXA2 synthase inhibitor, in guinea-pigs.

An intravenous injection of oleic acid into animals can produce a lung injury with hypoxaemia and pulmonary vascular hyper-permeability. Although oleic acid lung injury is used as a model of acute respiratory distress syndrome (ARDS), the precise mechanisms of the lung injury are still unclear. We have investigated whether thromboxane A(2) (TXA(2)) participated in the lung injury and have evaluated the efficacy of ozagrel, a TXA(2) synthase inhibitor, on the lung injury in guinea-pigs. Oleic acid injection increased the plasma level of TXB(2), a stable metabolite of TXA(2), and the time-course of plasma TXB(2) was similar to that of the decreased partial oxygen pressure of arterial blood (Pao(2)) induced with oleic acid. Ozagrel administered intravenously 30 min before oleic acid injection prevented the decrease in Pao(2) and pulmonary vascular hyper-permeability. It also prevented increases in lactate dehydrogenase activity, a measure of lung cell injury, TXB(2 )and its weight ratio to 6-keto prostaglandin F(1alpha) in bronchoalveolar lavage fluid. Although ozagrel administered simultaneously with oleic acid ameliorated the decrease in Pao(2), post treatment showed little effect. We suggest that TXA(2) participated in the oleic acid lung injury, as an "early phase" mediator, and rapidly-acting TXA(2) synthase inhibitors were effective in the prevention of acute lung injury.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Method development for the analysis of trans-fatty acids in hydrogenated oils by capillary electrophoresis.

A novel capillary electrophoresis methodology using UV indirect detection (224 nm) for the analysis of trans-fatty acids in hydrogenated oils was proposed. The electrolyte consisted of a pH 7 phosphate buffer at 15 mmol x L(-1) concentration containing 4 mmol.L(-1) sodium dodecylbenzenesulfonate, 10 mmol x L(-1) polyoxyethylene 23 lauryl ether (Brij 35), 2% 1-octanol and 45% acetonitrile. Under the optimized conditions, ten fatty acids, C12:0, C13:0 (internal standard), C14:0, C16:0, C18:0, C18:1c, C18:1t, C18:2cc, C18:2tt and C18:3ccc were baseline-separated in less than 12 min. The proposed methodology was applied to monitor the formation of trans-fatty acids during hydrogenation of Brazilnut oil. A crude oil sample (42.1% linoleic acid, 37.3% oleic acid, 13.4% palmitic acid, and 7.0% stearic acid) was mixed with 0.25% of a nickel-based catalyst and submitted to two independent hydrogenation conditions: 175 degrees C, 3 atm, 545 rpm for 60 min (GH(1) sample), and 150 degrees C, 1 atm, 545 rpm for 30 min (GH(2) sample). For the most severe hydrogenation condition (higher temperature and pressure, under longer reactional period), a more complete conversion of linoleic and oleic acids into stearic acid occurred with concomitant formation of the trans-species, elaidic acid (C18:1t). For the milder hydrogenation procedure that generated sample GH(2), larger amounts of linoleic and oleic acids remained, in addition to the transformations already observed in the GH(1) sample.

Electrophoresis, Capillary↗
PubMed1994

Inhibition of diphosphatidylglycerol synthesis by u.v. A radiations in N.C.T.C. 2544 human keratinocytes.

The effects of u.v. A radiations on phospholipid synthesis were studied in the N.C.T.C. 2544 human keratinocyte cell line, by using [14C]arachidonic acid, [14C]oleic acid or sodium [32P]orthophosphate as precursors. Cells were irradiated in Hanks' medium with 365 nm light at doses up to 19 J/cm2, and then phospholipid synthesis from the three precursors was studied. Under these conditions, only small alterations in the incorporation pattern of [14C]arachidonic into phospholipids [phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylinositol (PI)] were observed, for u.v. A irradiation doses up to 19 J/cm2. In contrast, with [14C]oleic acid as precursor, two additional spots were observed, which co-migrate with pure phosphatidylglycerol (PG) and diphosphatidylglycerol (DPG) standards. The incorporation of [14C]oleic acid into PG and DPG was decreased in a dose-dependent manner after u.v. A exposure, with about 50% and 75% decreases at 9.5 J/cm2 and 19 J/cm2 respectively. As for arachidonic acid incorporation, no significant differences in the synthesis of the major phospholipids (PC, PE, PI) were noted upon u.v. A exposure. The dramatic and selective decrease in PG and DPG syntheses was confirmed with [32P]orthophosphate as precursor. As DPG is a specific component of the mitochondrial inner membrane, it appears that one of the early kinds of damage induced by u.v. A irradiation could be the impairment of mitochondrial functions.

