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Pulmonary clearance of three aerosolized solutes in oleic acid-induced lung injury.

We studied the effects of oleic acid (OA) on pulmonary clearance of three aerosolized radioactive solutes: 99mTc-diethylenetriamine pentaacetate (99mTc-DTPA), 67Ga-desferoxamine (67Ga-DFOM), and 111In-transferrin (111In-TF). Either 0.09 ml/kg OA or an equivalent volume of 0.9% NaCl (controls) was administered intravenously to 48 anesthetized, paralyzed dogs. Each animal received one aerosolized solute either 60 min after (protocol A) or 30 min before (protocol B) the infusion of OA or NaCl. In protocol A clearances of all three solutes were similar in OA and control animals. In contrast, in protocol B clearances of all three solutes increased significantly during OA infusion; during the next 60 min clearances of 99mTc-DTPA and 67Ga-DFOM returned to control values but 111In-TF remained increased. We conclude that 1) in OA-induced permeability edema pulmonary clearance of aerosolized solutes is increased when the aerosol is delivered 30 min before but not 60 min after injury, and 2) increased clearance persists only for large molecules, presumably because smaller molecules cross injured epithelium quickly and completely. These phenomena are best explained by a nonhomogeneous distribution of OA-induced injury.

Aerosols↗

Candida rugosa lipase LIP1-catalyzed transesterification to produce human milk fat substitute.

Structured lipids (SLs) containing palmitic and oleic acids were synthesized by transesterification of tripalmitin with either oleic acid or methyl oleate as acyl donor. This SL with palmitic acid at the sn-2 position and oleic acid at sn-1,3 positions is similar in structure to human milk fat triacylglycerol. LIP1, an isoform of Candida rugosa lipase (CRL), was used as biocatalyst. The effects of reaction temperature, substrate molar ratio, and time on incorporation of oleic acid were investigated. Reaction time and temperature were set at 6, 12, and 24 h, and 35, 45, and 55 degrees C, respectively. Substrate molar ratio was varied from 1:1 to 1:4. The highest incorporation of oleic acid (37.7%) was at 45 degrees C with methyl oleate as acyl donor. Oleic acid resulted in slightly lesser (26.3%) incorporation. Generally, higher percentage incorporation of oleic acid was observed with methyl oleate (transesterification) than with oleic acid (acidolysis). In both cases percentage incorporation increased with reaction time. Incorporation decreased with increase in temperature above 45 degrees C. Initially, oleic acid incorporation increased with increase in substrate molar ratio up to 1:3. LIP1 was also compared with Lipozyme RM IM as biocatalysts. The tested reaction parameters were selected on the basis of maximum incorporation of C18:1 obtained during optimization of LIP1 reaction conditions. Reaction temperature was maintained at 45, 55, and 65 degrees C. Lipozyme RM IM gave highest oleic acid incorporation (49.4%) at 65 degrees C with methyl oleate as acyl donor. Statistically significant (P < 0.05) differences were observed for both enzymes. SL prepared using Lipozyme RM IM may be more suitable for possible use in human milk fat substitutes.

Animals↗

Neutrophil apoptosis during the development and resolution of oleic acid-induced acute lung injury in the rat.

The oleic acid (OA) model of acute lung injury in rats is characterized by a massive and rapid influx of polymorphonuclear neutrophils (PMN) within 1 h, with a peak inflammatory response at 4 h and resolution by 72 h. We hypothesized that PMN apoptosis is involved in the resolution of OA-induced acute lung injury. To test this hypothesis, healthy adult Fischer 344 rats were given 30 microl OA in 0.1% bovine serum albumin (BSA) intravenously; controls were given BSA alone and killed at 1, 4, 24, and 72 h after OA to obtain bronchoalveolar lavage fluid (BALF) and lung tissue. Cell pellets from BALF and formalin-fixed, paraffin-embedded tissue section samples were processed for terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) to identify apoptotic cells. Propidium iodide was used to counterstain nuclei. Percentage of nuclei undergoing apoptosis was counted under a fluorescent microscope. Control rats showed only resident alveolar macrophages (AM) in the BALF with no apoptosis. At the peak of injury, 1 h and 4 h after OA injection, we observed a massive PMN response without any evidence of apoptosis. At 24 h, when the OA injury is clinically and histologically in early resolution, we observed intense apoptosis of PMN nuclei along with evidence of apoptotic bodies in the cytoplasm of AM. Some of the AM also showed apoptotic nuclei at 72 h. Similar observations were made in the lung tissue sections. The results of the TUNEL assay were confirmed by DNA ladders and electron microscopy. We conclude that apoptosis of PMN and clearance by AM is an important mechanism in resolution of OA- induced acute lung injury.

