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PubMed1974

Utilization of ascites plasma very low density lipoprotein triglycerides by Ehrlich cells.

Much of the lipid present in the ascites plasma in which Ehrlich cells grow is contained in very low density lipoproteins (VLDL). Chemical measurements indicated that triglycerides were taken up by the cells during in vitro incubation with ascites VLDL. When tracer amounts of radioactive triolein were incorporated into the ascites VLDL, the percentage uptakes of glyceryl tri[1-(14)C]oleate and triglycerides measured chemically were similar. The cells also took up [2-(3)H]glyceryl trioleate that was added to VLDL, but the percentage of available (3)H recovered in the cell lipids was 30-40% less than that of (1 4)C from glyceryl tri[1-(1 4)C]oleate. This difference was accounted for by water-soluble (3)H that accumulated in the incubation medium, suggesting that extensive hydrolysis accompanied the uptake of VLDL triglycerides. Radioactive fatty acids derived from the VLDL triglycerides were incorporated into cell phospholipids, glycerides, and free fatty acids, and they also were oxidized to CO(2). Triglyceride utilization increased as the VLDL concentration was raised. These results suggest that one function of the ascites plasma VLDL may be to supply fatty acid to the Ehrlich cells and that the availability of fatty acid to this tumor is determined in part by the ascites plasma VLDL concentration. Although Ehrlich cells incorporate almost no free glycerol into triglycerides, considerable amounts of [2-(3)H]glyceryl trioleate radioactivity were recovered in cell triglycerides. This indicates that at least some VLDL triglycerides were taken up intact. The net uptake of VLDL protein and cholesterol was very small relative to the triglyceride uptake, suggesting that intact triglycerides are transferred from the ascites VLDL to the Ehrlich cells and that hydrolysis occurs after the triglyceride is associated with the cells.

Animals↗

PubMed1982

Maternal-fetal fat transport versus new fat synthesis in the pregnant diabetic rat.

Rats were made diabetic by the injection of streptozotocin on day 12 of pregnancy and were investigated on days 17 and 20 of pregnancy. A significant correlation between both maternal plasma triglyceride and nonesterified fatty acid levels with placental or fetal triglyceride content was found, although fetal weight did not change significantly. In order to investigate the source of the placental and fetal fat the rats received, intragastrically 24 h earlier, 1-14C-triolein (as a preformed fatty acid tracer) and tritiated water (as a marker of de novo fatty acid synthesis). Several maternal tissues, placenta, and fetuses were extracted and analysed for fatty acid radioactivity. Compared with non-diabetic pregnant rats, maternal 14C-label storage was reduced. In contrast, the placental and fetal tissues demonstrated a significant rise in 14C-label, similar in magnitude to the rise in their triglyceride content. The pattern of 3H incorporation also indicated a pronounced decrease in maternal fatty acid synthesis, but no increase in de novo fatty acid synthesis in the fetus or placenta. The findings show that fetal lipids in the pregnant rat originate both from maternal fatty acids and those synthesized in situ. The diabetes-induced increment in fetal triglyceride content is derived, however, from preformed maternal triglycerides or non-esterified fatty acids secondary to the increase in their concentration in the maternal circulation.

Animals↗

PubMed1975

Effects of thyroid hormones on enzymes involved in fatty acid and glycerolipid synthesis.

The influence of thyroid hormones on lipid biosynthesis was studied after administration of L-thyroxine to rats for 5 days. Their weights remained the same as those of control animals, despite an approximately 3-fold increment in plasma L-thyroxine and L-triiodothyronine concentrations. The activity of acetyl-CoA carboxylase and fatty acid synthetase as well as incorporation of tritium into fatty acids were depressed significantly in epididymal adipose tissue and enhanced significantly in livers of thyroxine-treated rats. Using antibodies specific against rat liver fatty acid synthetase, it was determined that the changes in activity of this multienzymic complex were due to alterations in amount of enzyme protein. In the presence of optimal concentrations of fatty acids, radioactive sn-glycero-3-phosphate, and co-substrates, total glycerolipid synthesis (defined in this study as the sum of newly formed radioactive mono- and diacyl-sn-glycero-3-phosphate, diglyceride, and triglyceride) was decreased significantly in adipose tissue and increased in liver and heart. Thus, administration of thyroid hormone results in tissue-specific alterations in lipid biosynthesis which, at least in the case of fatty acid synthetase, are due to changes in enzyme protein content.

