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Stable and reproducible porcine model of acute lung injury induced by oleic acid.

BACKGROUND AND METHODS: Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (SVO2) and arterial oxygen saturation (SaO2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. RESULTS: During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, SaO2, and SVO2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in SaO2, SVO2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables. CONCLUSION: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion.

Animals↗

Efficient synthesis of 3-trifluoromethylphenyldiazirinyl oleic acid derivatives and their biological activity for protein kinase C.

3-trifluoromethylphenyldiazirine based oleic acids derivatives are synthesized to elucidate the functions of specific activation of protein kinase C (PKC) with oleic acid. The synthetic route is based on the alkylation of phenolic derivative with oleic acid equivalent and the post-functionalization of the compound to achieve radiolabeling. Several compounds have biological activity for PKC with similar efficacy with that of oleic acid. The results indicated that the diaizinyl oleic acid derivatives should be useful to study the specific functions of oleic acid for PKC.

Aziridines↗

Conversion of oleic acid to 10-hydroxystearic acid by two species of ruminal bacteria.

Bacteria able to convert oleic acid to 10-hydroxystearic acid were isolated from the ovine rumen. The solid hydroxy fatty acid produced from bacterial fermentations containing oleic acid was recovered by filtration, extraction into ether and crystallisation. The identity of the product was confirmed by HPLC and gas chromatography/mass spectrometry. One 10-hydroxystearic-acid-producing bacterial group was represented by two strains of an anaerobic gram-negative curved rod with tufts of flagella on the concave surface of the cell. The morphology and other characteristics enabled the strains to be tentatively identified as Selenomonas ruminantium. Another bacterium capable of the same transformation, represented by two strains of a facultatively anaerobic gram positive chain-forming coccus, was identified as Enterococcus faecalis. Since unsaturated fatty acids entering the rumen are normally hydrogenated, hydration of oleic acid represents an alternative fate of unknown significance in vivo.

Animals↗

Effects of triolein or oleic acid on lymphatic recovery of docosahexaenoic acid given as ethyl ester and their intramolecular distribution in lymph triglyceride of rats.

Effects of oleic acid or triolein on lymphatic recovery of docosahexaenoic acid (DHA) given as an ethyl ester were examined in rats with cannulated thoracic ducts. Lymphatic recovery of ethyl DHA given with oleic acid or triolein was significantly higher than in rats given ethyl DHA alone. DHA distributed almost exclusively at the 1- and 3-position of triglyceride in lymph collected at 0-3 h after the administration, when it was given with oleic acid or triolein. A small part of DHA distributed at the 2-position when ethyl DHA was the sole fatty acid given. Oleic acid given as free acid or triolein with ethyl DHA was a major fatty acid at the 2-position. Intramolecular distribution of DHA and oleic acid in lymph triglyceride was similar when ethyl DHA was given with oleic acid or triolein.

Absorption↗

Cardiovascular and blood gas responses to ketanserin in canine pulmonary edema induced by oleic acid.

This study was performed to determine the cardiovascular and respiratory effects of ketanserin, a specific 5-HT2 antagonist, following oleic acid lung injury in anesthetized dogs. Following intravenous administration of oleic acid (0.1 ml/kg) to a control group (N = 7), systemic blood pressure decreased significantly. This lowered level of systemic blood pressure was maintained throughout the experiment. Cardiac output gradually decreased following oleic acid administration, while total peripheral resistance, pulmonary vascular resistance, and pulmonary arterial pressure were increased significantly. In a group treated with intravenous ketanserin (0.16 mg/kg, N = 7) 60 min after the injection of oleic acid, no decrease in cardiac output was seen. The increased total peripheral resistance, pulmonary vascular resistance, and pulmonary arterial pressure following injection of oleic acid also were returned toward preoleic acid levels. However systemic blood pressure showed no significant improvement after treatment with ketanserin nor did ketanserin protect against progressive hypoxemia following pulmonary injury with oleic acid. A progressive increase in hemoglobin concentration was seen after oleic acid in the control group. This recovered toward the preoleic acid level following treatment with ketanserin. The postmortem lung wet-dry weight ratio was significantly lower in the treated group compared with the control group. In conclusion, these data suggest that serotonin may have a role in including cardiopulmonary hemodynamic disturbances and in producing increases in extravascular lung water when pulmonary edema is induced by oleic acid injection in anesthetized dogs.

Animals↗

Translocation of oleic acid across the erythrocyte membrane. Evidence for a fast process.