Animals↗

Inhibition of apolipoprotein secretion and phosphatidate phosphohydrolase activity by eicosapentaenoic and docosahexaenoic acids in the perfused rat liver.

Infusion of albumin-bound eicosapentaenoic acid (EPA) docosahexaenoic acid (DHA), or oleic acid (OA) in perfused rat livers was carried out for two hours at a rate that maintained the perfusate concentration at 1 mmol/L. When compared with fatty acid-poor albumin alone, triacylglycerol (TAG) output was not significantly increased with DHA or EPA, whereas OA infusion resulted in a twofold increase. Incorporation of labeled leucine into VLDL apo B-100, apo B-48, apo E, and apo Cs was decreased by 50% by DHA or EPA compared with OA. The total phosphatidate phosphohydrolase activity was decreased by 35% with DHA or EPA compared to oleic acid or albumin alone. In no case was there a significant change in the distribution of activity between the microsomal and cytosolic factions. Fatty acid infusion did not significantly change the liver TAG content. Total liver lipids, microsomal lipids, and lipids of secreted VLDL were enriched with the infused fatty acids. The degree of enrichment for secreted TAG averaged 24% for OA and 36% for DHA or EPA. The effects of DHA and EPA on PPH activity and on apo B secretion in feeding experiments with marine oils rich in these acids may relate to changes in the fatty acid composition of liver membranes.

Animals↗

Cis-unsaturated fatty acids induce both lipogenesis and calcium binding in adipocytes.

The addition of 0.4-3 mM of cis-unsaturated fatty acids such as oleic acid (18:1) or linoleic acid (18:2) to intact rat adipocytes stimulated lipogenesis at 37 degrees C. Saturated or trans-unsaturated fatty acids were ineffective. Fluorescence photobleaching recovery studies performed under similar conditions indicated that the cis-unsaturated fatty acids do not alter lateral mobility of either a lipid probe or a general protein marker in the plasma membrane. A high concentration (7 mM) of Ca2+, which by itself has some stimulatory effect on lipogenesis, significantly potentiated the effect of oleic acid on this insulin-like activity. Measurement of 45Ca2+ binding by fat cells has indicated that cis-unsaturated (but not saturated) fatty acids increased 12- to 20-fold the amount of Ca2+ associated with the cells. The dependence of this effect on the fatty acid concentration correlates well with the effect of the fatty acid on the induction of lipogenesis. Our results suggest that cis-unsaturated fatty acids affect membrane organization in a manner which induces a significant increase in membrane associated or intracellular Ca2+. This increase may be responsible for inducing exocytotic-like processes which facilitate translocation of glucose transport activity from storage sites to the plasma membrane and thus produce an insulin-like effect.

Adipose Tissue↗

Effects of continuous positive airway pressure after oleic acid-induced lung injury in dogs.

The physiologic effects of continuous positive airway pressure (CPAP) of 5,10,15, and 20 cm H2O during spontaneous ventilation were studied in six anesthetized dogs with simulated respiratory distress syndrome (RDS) induced by iv infusion of oleic acid and in three normal controls. After oleic acid, mean PaO2 dropped to 63.6 +/- 3.1 mm Hg while breathing 100% oxygen and mean shunt fraction was 48.3 +/- 3.0%. PaO2 and shunt fraction improved significantly at the two highest levels of CPAP (e.g.,PaO2 271.3 +/- 41.3 mm Hg and shunt fraction 17.8 +/-2.2% at 20 cm H2O CPAP). Mean mixed venous PO2 rose from 37.4 +/- 1.5 mm Hg with no CPAP TO 60.8 +/- 3.1 mm Hg at 20 cm H2O CPAP. Tissue oxygenation appeared to improve during CPAP, since cardiac output, oxygen delivery, and serum lactate were not significantly affected and mixed venous PO2 rose significantly. However, significant hypoventilation occurred at all but the lowest level of CPAP, mean PaCO2 rising from 44.1 +/- 1.8 mm Hg with no CPAP to 77.6 +/-6.8 mm Hg at 20 cm H2O CPAP. The hypoventilation during CPAP is consistent with increased work of breathing due to a combination of decreased lung compliance and increased dead space ventilation due to rapid, shallow breathing.