Acetyl-CoA Carboxylase↗

PubMed1975

On the effect of brain phospholipase A1 on specifically labelled glycerophospholipids in the course of subacute sclerosing panencephalitis.

The effect of phospholipase A1 of human brain on 1,2-diacyl-sn-glycero-3-phosphorylcholine, -ethanolamine and -serine, specifically labelled with different fatty acids at either the 1 or 2 position, was determined in subacute sclerosing panencephalitis. An increase of approximately 40% in the specific activity of phospholipase A1 could be observed for all substrates investigated during the demyelinating disorder. On investigating the specific activity of the enzyme with various molecular species of phosphatidylcholine and -ethanolamine, labelled at the 1 position with different radioactive fatty acids, we found that the phospholipase A1 preferentially removed those fatty acids from the 1 position of phosphatidylcholines that have the fewest double bonds, while oleic and linoleic acid were released at almost similar rates from phosphatidylethanolamine.

Adolescent↗

PubMed1995

Incorporation of arachidonic and eicosapentaenoic acids into phospholipids of non-transformed and spontaneously-transformed rat liver epithelial cells: effects on DNA-synthesis.

We compared the incorporation of arachidonic acid (AA) and eicosapentaneoic acid (EPA) into phospholipids of non-transformed (NT-) and spontaneously-transformed (T-) rat liver epithelial cells (RLEC), and their consequences on DNA-synthesis. In NT-cells, both radioactive fatty acids were preferentially incorporated into phosphatidylcholine (PC). In T-cells, in contrast, AA was predominantly incorporated into phosphatidylethanolamine (PE), whereas EPA remained preferentially incorporated into PC. After pulse labelling, we observed in both cell types a progressive decrease in AA- and EPA-labelled PC associated with an increase in AA- and EPA-labelled PE. Preincubation of NT-cells with increasing concentrations of AA or EPA (0.1 microM to 20 microM) resulted in a concentration-dependent DNA-synthesis stimulation with a stronger effect of AA compared with EPA. In T-cells, the same treatment had no effect on DNA-synthesis.

Animals↗

PubMed1983

Incorporation and metabolism of exogenous fatty acids by cultured normal and tumoral glial cells.

We have investigated the transformation of exogenous radioactive free fatty acids by cultured glial cells and their incorporation into complex lipids. The cells were either tumor lines (C6 and NN) or primary cultures from newborn rat hemispheres. The tumor lines could undergo morphological differentiation with dibutyryl cyclic AMP or bromodeoxyuridine. The fatty acid precursors used were palmitic, stearic, oleic, linoleic and linolenic acids. Tumor cells presented a higher incorporation of the precursors in the cell lipid acyl groups than did normal cells. Tumor cells desaturated and/or elongated palmitic, stearic and oleic acid to a higher extent than did normal cells. In contrast, tumor cells transformed linoleic and linolenic acids to their polyunsaturated derivatives to a lower extent than did normal cells. In differentiated tumor cells, these patterns of metabolism were shifted toward the patterns of normal cells. Tumor cells did not exhibit delta 4-desaturase activity, but such activity was restored in the C6 line upon dibutyryl cyclic AMP-induced differentiation. Transformation of linoleic and linolenic acid is likely to proceed through initial delta 6 desaturation. Phospholipids were preferentially labelled with the radioactive fatty acids, and only a little radioactivity was found in the neutral lipid fraction, mainly in diacylglycerols. Each fatty acid precursor label was incorporated in individual phospholipids to a proportion which reflected the typical acyl group composition of glycerophospholipids; we observed high levels of incorporation of palmitic acid and its derivatives into choline glycerophospholipids, and high levels of incorporation of linolenic acid and its derivatives into ethanolamine glycerophospholipids. This pattern was more marked in tumor cells than in normal cells, and the differentiation of tumor cells partially restored the normal pattern, mainly in bromodeoxyuridine-treated NN cells. Both types of differentiation of glial cell lines can be useful as models for the understanding of membrane physiology in normal and tumor cells.

Animals↗

PubMed1987

A kinetic model of chylomicron core lipid metabolism in rats: the effect of a single meal.