To clarify divergent views concerning the mechanism of fatty acid translocation across biomembranes this issue was now investigated in human erythrocytes. Translocation rates of exogenously inserted radioactive oleic acid across the membrane of native cells were derived from the time-dependent increase of the fraction of radioactivity becoming non-extractable by albumin. No accumulation of non-extractable unesterified oleic acid occurred. The rate of transfer was markedly suppressed by SH-reagents and by ATP-depletion. The suppression, however, resulted from a mere decrease of incorporation of oleic acid into phospholipids and was not accompanied by an increase of non-extractable unesterified oleic acid. These findings were reconcilable with the concept of a slow, possibly carrier-mediated fatty acid transfer as well as a very fast presumably, diffusional process not resolvable by the albumin extraction procedure. This ambiguity was resolved by using resealed ghosts, which are unable to incorporate oleic acid into phospholipids. In such ghosts all of the oleic acid inserted into the membrane remains extractable by albumin even after prolonged incubation. On the other hand, ghosts containing albumin accumulated non-extractable oleic acid. The rate of accumulation was beyond the time resolution of the albumin extraction procedure at 4 degrees C. Oleic acid uptake into albumin-containing ghosts became kinetically resolvable when the fatty acid was added as a complex with albumin. Correspondingly, time-resolvable release of oleic acid, originally complexed to internal albumin, into an albumin-containing medium was demonstrated at 4 degrees C. Rate and extent of these redistributions of oleic acid were dependent on the concentrations of internal and external albumin. This indicates limitation by the dissociation of oleic acid from albumin and not its translocation across the membrane. Translocation of oleic acid, which is probably a simple diffusive flip-flop process, must therefore occur with a half-time of less than 15 s. These findings raise doubts on the physiological role of presently discussed concepts of a carrier-mediated translocation of fatty acids across plasma membranes.

Acyl Coenzyme A↗

The neurotrophic effect of oleic acid includes dendritic differentiation and the expression of the neuronal basic helix-loop-helix transcription factor NeuroD2.

We have shown recently that the presence of albumin in astrocytes triggers the synthesis and release of oleic acid, which behaves as a neurotrophic factor for neurons. Thus, oleic acid promotes axonal growth together with the expression of the axonal growth-associated protein, GAP-43. Here we attempted to elucidate whether the neurotrophic effect of oleic acid includes dendritic differentiation. Our results indicate that oleic acid induces the expression of microtubule associated protein-2 (MAP-2), a marker of dendritic differentiation. In addition, the presence of oleic acid promotes the translocation of MAP-2 from the soma to the dendrites. The time course of MAP-2 expression during brain development coincides with that of stearoyl-CoA desaturase, the limiting enzyme of oleic acid synthesis, indicating that both phenomena coincide during development. The effect of oleic acid on MAP-2 expression is most probably independent of autocrine factors synthesized by neurons because this effect was also observed at low cellular densities. As oleic acid is an activator of protein kinase C, the possible participation of this transduction pathway was studied. Our results indicate that added oleic acid or oleic acid endogenously synthesized by astrocytes exerts its neurotrophic effect through a protein kinase C-dependent mechanism as the effect was inhibited by sphingosine or two myristoylated peptide inhibitors of protein kinase C. The transduction pathway by which oleic acid induces the expression of genes responsible for neuronal differentiation appears to be mediated by the transcription factor NeuroD2, a regulator of terminal neuronal differentiation.

Animals↗

[Intraenterocytic metabolism and blood uptake of caproic and oleic acids in control and actidione-cycloheximide-treated rats].

Intestinal absorption of capric and oleic acids from the intestinal lumen into mesenteric portal vein blood was investigated in control and actidione-cycloheximide-treated rats using the ex vivo vascular perfusion technique. The measurement of 14C-labeled lipids, 14CO2 and 14C-labeled acid-soluble products was simultaneously carried out with blood collected at 5-min intervals for 60 min. The enterocyte catabolism of capric and oleic acids, one of which was preferentially absorbed via the blood, has been interpreted by the different processes of absorption. The greater enterocyte catabolic activity with capric acid, compared to oleic acid, could be related to the slight affinity of FABP Z for this medium-chain fatty acid and also to lack of capric acid esterification; a non-negligible fraction of this fatty acid actually disappeared from the lumen and was catabolized into the enterocyte at an early stage of its absorption. The actidione-cycloheximide treatment affected oleic acid absorption via the blood to a greater degree than that of capric acid. But it modified both intestinal blood absorption and the catabolism of the two fatty acids in the same manner.