Animals↗

Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY.

BACKGROUND: Upper gastrointestinal motility is regulated by the presence of nutrients in the distal gut. The present study evaluated whether lipid-induced ileal brake on gastric emptying (1) can be elicited by low fat concentrations; (2) is a dose-dependent phenomenon; and (3) is related to gastrointestinal peptide release. METHODS: Seven patients were studied in the defunctionalized stage of total colectomy, on three separate occasions. On each study day, patients ate a meal labeled in the solid component; 30 minutes later, one of the following solutions was randomly infused into the ileal pouch: 0.9% saline, 2% oleic acid, and 20% oleic acid. Plasma concentrations of peptide YY (PYY), enteroglucagon, neurotensin, and motilin were measured. RESULTS: Both oleic acid solutions slowed gastric emptying compared with saline (P < 0.001), the effect being dose dependent (P < 0.001). Ileal infusions did not modify neurotensin and enteroglucagon levels but induced a dose-dependent increase of PYY (P < 0.01) and a borderline decrease of motilin (P = 0.05) levels. Slower rates of gastric emptying were related to increased plasma concentrations of PYY (r = 0.615; P < 0.05). CONCLUSIONS: This study shows that (1) the ileal brake on gastric emptying can be evoked by low doses of lipids in the distal ileum; (2) the delay of gastric emptying is related to the release of PYY; and (3) both phenomena are dose dependent.

Adult↗

Locations of the three primary binding sites for long-chain fatty acids on bovine serum albumin.

Binding of 13C-enriched oleic acid to bovine serum albumin and to three large proteolytic fragments of albumin--two complementary fragments corresponding to the two halves of albumin and one fragment corresponding to the carboxyl-terminal domain--yielded unique patterns of NMR resonances (chemical shifts and relative intensities) that were used to identify the locations of binding of the first 5 mol of oleic acid to the multidomain albumin molecule. The first 3 mol of oleic acid added to intact albumin generated three distinct NMR resonances as a result of simultaneous binding of oleic acid to three heterogeneous sites (primary sites). Two of these resonances were seen upon addition of 1 or 2 mol of oleic acid to fragments representing either the carboxyl-terminal half (residues 307-582) or the carboxyl-terminal domain (residues 377-582); the third resonance was seen upon addition of 1 mol of oleic acid to the fragment representing the amino-terminal half (residues 1-306). The resonance patterns for the fourth and fifth moles of oleic acid added to albumin (secondary sites) could not be duplicated by addition of more oleic acid to individual fragments. These resonance patterns were generated, however, when the two complementary fragments were mixed in equimolar proportions to form an albumin-like complex with a reconstituted middle domain. Thus, two primary fatty acid binding sites are assigned to the carboxyl-terminal domain, one primary site is assigned to the amino-terminal half, and the secondary sites are assigned to the middle domain. This distribution suggests albumin to be a less symmetrical binding molecule than theoretical models predict. This work also demonstrates the power of NMR for the study of microenvironments of individual fatty acid binding sites in specific domains.

Binding Sites↗

Effect of pancreatic juice and trypsin on oleic acid-stimulated pancreatic secretion and plasma secretin in dogs.

We have investigated a negative feedback mechanism in the intestinal phase of pancreatic exocrine secretion in dogs with gastric cannulas and Thomas duodenal cannulas in whom pancreatic juice was collected by cannulation of the main pancreatic duct. Intraduodenal infusion of oleic acid emulsion in a dose of 18 mmol/h resulted in a significant increase in pancreatic secretion of water, bicarbonate, and protein, which was accompanied by increased plasma concentrations of both secretin and cholecystokinin. Infusion of pancreatic juice or bovine trypsin into the duodenum significantly inhibited the oleic acid-stimulated pancreatic secretion. This inhibition coincided with a significant decrease in plasma secretin level, whereas plasma cholecystokinin concentration was not affected by either pancreatic juice or trypsin. Neither pancreatic secretion nor plasma secretin concentration was affected by intraduodenal administration of NaHCO3 solution. The trypsin-induced suppression of pancreatic secretion was prevented by intravenous administration of secretin in a dose that achieved a plasma secretin level comparable to that during the oleic acid administration. This study indicates that a negative feedback mechanism is operative in the intestinal phase of pancreatic exocrine secretion in dogs, and endogenous secretin plays a significant role in the mechanism.

Animals↗

Interaction of glucose and long chain fatty acids (C18) on antioxidant defences and free radical damage in porcine vascular smooth muscle cells in vitro.