A detailed quantitative description of the metabolism of the core lipids of chylomicrons was developed with data obtained from rats injected intravenously with radioactive chylomicrons. Groups of recipient rats were starved or else fed a single meal that was either fat-free or contained 5% fat. The kinetic model included chains of delipidation compartments and a remnant particle. Compartments for recirculation of portions of triglyceride, cholesteryl ester, and unesterified fatty acid radioactivities were all included and necessary to obtain good fits to the data. Making the simplifying assumption that remnants could be represented as particles retaining cholesteryl esters but depleted in triglycerides, a 'delipidation index' was calculated as the ratio of the cholesteryl ester residence time divided by the triglyceride residence time. Significant differences were found in the delipidation index between the starved group and both the normal-fed and fat-free-fed groups. Compared with rats fed a meal of the usual diet which contained 5% fat, starved rats showed more extensive delipidation and a trend toward a longer residence time of remnant particles. A longer residence time of triglycerides in rats fed a fat-free meal was explained by less delipidation, but remnant removal appeared to be accelerated. The kinetic model makes possible an interpretation of the patterns of metabolism in terms of the known underlying physiological mechanisms.

Animals↗

PubMed1995

Glutamate stimulates the formation of N-acylphosphatidylethanolamine and N-acylethanolamine in cortical neurons in culture.

The formation of anandamide (N-arachidonoylethanolamine), N-acylethanolamine, and N-acylphosphatidylethanolamine was studied in primary cultures of rat cortical neurons. The cells were incubated for 22 h with [14C]ethanolamine, [U-14C]arachidonic acid, [3H]arachidonic acid, [32P]phosphate, [14C]stearic acid, or [3H]myristic acid. The lipids from the cells and media were separated by thin layer chromatography. [14C]Ethanolamine labelling revealed two compounds (I and II), which on different thin layer chromatography systems migrated as N-acylethanolamine (0.06-0.55% of total radioactivity) and N-acylphosphatidylethanolamine (0.66-6.49% of total radioactivity), respectively. Compound II was also labelled with [32P]phosphate, and radioactive fatty acids. Treatment of compound II with phospholipase D (Streptomyces chromofuscus) resulted in two compounds, one comigrating as phosphatidic acid and the other as N-acylethanolamine. Compound I could be labelled with [14C]stearic acid and [3H]myristic acid, but not with [3H]- or [14C]arachidonic acid. Exogenous [3H]anandamide was metabolised with a t1/2 of 2.6 h. The labelling of the two compounds identified as N-acylethanolamine and N-acylphosphatidylethanolamine were more pronounced the older the culture. The neurotoxic amino acid, glutamate, stimulated within 2 h dose-dependently (ED50 = 40 microM) the formation of both compounds. It is suggested that N-acylethanolamine and N-acylphosphatidylethanolamine are formed in relation to the cytotoxicity induced by glutamate, and that these compounds may be markers of neurotoxicity. We could not detect any formation of anandamide using radioactive arachidonic acid.

Animals↗

PubMed1969

Synthesis of lipids from acetate by human preputial and abdominal skin in vitro.

Lipogenesis in vitro from acetate-1-(14)C was studied in human preputial skin and abdominal skin. Radioactive lipids were separated by column chromatography on Florisil and by thin-layer chromatography on silica gel. Radioactivity was incorporated chiefly into the triglyceride, sterol, and polar lipid fractions, while lesser amounts of (14)C were found in the hydrocarbon, wax, diglyceride, monoglyceride, and fatty acid fractions; labeling of steryl esters was minimal. On thin-layer chromatography, the radioactive polar lipids had mobilities similar to lysolecithin, phosphatidyl choline, phosphatidyl ethanolamine, and phosphatidic acid. The radioactive fatty acids of the different lipid fractions were separated by gas-liquid chromatography. The major (14)C-labeled acids were 16:0 and 18:0. Radioactivity was also detected in acids 14:0, 15:0, 16:1, 18:1, 18:2, 20:0, 20:1, 22:0, 24:0, 24:1, and 26:0. No radioactivity could be detected in arachidonic acid, although this fatty acid comprises 9% of the chromatographed fatty acids. The pattern of incorporated (14)C was different from the percentage mass composition of the fatty acids. Skin is therefore active in the biosynthesis of a wider variety of lipids than previously demonstrated.

Abdomen↗

PubMed1992

Membrane protein acylation. Preference for exogenous myristic acid or endogenous saturated chains in Acholeplasma laidlawii.