Cardiolipins↗
PubMedDate not supplied

Morphology of oleic acid-induced lung injury. Observations from computed tomography, specimen radiography, and histology.

Previously, we reported that oleic acid infusion in dogs produced a patchy and predominantly peripheral increase in lung density. The present study examines in more detail the morphology of the early stages of development of the oleic acid lesion using computed tomography (CT), specimen radiography, and conventional histology. Dogs were sacrificed 10, 30, 60, and 240 minutes after infusion of oleic acid (.05 ml/kg). After freezing in dry-ice, the thorax was scanned and cut into 1-cm thick sections. Frozen sections were then contact radiographed and sampled for histology. Within 10 minutes of infusion, subtle increases in peripheral lung density were visible on the contact radiographs. Patchy areas of peripheral density, resembling secondary lobules, were especially prominent 60 and 240 minutes after infusion. These lesions were often clearly associated with the distal bronchovascular structures. Histologic signs of edema were present in all animals sacrificed 30 or more minutes after receiving oleic acid. These correlative studies provide additional insight into the early subgross development of oleic acid-induced injury by showing the relationship between the developing edema and the bronchovascular structure of the lung.

Animals↗
PubMed1995

Recognition system for dietary fatty acids in the rat small intestine.

Linoleic acid and oleic acid markedly increased the influx of 45Ca into isolated intestinal epithelial cells, and this increase reflected a rise in the intracellular calcium level. Methyl linoleate had no effect, while glutamic acid and somatostatin both inhibited the linoleic acid-induced influx of 45Ca. In addition, methyl linoleate had no effect, while glutamic acid inhibited linoleic acid-induced hormone-responsive pancreatic exocrine secretion.

Animals↗
PubMed1990

Phosphatidylcholine stimulates the activity of UDP-Gal beta 1-4 galactosyltransferase in normal human kidney proximal tumour cells.

Effects of various lipid components of low density lipoproteins (LDL) and serine on the regulation of UDP-Gal-beta 1-4-galactosyltransferase (GalT-2) activity have been investigated in normal proximal tubular (PT) cells. Addition of exogenous serine (0.1-0.75 mM), cholesterol (0-200 micrograms/ml medium), linoleic acid and oleic acid (0.1-0.75 mM) for 4 hr at 37 degrees C did not suppress the activity of GalT-2 in PT cells. Similarly, incubation of cells with glucosylceramide and lactosylceramide (25-50 micrograms/ml medium) did not alter GalT-2 activity in cells as compared to control. In contrast, palmitic acid (0-0.75 mM), phosphatidylethanolamine and sphingomyelin (0-200 micrograms/ml) stimulated GalT-2 activity by 20-36% as compared to control. Incubation of PT cells with D-alpha-dipalmitoyl phosphatidylcholine (0-200 micrograms/ml medium) also stimulated the activity of GalT-2, maximum stimulation (200%) occurring with 25 micrograms phosphatidylcholine/ml medium. However, at a higher concentration (200 micrograms/ml), the stimulation of the activity of GalT-2 was in the order of 27% compared to control. Dioleylphosphatidylcholine did not alter GalT-2 activity in PT cells. Thus, it is concluded that (i) various lipid components, sphingosine and serine present in LDL are not involved in the LDL-mediated suppression of GalT-2 activity in normal PT cells, and (ii) stringent structural requirements in the phosphatidylcholine molecule are necessary to exert a time and concentration dependent stimulation of GalT-2 activity.

Cells, Cultured↗
PubMed1986

Oleic acid-induced cholelithiasis in rabbits. Changes in bile composition and gallbladder morphology.