AIMS/HYPOTHESIS: Abnormalities of glucose and fatty acid metabolism in diabetes are believed to contribute to the development of oxidative stress and the long term vascular complications of the disease; therefore the interactions of glucose and long chain fatty acids on free radical damage and endogenous antioxidant defences were investigated in vascular smooth muscle cells. METHODS: Porcine vascular smooth muscle cells were cultured in 5 mmol/l or 25 mmol/l glucose for 10 days. Fatty acids, stearic acid (18:0), oleic acid (18:1), linoleic acid (18:2) and alpha-linolenic acid (18:3) were added with defatted bovine serum albumin as a carrier for the final three days. RESULTS: Glucose (25 mmol/l) alone caused oxidative stress in the cells as evidenced by free radical-mediated damage to DNA, lipids, and proteins. The addition of fatty acids (0.2 mmol/l) altered the profile of free radical damage; the response was J-shaped with respect to the degree of unsaturation of each acid, and oleic acid was associated with least damage. At a lower concentration alpha-linolenic acid (0.01 mmol/l) was markedly different in that, when added to 25 mmol/l glucose it resulted in a decrease in free radical damage to DNA, lipids and proteins. This was accompanied by a marked increase in antioxidant and glutathione concentrations as well as by increased gene expression is of gamma-glutamylcysteine synthetase, the rate-limiting enzyme in glutathione synthesis. CONCLUSIONS/INTERPRETATION: The results clearly show that glucose and fatty acids interact in the production of oxidative stress in vascular smooth muscle cells.

Animals↗

Dietary and hormonal interrelationships in premenopausal women: evidence for a relationship between dietary nutrients and plasma prolactin levels.

To investigate possible differences in tissue exposures to reproductive hormones and to determine hormone-nutrient interrelationships, we studied 10 vegetarian and 10 nonvegetarian premenopausal Seventh-day Adventist women. Over 3 d in each of three consecutive menstrual cycles, we collected diet records, fasting midluteal phase blood, and 24-h urine samples. During each study period, we measured plasma and urinary estrogens, plasma free and protein bound-estradiol-17 beta, the binding capacity of sex-hormone-binding globulin (SHBG), androgens, progesterone, and prolactin levels. The omnivores consumed significantly more protein, total and saturated fatty acids, oleic and linoleic acids, and cholesterol than did the vegetarians. Hormonal status and binding capacity of SHBG were similar in both groups. However, for nonvegetarians, prolactin levels were positively correlated with dietary energy, protein, total and saturated fatty acids, and oleic acid. Further study delineating the effects of specific dietary nutrients on the basal level of prolactin secretion is warranted.

Adult↗

n-3 and n-6 polyunsaturated fatty acids have different effects on acyl-CoA:cholesterol acyltransferase in J774 macrophages.

The effects of incubating J774 mouse macrophages with different fatty acids on cholesterol esterification were investigated. In cells incubated with n-3 polyunsaturated fatty acids, the rate of cholesterol esterification was significantly reduced compared with cells incubated with n-6 polyunsaturated fatty acids or with oleic acid. This change in cholesterol esterification appears to be the result of reductions in the activity of acyl-CoA:cholesterol acyltransferase (ACAT) in the endoplasmic reticulum of the macrophages incubated with the n-3 polyunsaturated fatty acids. No differences in microsomal cholesterol were observed among cells incubated with different fatty acids. However, cellular cholesterol levels were lower in cells incubated with n-3 polyunsaturated fatty acids. In microsomes from cells incubated with n-3 polyunsaturated fatty acids, both the Km and the Vmax of ACAT were lower than in microsomes from cells incubated with n-6 fatty acids or oleic acid. These findings may explain some of the reduction in atherosclerotic lesions that are observed with dietary fish oils that contain high levels of n-3 polyunsaturated fatty acids.

Animals↗

[Studies of the effects of cis, cis and trans, trans-octadecadienoic acids on lipid metabolism in essential fatty acid deficient rats (author's transl)].