Mycoplasmas are small bacteria without a cell wall, often found as surface parasites on eukaryotic cells. Of the more than 200 membrane proteins from Acholeplasma laidlawii resolved by two-dimensional PAGE, 23 were covalently modified with acyl chains. These acyl proteins had lower pI values than average and were all labelled by different exogenously supplied radioactive fatty acids attached by O-ester bonds. The fatty acids were selectively incorporated in the order myristic acid (14:0) greater than palmitic acid (16:0) greater than stearic acid (18:0) greater than oleic acid (18:1). However, endogenously synthesised saturated fatty acids, most of which were 16:0, were preferred over the supplied ones. A fraction of the exogenous 14:0 was elongated to 16:0. Absence of saturated fatty acids increased the incorporation of 18:1. The maximum extent of modification was one acyl chain for protein T2, on the exterior surface and two acyl chains for protein D12, spanning them membrane. Exogenously supplied fatty acids were incorporated into membrane lipids in proportion to their occurrence. However, the acylated proteins always contained 8-10 times more saturated chains than did the lipids. When exogenously supplied, all A. laidlawii polar membrane lipids could donate acyl chains to the acylated proteins but the neutral fraction (fatty acids and diacylglycerol) was most efficient. An incorporation into the acylated proteins of labelled cysteine, but not glucose or glycerol, was observed. Acylated proteins with different chains interacted similarly with a Triton X-114 detergent phase, and no full-size proteins (or acylated fragments) were released from cells by proteolytic enzymes. The results indicate an anchoring with peptide segments in addition to the acyl chains. Both 14:0 and 16:0 were attached at one end of both T2 and D12, but the N-terminal methionine of T2 was not acylated. The extent of modification and preference for saturated chains in the A. laidlawii membrane acylated proteins is more similar to eukaryotic than to eubacterial proteins.

Acholeplasma laidlawii↗

PubMed2000

Microsomal fatty aldehyde dehydrogenase catalyzes the oxidation of aliphatic aldehyde derived from ether glycerolipid catabolism: implications for Sjögren-Larsson syndrome.

The enzyme that catalyzes the oxidation of fatty aldehyde derived from ether glycerolipid catabolism has not been identified. To determine whether microsomal fatty aldehyde dehydrogenase (FALDH) is responsible, we investigated the metabolism of 1-O-[9, 10-(3)H-octadecyl]-glycerol ([(3)H]OG) in FALDH-deficient cultured cells from patients with Sjögren-Larsson syndrome (SLS) and in mutant Chinese hamster ovary (CHO) cells. Intact fibroblasts from SLS patients incubated with [(3)H]OG showed a selective deficiency (38+/-7% of normal) in the incorporation of radioactivity into fatty acid, but no decrease in incorporation of radioactivity into fatty alcohol, total lipids and phosphatidylethanolamine (PE). Consistent with fatty aldehyde accumulation, incorporation of radioactivity into N-alkyl-phosphatidylethanolamine, which is derived from Schiff base formation of free aldehyde with PE, was 4-fold higher in SLS fibroblasts compared to normal controls. Similar results were seen with SLS keratinocytes, whereas FALDH-deficient CHO cells showed a more profound reduction in radioactive fatty acid to 12+/-2% of normal. These results implicate FALDH in the oxidation of ether-derived fatty aldehyde in human and rodent cells. Metabolism of ether glycerolipids is a previously unrecognized source of fatty aldehyde that may contribute to the pathogenesis of SLS.

Aldehyde Oxidoreductases↗

PubMed1984

Inability of skin enzyme preparations to biosynthesize arachidonic acid from linoleic acid.

The lack of any information as to the origin of epidermal arachidonic acid, an important precursor of eicosanoids in the epidermis, prompted us to determine in vitro whether or not microsomal preparations from rat and guinea pig epidermis possess the delta 6 and delta 5 desaturase activities. The incubations were performed in parallel with microsomal preparations from liver of these animals where activities for these enzymes have previously been reported. The conversions of radioactive fatty acids were determined after methylation and separation of the 14C-fatty acid methyl esters by argentation thin layer chromatography. Data from these studies demonstrated that delta 5 desaturase activity is markedly lower in guinea pig liver than in rat liver. Interestingly, preparations from rat and guinea pig epidermis at all concentrations tested lacked the capacity to transform either linoleic acid into gammalinolenic acid or dihomogammalinolenic acid into arachidonic acid. This observation implies that arachidonic acid that is present in the epidermal phospholipids is biosynthesized elsewhere endogenously and transported to the epidermis for esterification into the phospholipids. The site of this biosynthesis is presumably the liver and the mode of transport to the epidermis remains to be determined. These studies indicate arachidonic acid per se as an essential fatty acid for the epidermis.