Feeding oleic acid to rabbits resulted in a progressive rise in bile concentration of allodeoxycholic acid, expansion of the bile salt pool, and depression of de novo hepatic bile acid synthesis. There was also an increase in cholesterol saturation in bile. The gallstones that formed contained traces of cholesterol but were composed mainly of salts of allodeoxycholic acid. The data suggest that oleic acid feeding results in increased rate of cholestanol and allodeoxycholic acid metabolism. Morphologically, these biochemical events were accompanied by early reactive changes in the gallbladder epithelium characterized by marked increase in cell proliferation and mucus hypersecretion. In addition, there was the early formation of interepithelial cell vacuoles and, later, Rokitansky-Aschoff sinuses. These cellular reactions reflect the dramatic and important changes that take place in the gallbladder before gallstone formation.

Administration, Oral↗
PubMed1998

Divergent incorporation of dietary trans fatty acids in different serum lipid fractions.

Trans fatty acids may be involved in atherosclerotic vascular diseases. We investigated the incorporation of dietary trans fatty acids and oleic acid into the serum triglycerides (TG), cholesterol esters (CE), and phospholipids (PL). Fourteen healthy female volunteers, aged 23.2+/-3.1 yr (mean+/-SD), body mass index 20.8+/-2.1 kg/m2 participated in this study. All subjects consumed both a trans fatty acid-enriched diet (TRANS diet) and an oleic acid-enriched diet (OLEIC diet) for 4 wk according to a randomized crossover design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 wk which supplied 37% of total energy (E%) as fat: 18 E% from saturated fatty acids (SFA), 12 E% from monounsaturated fatty acids, and 6 E% from polyunsaturated fatty acids. Five E% of the SFA in the baseline diet was replaced by trans fatty acids (18:1t and 18:2c,t + 18:2t,t, where c is cis and t is trans) in the TRANS diet and by oleic acid (18:1n-9) in the OLEIC diet. After the TRANS diet, the proportions of 18:1t and 18:2t increased (P<0.001) in all serum lipid fractions analyzed. The increase of 18:1t in TG and PL (1.80+/-0.28 vs. 5.26+/-1.40; 1.07+/-0.34 vs. 3.39+/-0.76 mol% of total fatty acids, respectively) was markedly higher than that in CE (0.44+/-0.07 vs. 0.92+/-0.26), whereas that of 18:2t was nearly the same in all three fractions. The proportions of palmitic, stearic, arachidonic, and eicosapentaenoic acids in TG, CE, and PL and that of oleic acid in TG and CE were decreased when compared with the baseline value. In contrast, the proportion of palmitoleic acid in TG and PL and that of linoleic acid in PL increased on the TRANS diet. After consumption of the OLEIC diet, the proportion of oleic acid increased in all three lipid fractions analyzed, and the percentage increase was nearly the same in all fractions. In contrast, the proportions of 18:1t in TG and PL and 18:2t in TG and CE decreased when compared with the baseline value. In conclusion, a moderate increase in dietary trans fatty acids resulted in a marked incorporation into serum lipids and decreased the conversion of linoleic acid to its more unsaturated long-chain metabolites. Analysis of 18:1t from serum TG and PL seems to reflect reliably the dietary intake of this fatty acid.

Adult↗
PubMed1993

Disparity of in vitro and in vivo oleic acid-enhanced beta-estradiol percutaneous absorption across human skin.

The permeation enhancing property of 5% oleic acid in ethanol on beta-estradiol was investigated in vitro and in vivo using symmetrical and asymmetrical side-by-side diffusion cells and the human skin sandwich flap, respectively. beta-Estradiol permeability in vitro and in vivo was similar in 75% ethanol (ETOH). Oleic acid (5%) did not alter beta-estradiol permeability in vivo but increased permeability six-fold in vitro in symmetrical diffusion cells. beta-Estradiol permeability in oleic acid was not different from that in ETOH, however, using asymmetrical diffusion cells. Stratum corneum-to-vehicle partition coefficients of beta-estradiol in the vehicles were similar, yet fourfold more steroid was detected in skin biopsies from the in vitro symmetrical diffusion cells. Thus, oleic acid increased beta-estradiol permeability in vitro only when skin was equilibrated with fatty acid. Attention to in vitro diffusion cell design and its relevance in vivo is critical to defining the mechanisms of enhanced solute permeation.

Administration, Cutaneous↗
PubMed2003

Endothelin receptor blockade in canine oleic acid-induced lung injury.