The effect of an essential fatty acid [EFA] deficiency in male Sprague-Dawley rats and its excerbation by inclusion of trans fatty acids in the diet were observed from the level and composition of serum lipoproteins. Male Sprague-Dawley rats were fed from weaning diet containing all essential nutrients and 10% of a fat supplement as safflower oil (SAFF] or hydrogenated coconut oil [HCO] for 28 weeks. At the end of 28 weeks, the blood was withdrawn from the retro-ocular plexes of 4 animals of each group, and lipoprotein lipid and fatty acids were analyzed. Another 5 animals of each group were switched to a 5% supplement of ethyl linolelaidate [TRANS]. In addition, the remaining 5 animals of HCO group were switched to SAFF diet. Lipoprotein lipid and fatty acid analyses were performed on the pooled serum in each group at 3, 7 and 14 days after switching the diet, and after 21 days serum was analyzed on the individual animal of each group. The results obtained were as follows: [1] With the development of an EFA deficiency in HCO group, there was a decrease in the high density lipoprotein [HDL] and increase in the very low density lipoprotein [VLDL] plus low density lipoprotein [LDL] fraction. [2] In a switching group from the SAFF to the TRANS supplement, the level of arachidonate in the serum lipid was decreased with a corresponding decrease in HDL, whereas linoleate, at least for the initial 3 weeks, decreased only in triglyceride fraction. [3] In a EFA deficient rat [HCO group] after switched to the TRANS supplement, HDL was further decreased and increase o VLDL-LDL was progressed. Consequently, the HDL: VLDL-LDL ratio was lowered strikingly. These changes in the EFA deficiency were accompanied by a large increase in monoenoic acids and a decrease in eicosatrienoic acid converted from oleic acid. [4] The administration of SAFF diet to the EFA deficient group induced a rapid increase in arachidonate in HDL, and decrease in eicosatrienoic acid and oleic acid. These changes were accompanied by a marked decrease in VLDL-LDL. It is suggested that the normal HDL might play an important role on catabolism of VLDL-LDL. These results suggest that polyunsaturated fatty acid, especially arachidonic acid rather than linoleic acid is essential to the formation and the function of HDL in the rats.

Animals↗

Increased erythrocyte stearic acid desaturation in rats with chemically induced colorectal carcinomas.

Our previous studies have demonstrated a desaturation of stearic acid related to oleic acid in the lipid layer of erythrocytes in patients with malignancies. This study investigated the stearic acid desaturation in red blood cell membranes of rats during the induction of colorectal tumours. Male Sprague-Dawley rats were injected weekly with dimethylhydrazine (DMH) and sacrificed at 4-week intervals. Blood was withdrawn via heart puncture, collected in EDTA bottle and erythrocytes separated by centrifugation. Total lipid extraction was carried out and analysed with gas liquid chromatography. In the control rats (injected with normal saline) the mean of the stearic to oleic acid ratio in erythrocyte membranes was 2.0 +/- 0.3 (n = 28, range 1.51-2.62) compared to a mean of 0.94 +/- 0.16 (n = 0.5-1.23) in tumour bearing rats (p less than 0.001). The increased desaturation occurred in parallel with appearance of tumours. These data suggest the regulation of stearic acid desaturation is an important adaptive mechanism of membrane fluidity and could be a useful chemical marker for malignancy.

Animals↗

Mapping of the loci controlling oleic and linolenic acid contents and development of fad2 and fad3 allele-specific markers in canola (Brassica napus L.).

The quality of canola oil is determined by its constituent fatty acids such as oleic acid (C18:1), linoleic acid (C18:2) and linolenic acid (C18:3). Most canola cultivars normally produce oil with about 55-65% oleic acid and 8-12% linolenic acid. High concentrations of linolenic acid lead to oil instability and off-type flavor, while high levels of oleic acid increase oxidative stability and nutritional value of oil. Therefore, development of canola cultivars with increased oleic acid and reduced linolenic acid is highly desirable for canola oil quality. In this study, we have mapped one locus that has a major effect and one locus that has a minor effect for high oleic acid and two loci that have major effects for low linolenic acid in a doubled haploid population. The major locus for high C18:1 was proven to be the fatty acid desaturase-2 (fad2) gene and it is located on the linkage group N5; the minor locus is located on N1. One major QTL for C18:3 is the fatty acid desaturase-3 gene of the genome C (fad3c) and it is located on N14. The second major QTL resides on N4 and is the fad3a gene of the A genome. We have sequenced genomic clones of the fad2 and fad3c genes amplified from an EMS-induced mutant and a wild-type canola cultivar. A comparison of the mutant and wild-type allele sequences of the fad2 and fad3c genes revealed single nucleotide mutations in each of the genes. Detailed sequence analyses suggested mechanisms by which both the mutations can cause altered fatty acid content. Based on the sequence differences between the mutant and wild-type alleles, two single nucleotide polymorphism (SNP) markers, corresponding to the fad2 and fad3c gene mutations, were developed. These markers will be highly useful for direct selection of desirable fad2 and fad3c alleles during marker-assisted trait introgression and breeding of canola with high oleic and low linolenic acid.

