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A A Spector

Publications and source records attributed to A A Spector.

At least 55 records · Page 3Linked to original sources
PubMed1997

Fatty acid binding proteins reduce 15-lipoxygenase-induced oxygenation of linoleic acid and arachidonic acid.

Free fatty acids in plasma and cells are mainly bound to membranes and proteins such as albumin and fatty acid binding proteins (FABP), which can regulate their biological activities and metabolic transformations. We have investigated the effect of FABP and albumin on the peroxidation of linoleic acid (18:2) and arachidonic acid (20:4) by 15-lipoxygenase (15-LO). Rabbit reticulocyte 15-LO produced a rapid conversion of [1-14C]18:2 to 13-hydroxyoctadecadienoic acid (13-HODE) and [3H]20:4 to 15-hydroxyeicosatetraenoic acid (15-HETE). 13-HODE formation was reduced when intestinal FABP (I-FABP). liver FABP (L-FABP) or albumin was added. The relative ability of these proteins to reduce 15-LO induced formation of 13-HODE and 15-HETE was BSA > L-FABP > I-FABP. Smaller reductions in activity were observed with 20:4 as compared to 18:2. The IC50-values of I-FABP and L-FABP, using either 18:2 (3.4 microM) or 20:4 (3.4 microM), were 4.6 +/- 0.6 and 1.9 +/- 0.2 microM, respectively, for reduction of 13-HODE and 6.8 +/- 0.3 and 3.1 +/- 0.2 microM, respectively, for reduction of 15-HETE formation. The smaller 15-HETE reduction correlated with decreased binding of 20:4 to the FABP. Titration calorimetry also showed that the I-FABP IC50 for 18:2, 0.25 microM, was lower then for 20:4, 0.6 microM. Thus the reduction in fatty acid lipid peroxidation relates to the binding capacity of each FABP. We also demonstrated that 18:2 rapidly diffuses (flip-flops) across the phospholipid bilayer of small unilamellar vesicles (SUV) and measured partitioning of 18:2 between proteins and SUV by the pyranin fluorescence method [Kamp, F. and Hamilton, J.A. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 11367-11370]. Addition of proteins to SUV in buffer resulted in a complete desorption of 18:2 from SUV with a relative effect of BSA > L-FABP > I-FABP. This suggests that the relative effects of these proteins on 18:2 peroxidation will not be altered by the presence of membranes. Our results indicate that FAPBs protect intracellular polyunsaturated fatty acids against peroxidation and, through differential binding of 18:2 and 20:4, they may modulate the availability of these polyunsaturated fatty acids to intracellular oxidative pathways.

Animals↗
PubMed1997

Polyunsaturated fatty acids increase the sensitivity of 36B10 rat astrocytoma cells to radiation-induced cell kill.

Polyunsaturated fatty acids (PUFA) such as gamma-linolenic acid (GLA, 18:3n-6), eicosapentaenoic acid (EPA, 20:5n-3), and docosahexaenoic acid (DHA, 22:6n-3) have been shown to be cytotoxic to tumor cells. The objective of this work was to study the effects of PUFA on the radiation response of a 36B10 rat astrocytoma cell line. Supplementation of the astrocytoma cells with 15-45 microM GLA, EPA, or DHA produced marked changes in the fatty acid profiles of their phospholipids and neutral lipids. The methylene bridge index of these lipids increased significantly. These PUFA also exerted cytotoxic effects, as determined using the clonogenic cell survival assay. While GLA and DHA produced a moderate cell-killing effect, EPA was extremely cytotoxic, especially at a concentration of 45 microM. The monounsaturated oleic acid (OA, 18:1n-9) did not affect cell survival. Further, all three PUFA, and particularly GLA, increased the radiation-induced cell kill; OA did not enhance the effect of radiation. alpha-Tocopherol acetate blocked the enhanced radiation sensitivity of GLA- and DHA-supplemented cells. In conclusion, GLA, EPA, and DHA supplementation prior to, during, and after irradiation can enhance the radiation-induced cytotoxicity of rat astrocytoma cells. GLA and DHA supplementation post-irradiation also enhanced the radiation response of the 36B10 cells. Because GLA maximally increases the radioresponsiveness of a rat astrocytoma, this PUFA might prove useful in increasing the therapeutic efficacy of radiation in the treatment of certain gliomas.