Animals↗

Increased liver oleic acid synthesis in cholesterol-fed rabbits.

Several investigators have observed increased levels of esterified oleic acid in tissue cholesterol esters and phospholipids of atherosclerotic humans and cholesterol-fed animals. However, the cause of this is still unknown. Increased synthesis, increased esterification, or both of oleic acid can account for this. In the present investigation, hepatic synthesis of oleic acid is studied in cholesterol-fed rabbits. A nearly 3-fold increase in oleic acid synthesis was observed after 3 weeks of cholesterol feeding. This increase continued for at least 6 weeks. Since acyl acceptors like glycerol-3-phosphate are known to increase liver oleic acid synthesis it is possible that the observed increased in oleic acid formation was partially due to an increased availability of acyl acceptors in the system.

Animals↗

Fibrinogen depletion and control of permeability in oleic acid lung injury.

To determine if the biphasic pulmonary clearance of aerosolized 99mTc diethylene penta acetate (99mTc-DTPA) observed in oleic acid lung injury represents acute epithelial damage followed by sealing as a result of intra-alveolar fibrin deposition, we examined the effect of fibrinogen depletion. 99mTc-DTPA clearance was assessed in three groups of rabbits: Group 1, normal fibrinogen + oleic acid injury; Group 2, fibrinogen-depleted + oleic acid injury; Group 3, fibrinogen-depleted with no oleic acid injury. In Group 3 animals with no lung injury, the 99mTc-DTPA clearance rate, expressed as k, the percent decrease in thoracic radioactivity, was similar to that previously reported for healthy rabbits (k = 1.16 +/- 0.57%/min, mean +/- SD). Oleic acid administration to Groups 1 and 2 resulted in significantly faster clearance rates, with identical biphasic curves in all animals, irrespective of fibrinogen status. There were no significant differences between either the initial fast phase (k, Group 1 = 5.26 +/- 1.83%/min, Group 2 = 5.70 +/- 1.77%/min) or the subsequent slow phase (k, Group 1 = 1.67 +/- 0.63%/min, Group 2 = 1.57 +/- 0.55%/min, p greater than 0.05). On histologic examination, Groups 1 and 2 showed greater cellular interstitial infiltrate, alveolar edema, and hemorrhage than did Group 3. Fibrinogen depletion plus oleic acid injury resulted in greater alveolar cellular exudate, edema, and hemorrhage than did either oleic acid or fibrinogen depletion alone. We conclude that fibrinogen is not necessary to produce biphasic 99mTc-DTPA clearance in oleic acid lung injury.

Animals↗

NTP Toxicology and Carcinogenesis Studies of Oleic Acid Diethanolamine Condensate (CAS No. 93-83-4) in F344/N Rats and B6C3F1 Mice (Dermal Studies).