Animals↗

PubMed1982

Changes in the metabolism of fatty acids in adipose tissue in obese patients with primary hypertriacylglycerolemia.

Changes in the release and esterification of free fatty acids (FFA) in adipose tissue were looked for as a cause of moderate primary hypertriacylglycerolemia (HTG) in five obese subjects. Comparison was made with six obese normolipidemic subjects. The two groups were matched for body weight, tolerance of intravenous glucose, fat cell size, fasting levels of serum immunoreactive insulin, and serum insulin response to an intravenous glucose load. Subcutaneous adipose tissue was incubated in vitro with [1-14C]palmitic acid for 30, 60, and 120 min. There was a significant, twofold increase in the rate of FFA mobilization, but no change of glycerol release in HTG patients. The adipose tissue levels of mono- and diacylglycerols were similar in the two groups of subjects and did not change during incubation. Re-esterification of FFA, calculated from the net changes in medium and in tissue FFA and glycerol release, was lower in HTG patients than in the controls (3 and 12 mumol/10(7) cells/hr, respectively; P less than 0.025). In adipose tissue of HTG patients, the amount of radioactive fatty acids incorporated into triacylglycerols (TG) was 50% lower (P less than 0.025), whereas that incorporated into tissue FFA was three times higher (P less than 0.01) when compared with control patients. It is concluded that, in adipose tissue of obese patients with primary hypertriacylglycerolemia, the esterification of free fatty acids to triacylglycerol is decreased. As a consequence, free fatty acids are mobilized at an increased rate.

Adipose Tissue↗

PubMed1967

Distribution of radioactive glycerol and fatty acids among adipose tissue triglycerides after administration of glucose-U-14C.

Adipose lipid obtained from fed rats 15 or 60 min after injection of radioactive glucose was separated into 10 triglyceride classes of differing fatty acid compositions. The distribution among these classes of total and radioactive triglyceride-glycerol was determined and found to be the same. Thus newly synthesized adipose triglycerides resemble in kind and proportion the triglycerides which exist in the tissue. This finding is in accord with the concept that the structures of adipose triglycerides are stable over long periods and that the turnover rate of the several triglyceride species are similar. After administration of radioactive glucose, the specific activity of saturated fatty acids was higher in the more saturated triglyceride species. These data indicate that newly formed saturated acids do not mix completely with all adipose tissue fatty acids available for esterification. Fatty acids derived from plasma triglyceride influenced the composition of newly synthesized adipose tissue triglyceride and thus constitute an important source of adipose tissue lipid.

Adipose Tissue↗

PubMed1987

Incorporation of radioactivity into amino acids and fatty acids after administration of 14C-geranylgeranylacetone to rats.

The radioactive components present in plasma proteins and adipose tissue after oral dosing of 14C-geranylgeranylacetone (GGA) to rats were characterized by gel filtration, paper electrophoresis, t.l.c. and reversed-phase column chromatography. The radioactivity associated with the plasma proteins was identified as 14C-labelled amino acids (Glu, Asp, Ala, Pro, Gly and probably Ser); however, no 14C was detectable in the essential amino acids. Radioactivity accumulated in adipose tissue as 14C-labelled fatty acids of triglycerides. The incorporation of 14C into amino acids and fatty acids may be due to the formation of 14C-propionyl-CoA resulting from omega-oxidation and successive beta-oxidations of 14C-GGA. This view was supported by the finding that 14C-acetate was incorporated into amino acids and fatty acids in a similar manner to 14C-GGA.

Acetates↗

PubMedDate not supplied

Immobilization antigens from Tetrahymena thermophila are glycosyl-phosphatidylinositol-linked proteins.

We have studied four strains of Tetrahymena thermophila, each of which expresses a different allele of the SerH gene and produces a distinctive surface protein of the immobilization antigen (i-antigen) class. Following exposure of the strains to [3H]ethanolamine or [3H]myristic acid, a protein corresponding in molecular mass to the characteristic i-antigen for that strain became highly labeled, as determined by mobility in sodium dodecylsulfate-polyacrylamide electrophoresis gels. Furthermore, antibodies raised to the i-antigens of the T. thermophila strains selectively immunoprecipitated radioactive proteins having molecular mass identical to that of the i-antigen characteristic for that particular strain. The lipid moieties labeled by [3H]myristate were not susceptible to hydrolysis by exogenous phosphatidylinositol-specific phospholipase C from bacteria. However, when protein extraction was carried out in the absence of phospholipase C inhibitors, radioactive fatty acids derived from [3H]myristate were rapidly cleaved from the putative i-antigens. On the basis of available data, it was concluded that T. thermophila i-antigens contain covalently-linked glycosyl-phosphatidylinositol anchors.