OBJECTIVE: To investigate the effects of endogenous endothelins on pulmonary haemodynamics and gas exchange in oleic acid lung injury. DESIGN: Prospective experimental study in dogs. SETTING: Animal research laboratory in a university teaching hospital. SUBJECTS. Seventeen anaesthetised and ventilated mongrel dogs. INTERVENTIONS: Nine pretreated dogs received an infusion of the endothelin A and B receptor antagonist bosentan (10 mg/kg) started before oleic acid. Eight treated dogs received bosentan started 90 min after oleic acid. Cardiac index (CI) was manipulated by inflating an inferior vena caval balloon or by opening a femoral arterio-venous bypass. MEASUREMENTS AND RESULTS: Pulmonary vascular resistance was defined by measuring the gradient between mean pulmonary artery pressure (MPAP) and occluded PAP (PAOP) at five levels of CI. Intrapulmonary shunt was measured using the inert gas SF(6). Pretreatment with bosentan prevented the oleic acid-induced shift of (MPAP-PAOP)/CI plots to higher pressures, but did not affect the increase in intrapulmonary shunt. Treatment of established oleic acid lung injury with bosentan had no effect. CONCLUSIONS: Pretreatment, but not treatment, with bosentan, in the dose used, blunted the oleic acid-induced increase in pulmonary vascular resistance, suggesting that endothelins contribute to the increase in pulmonary vascular tone in the early stages of oleic acid lung injury.

Animals↗
PubMed1999

Fatty acid metabolism in human breast cancer cells (MCF7) transfected with heart-type fatty acid binding protein.

The human breast cancer cell line MCF7 does not express heart-type fatty acid binding protein (H-FABP), a marker protein for differentiated mammary gland. MCF7 cells transfected with the bovine H-FABP cDNA expressed the corresponding protein and were characterized by growth inhibition and lower tumorgenicity in nude mice [22]. By enzyme linked immunoassay we now determined the amount of bovine H-FABP in these cells as 638 +/- 80 ng/mg protein and used the transfected cells to study the role of H-FABP in fatty acid metabolism. Compared to control cells the uptake of radioactively labelled palmitic acid and oleic acid into MCF7 cells after 30 or 60 min was increased by 67% in H-FABP expressing transfectants, demonstrating a stimulatory role for this FABP-type in fatty acid metabolism. However, preferential targeting of [14C]oleic acid into neutral or phospholipid classes was not observed by the criterion of high performance thin layer chromatography followed by autoradiography. A reason for the modest increase of fatty acid uptake in H-FABP transfected MCF7 cells may be the basal expression of epidermal-type FABP, which was detected for the first time in these cells. It appears that the small amount of E-FABP expressed in MCF7 cells fulfils the need of the cells for a cytosolic fatty acid carrier under culture conditions and that even high concentrations of another FABP do only slightly increase the uptake due to limitations of fatty acid transport through the plasma membrane or of metabolism.

Animals↗
PubMed1998

Activation of polymorphonuclear leukocytes in oleic acid-induced lung injury.

OBJECTIVE: Oleic acid (OA) can produce a lung injury similar to the adult respiratory distress syndrome (ARDS). Elastase and superoxides are thought to have an effect in ARDS. However, the effect that elastase and superoxide have in OA lung injury is unclear. To examine their involvement in OA lung injury, we tested the effects of methoxysuccinyl-alanyl-alanyl-prolyl-valyl chloromethyl ketone (MAAPVCK), an elastase inhibitor, and N-acetyl-L-cysteine (NAC), an active oxygen scavenger, on the increase in pulmonary vascular permeability caused by OA. We also examined whether OA stimulated elastase and/or superoxide release from polymorphonuclear leukocytes (PMNs). DESIGN: Prospective trial. SETTING: University laboratory. INTERVENTIONS: (1) Guinea pigs were anesthetized. MAAPVCK (2.5 mg/ kg) or NAC (150 mg/kg) was infused over OA (15 microl/kg) injection. Evans blue was used to measure vascular permeability. (2) PMNs were isolated from the blood of guinea pigs and rats. Elastase release was measured with MeO-Suc-Ala-Ala-Pro-Val-7-amino-4-methylcoumarin. Superoxide production was measured by the ferricytochrome c reduction method. MEASUREMENTS AND RESULTS: OA caused pulmonary hemorrhage and an increase in vascular permeability. MAAPVCK and NAC significantly attenuated the increase in vascular permeability in distal bronchus and trachea, respectively. OA induced superoxide production from PMNs in guinea pigs, but elastase release from PMNs was not detected. CONCLUSIONS: These results suggest that elastase and superoxide are involved in OA lung injury.