Oleic acid diethanolamine condensate is widely used as an emollient, thickener, and foam stabilizer present in cosmetic formulations of bath additives, shampoos, conditioners, lipsticks, and hair dyes. Male and female F344/N rats and B6C3F1 mice received dermal applications of diethanolamine in 95% ethanol for 13 weeks or 2 years. Genetic toxicology studies were performed in Salmonella typhimurium and L5178Y mouse lymphoma cells. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats were admin istered 0, 25, 50, 100, 200, or 400 mg oleic acid diethanolamine condensate/kg body weight in ethanol dermally for 13 weeks. All male and female rats survived until the end of the study. The final mean body weights and body weight gains of 200 and 400 mg/kg males and the mean body weight gain of 400 mg/kg females were significantly less than those of the vehicle controls. The only chemical-related clinical finding was irritation of the skin at the site of application in most males administered 100 mg/kg or greater and in all females administered 50 mg/kg or greater. Segmented neutrophil counts were increased relative to the vehicle controls in the 400 mg/kg male group on days 5 and 19, in the 200 mg/kg female group on day 19 and at week 13, and in the 400 mg/kg female group on days 5 and 19 and at week 13. Alkaline phosphatase concentrations were significantly increased in the 200 mg/kg male group on day 19, the 200 mg/kg female group at week 13, and in the 400 mg/kg groups of males and females at week 13. Kidney weights of 200 and 400 mg/kg females were significantly greater than those of the vehicle controls. Lesions of the skin at the site of application included epidermal hyperplasia, parakeratosis, chronic active dermal inflammation, suppurative epidermal inflammation, and sebaceous gland hypertrophy in dosed rats. The severities of these lesions generally increased with increasing dose. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice were admin istered 0, 50, 100, 200, 400, or 800 mg oleic acid diethanolamine condensate/kg body weight in ethanol dermally for 13 weeks. All male and female mice except one 800 mg/kg male survived until the end of the study. Final mean body weights and body weight gains of 800 mg/kg males and females and 400 mg/kg females were significantly less than those of the vehicle controls. Clinical findings in dosed mice included irritation of the skin at the site of application. Irritation occurred in all surviving dosed males and in most females administered 100 mg/kg or greater and progressed to ulcer in one 800 mg/kg male. The heart weights of 400 and 800 mg/kg males and females and 200 mg/kg females and the kidney weights of 50, 100, and 400 mg/kg males were significantly greater than those of the vehicle controls. Relative to the vehicle controls, the liver weights were increased in all dosed groups. Lesions of the skin at the site of application in dosed mice included epidermal hyperplasia, parakeratosis, suppurative epidermal inflammation, chronic active dermal inflammation, sebaceous gland hypertrophy, and ulcer. The severities of these lesions generally increased with increasing dose. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were administered 0, 50, or 100 mg oleic acid diethanolamine condensate/kg body weight in ethanol dermally for 2 years. Survival, Body Weights, and Clinical Findings: Survival of dosed male and female rats was similar to that of the vehicle control groups. Mean body weights of 100 mg/kg males were slightly less than those of the vehicle controls throughout most of the study. Mean body weights of 100 mg/kg females were less than those of the vehicle controls beginning at week 24. The only significant treatment-related clinical finding was mild to moderate irritation of the skin at the site of application in dosed males and females. Pathology Findings: The predominant effects of oleic acid diethanolamine condensate administration were minimal to moderate nonneoplastic lesions of the skin at the site of application in dosed rats. These lesioe lesions included epidermal hyperplasia, sebaceous gland hyperplasia, hyperkeratosis, parakeratosis, chronic active dermal inflammation, and ulcer. 2-YEAR STUDY IN MICE: Groups of 55 male and 55 female mice were administered 0, 15, or 30 mg oleic acid diethanolamine condensate/kg body weight in ethanol dermally for 2 years. Five animals from each group were evaluated at 3 months for gross lesions and skin histopathology. Survival, Body Weights, and Clinical Findings: Survival of dosed male and female mice was similar to that of the vehicle control groups. Mean body weights of dosed males and of 15 mg/kg females were similar to those of the vehicle controls throughout the study. Mean body weights of 30 mg/kg females were less than those of the vehicle controls from week 76 until the end of the study. The only significant treatment-related clinical finding was irritation of the skin at the site of application in 30 mg/kg males. Pathology Findings: The incidences of epidermal hyperplasia, sebaceous gland hyperplasia, and chronic active inflammation of the dermis in all dosed groups were significantly increased relative to the vehicle controls at 3 months and at 2 years. The increased incidences of hyperkeratosis in dosed males at 3 months and in dosed males and females at 2 years, of parakeratosis in 30 mg/kg males at 3 months and 2 years, and of ulcer in 30 mg/kg males and exudate in 30 mg/kg males and females at 2 years were also attributed to chem ical administration. GENETIC TOXICOLOGY: Oleic acid diethanolamine condensate was not mutagenic in S. typhimurium strain TA97, TA98, TA100, or TA1535, with or without S9 metabolic activation enzymes. In addition, it did not induce mutations in mouse L5178Y lymphoma cells treated with or without S9. CONCLUSIONS: Under the conditions of these 2-year dermal studies, there was no evidence of carcinogenic activity of oleic acid diethanolamine condensate in male or female F344/N rats administered 50 or 100 mg/kg or in male or female B6C3F1 mice administered 15 or 30 mg/kg. Dermal administration of oleic acid diethanolamine condensate to male and female rats was associated with epidermal hyperplasia, sebaceous gland hyper plasia, hyperkeratosis, parakeratosis, chronic active inflammation of the dermis, and ulceration of the skin at the site of application. Dermal administration of oleic acid diethanolamine condensate to mice was associated with epidermal hyperplasia, sebaceous gland hyperplasia, hyperkeratosis, chronic active inflammation of the dermis, and exudate of the skin at the site of application in males and females and parakeratosis and ulcer of the skin at the site of application in males. Synonyms: Diethanolamine oleate; diethanolammonium oleate; (Z)-9-octadecenoic acid, compound with 2,2.-imnobis(ethanol) (1:1); oleamide diethanolamine

Journal Article↗

Effects of oleic acid infusion on plasma free fatty acids and blood ketone bodies in the fasting rat.