Alleles↗

ApoB-100 secretion by HepG2 cells is regulated by the rate of triglyceride biosynthesis but not by intracellular lipid pools.

Triglycerides (TGs), cholesteryl esters (CEs), cholesterol, and phosphatidylcholine have been independently proposed as playing regulatory roles in apoB-100 secretion; the results depended on the cellular model used. In this study, we reinvestigate the role of lipids in apoB-100 production in HepG2 cells and in particular, we clarify the respective roles of intracellular mass and the biosynthesis of lipids in the regulation of apoB-100 production. In a first set of experiments, the pool size of cholesterol, CEs, and TGs was modulated by a 3-day treatment with either lipid precursors or inhibitors of enzymes involved in lipid synthesis. We used simvastatin (a hydroxymethylglutaryl coenzyme A reductase inhibitor), 58-035 (an acyl coenzyme A cholesterol acyltransferase inhibitor), 5-tetradecyloxy-2-furancarboxylic acid (TOFA, an inhibitor of fatty acid synthesis), and oleic acid. The secretion rate of apoB-100 was not affected by the large modulation of lipid mass induced by these various pre-treatments. In a second set of experiments, the same lipid modulators were added during a 4-hour labeling period. Simvastatin and 58-035 inhibited cholesterol and CE synthesis without affecting apoB-100 secretion. By contrast, treatment of HepG2 cells with TOFA resulted in the inhibition of TG synthesis and apoB-100 secretion. This effect was highly specific for apoB-100 and was reversed by adding oleic acid, which stimulated both TG synthesis and apoB-100 secretion. Moreover, a combination of oleic acid and 58-035 inhibited CE biosynthesis and increased both TG synthesis and apoB-100 secretion. These results show that in HepG2 cells TG biosynthesis regulates apoB-100 secretion, whereas the rate of cholesterol or CE biosynthesis has no effect.

Apolipoproteins B↗

Isolation and characterization of membranes from oleic acid-induced peroxisomes of Candida tropicalis.

We report a methodology for the isolation of peroxisome membranes from the yeast Candida tropicalis pK233 grown on oleic acid, and the characterization of the polypeptide and lipid compositions of these membranes. Peroxisomes purified in either sucrose or Nycodenz gradients are treated with Tris-HCl (pH 8.5) and then with sodium carbonate (pH 11.5) to yield a final peroxisome membrane preparation (hereafter called 'peroxisome membranes'). Electron microscopy revealed peroxisome membranes that are approximately 8.1 nm thick, have a typical trilaminar appearance, and form either flattened sheets or whorled structures. Peroxisome membranes contain 3.1% and 2.2% of the total protein of sucrose- and Nycodenz-gradient-purified peroxisomes, respectively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis showed three predominant polypeptide bands of 34 (PMP 34), 29 (PMP 29), and 24 (PMP 24) x 10(3) Mr in peroxisome membranes. Immunoblotting with an antiserum to PMP 24 showed that PMP 24 segregates with the peroxisome membrane fractions and is induced by growth of Candida tropicalis on oleic acid. Peroxisome membranes contain neutral lipids and phospholipids. The principal phospholipids are phosphatidyl choline and phosphatidyl ethanolamine. The phospholipid/protein ratio of peroxisome membranes is approximately 430 nmol mg-1.

Candida↗

Structural and related functional changes in sarcoplasmic reticulum induced by long-chain fatty acids.

The effect of palmitic and oleic acids on Ca2+-ATPase activity in coupled preparations of sarcoplasmic reticulum isolated from rabbit hind leg muscle have been compared with their effects on vesicles uncoupled with Ca2+ ionophore, A23187. Palmitate at 2 microM X mg protein-1 has no significant effect on enzyme activity and does not uncouple catalytic activity from calcium accumulation within the vesicles. Oleic acid at 1 microM X mg protein-1 uncouples the vesicles, whereas 2 microM X mg protein-1 completely inhibits Ca2+-ATPase activity. Fluorescence anisotropy of diphenylhexatriene is not significantly altered by palmitate, but a large transient increase in motion of the probe is observed with addition of oleic acid. The effects of oleic acid on enzyme activity are not mediated via an effect on the bulk properties of the hydrophobic domain of the membrane lipids.

Animals↗