Acetylcysteine↗
PubMed2002

The synthesis of short- and medium-chain-length poly(hydroxyalkanoate) mixtures from glucose- or alkanoic acid-grown Pseudomonas oleovorans.

Pseudomonas oleovorans NRRL B-778 accumulated mixtures of poly-3-hydroxybutyrate (PHB) and medium-chain-length poly(hydroxyalkanoates) (mcl-PHAs) when grown on glucose, octanoic acid or oleic acid, whereas growth on nonanoic acid or undecanoic acid resulted in copolymers of poly-3-hydroxybutyrate-co-3-hydroxyvalerate (PHB-co-HV). Acetone fractionation verified the presence of PHB/mcl-PHA mixtures. The acetone-insoluble (AIS) fractions of the polymers derived from glucose (PHA-glucose), octanoic acid (PHA-octanoic) and oleic acid (PHA-oleic) were exclusively PHB while the acetone-soluble (AS) fractions contained mcl-PHA composed of differing ratios of 3-hydroxy-acid monomer units, which ranged in chain length from 6 to 14 carbon atoms. In contrast, both the AIS and AS fractions from the polymers derived from nonanoic acid (PHA-nonanoic) and undecanoic acid (PHA-undecanoic) were composed of comparable ratios of 3-hydroxybutyrate (3HB) and 3-hydroxyvalerate (3HV). The unfractionated PHA-glucose, PHA-octanoic and PHA-oleic polymers had melting temperatures (Tm) between 177 and 179 degrees C, enthalpies of fusion (AHf) of 20 cal/g and glasstransition temperatures (Tg) of 3-4 degrees C. This was due to the large PHB content in the polymer mixtures. On the other hand, the PHA-nonanoic and PHA-undecanoic polymers had thermal properties that supported their copolymer nature. In both cases, the Tm values were 161 degrees C, deltaHf values were 7 cal/g and Tg values were - 3 degrees C.

Fermentation↗
PubMed1981

Interactions between permeability and hydrostatic pressure in perfused dogs' lungs.

To evaluate interactions between increased permeability of the pulmonary vasculature and increased hydrostatic pressure on lung fluid flux, we measured water and blood contents of five equally thick slices of in situ perfused dogs' lungs that had been vertically suspended and, after experimental manipulations, rapidly frozen. Measurements were made under four sets of conditions (4 dogs each): 1) control; 2) increased left atrial pressure (Pla), 25 cmH2O relative to the bottom of the lung; 3) oleic acid; and 4) oleic acid and increased Pla. Significant interactions on lung water content were found between 1) oleic acid and increased Pla (P less than 0.005) and 2) oleic acid and height of the slice of lung (P less than 0.003). Blood content was significantly affected by interactions between 1) oleic acid and height of the lung slice (P less than 0.001) and 2) increased Pla and height of the lung slice (P less than 0.001). We conclude that there are significant interactions between increased permeability and hydrostatic pressure that affect regional lung water content and intrapulmonary distribution of blood.

Animals↗
PubMed2004

N-acetylcysteine inhibits peroxynitrite-mediated damage in oleic acid-induced lung injury.

Since oleic acid (OA) induces morphologic and cellular changes similar to those observed in human acute lung injury (ALI) and acute respiratory distress syndrome, it has become a widely used model to investigate the effects of several agents on pathogenesis of lung injury. The antioxidant and anti-inflammatory properties of N-acetylcysteine (NAC) has been documented in many lung injury models. In this study, we evaluated the role of NAC in an OA-induced lung injury model by measuring myeloperoxidase (MPO) activity, malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels in lung tissue. Five groups labelled Sham, NAC, OA, Pre-OA-NAC and Post-OA-NAC were determined. ALI was induced by intravenous administration of OA. The pre-OA-NAC group received iv NAC 15 min before OA infusion and the post-OA-NAC group received iv NAC 2 h after OA infusion. In both of the NAC treatment groups' blood and tissue samples were collected 4 h after OA infusion, independent from the time of NAC infusion. The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in OA group and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (p = 0.0001) Lung histopathology was also affected by NAC in this OA-induced experimental lung injury model.

Acetylcysteine↗