Oleic acid emulsions stabilized with albumin were infused into fasted rats. Blood samples taken before and during infusion were analyzed for free fatty acids (FFA), ketone bodies, glucose, and insulin. Turnover rates of FFA and ketone bodies were also determined using constant infusion of radioactive tracers. During oleic acid infusions at a rate of 2 mumoles/min/100 g body weight, FFA concentrations increased for a short time and then decreased to preinfusion levels. The decreases in concentrations were due to decreases in the endogenous rates of appearance of FFA into the blood. When oleic acid was infused at a rate of 3.5 mumoles/min/100 g body weight, FFA concentrations increased and remained elevated throughout the infusion. Ketone body concentrations more than doubled during infusions at 2 and 3.5 mumoles/min/100 g body weight and showed no signs of decreasing even when FFA concentrations decreased. Insulin concentrations doubled during infusion and glucose concentrations decreased. Insulin injected during infusion had little effect on concentrations of FFA or ketone bodies. It was concluded that infusions of oleic acid inhibit adipose tissue lipolysis and increase blood ketone concentrations in intact fasted rats. The injection of insulin does not inhibit ketogenesis when blood FFA levels are maintained by infusion.

Animals↗

Effects of oleic acid and bile salts on canine villous motility.

The effects on canine villous motility of mucosal Tyrodes solution containing oleic acid (10 mM) and/or either taurocholic or cholic acid (15 mM) in the presence or absence of IV atropine (1 mg/kg) was used to assess the neural mediation of the effects of luminal nutrients. Villous motility was measured over 12 min periods by in vivo videomicroscopy of segments of jejunum. Neither bile salt had effects alone but villous motility increased after oleic acid was added to taurocholate and decreased after oleic acid was added to cholate. Villous motility increased when taurocholate and oleic acid were present initially and returned to control levels when removed. Villous motility was not affected by cholate and oleic acid but villous motility decreased when they were removed from the Tyrodes solution. Atropine blocked the increase in villous motility caused by taurocholate and oleic acid. Bile salts can modify the effect of oleic acid on villous motility and a cholinergic step is involved in the stimulation of motility.

Animals↗

Oleic acid enhances ACh receptor currents by activation of Ca2+/calmodulin-dependent protein kinase II.

Oleic acid, a cis-unsaturated free fatty acid, is proposed to be involved in the protein kinase C (PKC) activation pathway. Its biological actions, however, have not been well-characterized. We examined the effects of oleic acid on acetylcholine (ACh)-gated channel currents using Torpedo nicotinic ACh receptors expressed in Xenopus oocytes. Oleic acid (10 microM) enhanced the currents, reaching a maximum (140%) 20 min after treatment, while no enhancement was observed in Ca(2+)-free extracellular solution. The current potentiation by oleic acid was not inhibited by PKC inhibitors such as PKCI or GF109203X. Furthermore, oleic acid potentiated the currents in mutant ACh receptors lacking potential PKC phosphorylation sites. In contrast, the potentiation was fully inhibited by a CaMKII inhibitor, KN-62. These results strongly suggest that oleic acid potentiates ACh receptor currents by activation of calmodulin-dependent protein kinase II (CaMKII), independent of the PKC pathway.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Structures formed by the chiral assembly of racemic mixtures of enantiomers: iodination products of elaidic and oleic acids.

The self-assembled monolayer structure of the products of elaidic acid iodination (the racemic mixture of 9,10-(9S,10R)-diiodooctadecanoic acid and 9,10-(9R,10S)-diiodooctadecanoic acid) and the products of oleic acid iodination (the racemic mixture of 9,10-(9R,10R)-diiodooctadecanoic acid and 9,10-(9S,10S)-diiodooctadecanoic acid) are studied by high-resolution scanning tunneling microscopy. For the iodination products of elaidic acid, the separation of enantiomers into distinct chiral domains during the formation of the 2-D crystal on the highly ordered pyrolytic graphite (HOPG) surface is not observed. Instead, within the diiodooctadecanoic acid SAM, each row of molecules is composed of opposite racemates. The two opposite racemates pack alternately inside a row, using different faces to adsorb on the surface. The unit cell is composed of a pair of opposite racemates, forming a heterochiral structure. For the iodination products of oleic acid, the racemic mixture is observed to exhibit quasi-phase separation during the formation of the 2-D crystal on the HOPG surface. Each row is composed of homochiral acid molecules, either the 9,10-(9R,10R)-diiodooctadecanoic acid (R) or the 9,10-(9S,10S)-diiodooctadecanoic acid (S). The R row and the S row pack alternately, with a unit cell composed of four molecules. Two of the molecules in the unit cell are the 9,10-(9R,10R)-diiodooctadecanoic acid (R) molecules; two are the 9,10-(9S,10S)-diiodooctadecanoic acid (S) molecules. In the unit cell, the two molecules that have the same chirality pack antiparallel inside the homochiral row, using different faces to adsorb on the surface. These results suggest that several different types of chiral assembly are possible. Enantiomers with opposite chirality exhibit many chiral assembly patterns, forming heterochiral structures on the surface in addition to separation to form macroscopic chiral domains. By using different conformations, similar enantiomers with opposite chirality will display many chiral assembly patterns to form heterochiral structures on the surface.