Animals↗

PubMed1989

Association between inhibition of arachidonic acid release and prevention of calcium loading during ATP depletion in cultured rat cardiac myocytes.

The development of irreversible myocardial ischemic injury is associated with progressive degradation of membrane phospholipids, accumulation of arachidonate and other free fatty acids, and electrolyte derangements, including calcium accumulation. To study the relationship between arachidonate release and calcium loading during adenosine triphosphate (ATP) depletion in cardiac myocytes, the effects of two purported phospholipase inhibitors, mepacrine and U26,384, were evaluated. Cultured neonatal rat ventricular myocytes were pretreated for 90 minutes with 5 to 10 microM U26,384 (a steroidal diamine) or 10 to 50 microM mepacrine (an alkyl acridine) and then treated for 3 hours with 30 microM of the metabolic inhibitor, iodoacetic acid (IAA), with or without an additional dose of drug. IAA treatment resulted in a marked reduction in ATP level and a several-fold increase in free fatty acid radioactivity released from myocytes prelabeled with tritiated arachidonic acid (3H-AA). U26,384 produced substantial inhibition of the increased 3H-AA release, and was effective when given as a single pretreatment dose before IAA exposure or as continuous treatment before and during IAA exposure (for example, with 5 microM U26,384, the percentage of 3H-AA release versus IAA alone was 8% +/- 2% [SEM] [N = 15] for pretreatment only and 13% +/- 4% [N = 10] for continuous treatment). Mepacrine also resulted in significant reduction in 3H-AA release, but was more effective when given as continuous treatment (for example, with 50 microM mepacrine, the percentage of 3H-AA release versus IAA alone was 43% +/- 9% [N = 6] for pretreatment only and 22% +/- 7% [N = 9] for continuous treatment). More detailed analysis showed that U26,384 and mepacrine blocked the IAA-induced redistribution of 3H-AA into free fatty acids from other lipid species. Electron probe x-ray microanalysis of freeze-dried cryosections revealed marked electrolyte derangements in myocytes exposed to IAA, including a 24-fold increase in cellular Ca, a four fold increase in cellular Na, and a seven fold decrease in cellular K, and associated changes in cytoplasm and mitochondria. U26,384 treatment markedly reduced these electrolyte abnormalities, and maintained normal Ca levels in some protocols. Mepacrine treatment was less effective, but did produce normal Ca levels in 50% of myocytes. Prevention of IAA-induced cellular hypercontraction and blebbing also was observed. These data support the hypothesis that reduction of free fatty acid accumulation by inhibition of accelerated phospholipid degradation is associated with protection of myocytes from calcium loading and morphologic damage during inhibition of ene

Adenosine Triphosphate↗

PubMed1986

Docosatetraenoic acid in endothelial cells: formation, retroconversion to arachidonic acid, and effect on prostacyclin production.

Cultured bovine aortic endothelial cells convert arachidonic acid to docosatetraenoic acid and also take up docosatetraenoic acid from the extracellular fluid. After a 24-h incubation with biosynthetically prepared [3H]docosatetraenoic acid, about 20% of the cellular fatty acid radioactivity was converted to arachidonic acid. Furthermore, in pulse-chase experiments, the decrease in phospholipid docosatetraenoic acid content was accompanied by an increase in arachidonic acid, providing additional evidence for retroconversion. These findings suggest that one possible function of docosatetraenoic acid in endothelial cells is to serve as a source of arachidonic acid. The endothelial cells can release docosatetraenoic acid when they are stimulated with ionophore A23187, but they do not form appreciable amounts of eicosanoids from docosatetraenoic acid. Enrichment of the endothelial cells with docosatetraenoic acid reduced their capacity to produce prostacyclin (PGI2) in response to ionophore A23187. This may be related to the fact that docosatetraenoic acid enrichment caused a 40% reduction in the arachidonic acid content of the inositol phosphoglycerides. In addition, less prostacyclin was formed when the enriched cells were incubated with arachidonic acid, suggesting that docosatetraenoic acid also may act as an inhibitor of prostaglandin synthesis in endothelial cells.

Animals↗