Fatty Alcohols↗

Addition-order dependent modulation of the sensitivity of rabbit erythrocyte membrane to bee venom phospholipase A2 by oleic acid, lysophosphatidyl choline and albumin.

The addition of exogenous oleic acid to erythrocyte membranes induces a characteristic membrane crenation and sensitises the cells to the lytic action of phospholipase A2 enzymes. Both effects are extremely sensitive to inhibition by endogenous lysophosphatidyl choline (LPC), but the strength of inhibition depends of the order in which the reagents are added to the cells. These responses are further enhanced when the reagents are extracted from the cell membranes by treatment with albumin. Thus the inhibitory action of LPC added before oleic acid increases when the reagents have been extracted but that of LPC added after oleic acid decreases after extraction. The results are discussed in terms of the stimulation of PLA2 activity by enhanced membrane curvature.

Albumins↗

Screening bioavailable hydrophobic toxicants in surface waters with semipermeable membrane devices: role of inherent oleic acid in toxicity evaluations.

Semipermeable membrane devices (SPMDs) were deployed for 4 weeks in two rivers in Lithuania. The SPMD dialysates were tested in the Microtox assay and, surprisingly, the sample from the relatively clean Ula River exhibited three times more toxicity than the sample from the Vilnia River receiving discharge from several industrial enterprises and municipal waste-water. The whole dialysates were subjected to bioassay-directed fractionation on silica gel columns. Toxicity testing of each fraction revealed that most of the toxicity was contained in fraction 10, which was eluted with 100% acetone. GC/FID, GC/ECD, and GC/FTIR/MS analysis of the fractions indicated that the major component of this fraction was oleic acid. The oleic acid was most likely the hydrolysis product of methyl oleate, the major impurity of the SPMD triolein. It can be inferred that oleic acid was responsible for the toxicity of this fraction in Microtox, as a threefold difference in the toxicity between the two samples was also marked by a threefold difference in their oleic acid content. Toxicity of unsaturated fatty acids in various tests, including Microtox, has been demonstrated elsewhere. Vilnia fraction 2, which was eluted with 100% hexane, exhibited the most toxicity of the remainder of silica gel fractions. The spectral analysis demonstrated that other toxic fractions contained a number of halogenated compounds and PAHs. In general, SPMDs have proved to be a useful way to screen for hydrophobic toxicants in water. However, sample clean-up procedures to remove oleic acid may be required prior to toxicity testing for the estimation of the true toxic potential of the accumulated pollutants.

False Positive Reactions↗

Elongation of (omega-14C)oleic acid and (omega-14C)nervonic acid.

During feeding experiments with [omega-14C]oleic acid and [omega-14c]nervonic acid to adult rats, 14C-labelled C26, C28 and C30 fatty acids were recovered from the intestinal mucosa, liver, plasma, kidney and stools. The structures of these fatty acids were determined by g.l.c., radio-g.l.c. and mass spectrometry. The Schmidt and Ginger degradation methods indicated that most of the 14C found in these extra-long fatty acids remained in the omega position. These radioactive extra-long fatty acids were found mainly in the polar lipids of rats killed 3 or 15 h after being fed on labelled oleic acid or nervonic acid. Rats killed 63 h later yielded only traces of these extra-long fatty acids. When the rats were given antibiotics or received the same radioactive fatty acids by intravenous injection, the labelled extra-long fatty acids could not be detected in any of the tissues. We conclude that they were probably synthesized by elongation of oleic acid and nervonic acid by intestinal micro-organisms (probably yeasts) and then absorbed by the intestinal mucosa.

Animals↗