Animals↗
PubMed1997

Micropipette aspiration on the outer hair cell lateral wall.

The mechanical properties of the lateral wall of the guinea pig cochlear outer hair cell were studied using the micropipette aspiration technique. A fire-polished micropipette with an inner diameter of approximately 4 microm was brought into contact with the lateral wall and negative pressure was applied. The resulting deformation of the lateral wall was recorded on videotape and subjected to morphometric analysis. The relation between the length of the aspirated portion of the cell and aspiration pressure is characterized by the stiffness parameter, K(s) = 1.07 +/- 0.24 (SD) dyn/cm (n = 14). Values of K(s) do not correlate with the original cell length, which ranges from 29 to 74 microm. Theoretical analysis based on elastic shell theory applied to the experimental data yields an estimate of the effective elastic shear modulus, mu = 15.4 +/- 3.3 dyn/cm. These data were obtained at subcritical aspiration pressures, typically less than 10 cm H2O. After reaching a critical (vesiculation) pressure, the cytoplasmic membrane appeared to separate from the underlying structures, a vesicle with a length of 10-20 microm was formed, and the cytoplasmic membrane resealed. This vesiculation process was repeated until a cell-specific limit was reached and no more vesicles were formed. Over 20 vesicles were formed from the longest cells in the experiment.

Animals↗
PubMed1997

Cytochrome P450 metabolites of arachidonic acid: rapid incorporation and hydration of 14,15-epoxyeicosatrienoic acid in arterial smooth muscle cells.

Arachidonic acid is converted to epoxyeicosatrienoic acids (EETs) by cytochrome P450 monooxygenases. EETs produce arterial vasodilatation, and recent evidence suggests that they are endothelium-derived hyperpolarizing factors. In porcine coronary arteries contracted with a thromboxane mimetic agent, we find that relaxation is rapidly initiated by exposure to 14,15-EET. The relaxation slowly increases in magnitude, resulting in a response which is sustained for more than 10 min. Cultured porcine aortic smooth muscle cells rapidly take up [3H]14,15-EET. After 3 min, radioactivity is present in neutral lipids, phosphatidylcholine, and phosphatidylinositol. The cells also convert 14,15-EET to 14,15-dihydroxyeicosatrienoic acid (14,15-DHET), and some DHET is detected in the medium after only 1 min of incubation. Like 14,15-EET, 14,15-DHET produces relaxation of the contracted coronary artery rings. These findings suggest that the incorporation into phospholipids and conversion to 14,15-DHET can occur at a rate that is fast enough to modulate the vasorelaxation produced by 14,15-EET.

8,11,14-Eicosatrienoic Acid↗
PubMed1997

Conversion of arachidonic acid to tetradecadienoic acid by peroxisomal oxidation.

Human skin fibroblasts convert [5,6,8,9,11,12,14,15-3H]arachidonic acid to two radiolabeled polar metabolites that accumulate in the culture medium. Previous studies identified the most abundant of these products as 4,7,10-hexadecatrienoic acid (16:3). We have now identified the second metabolite as 5,8-tetradecadienoic acid (14:2). Fibroblasts deficient in mitochondrial long-chain acyl coenzyme A dehydrogenase produce increased amounts of 14:2 from arachidonic acid. By contrast, Zellweger fibroblasts which are deficient in peroxisomal beta-oxidation do not convert arachidonic acid to either 14:2 or 16:3. These results demonstrate that 14:2 can be synthesized from arachidonic acid, that this oxidative process occurs in the peroxisomes, and that the pathway does not function in Zellweger's syndrome and similar diseases where there is a genetic deficiency in peroxisomal beta-oxidation.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed1997

Potentiation of endothelium-dependent relaxation by epoxyeicosatrienoic acids.

Epoxyeicosatrienoic acids (EETs) are potent endothelium-derived vasodilators formed from cytochrome P-450 metabolism of arachidonic acid. EETs and their diol products (DHETs) are also avidly taken up by endothelial cells and incorporated into phospholipids that participate in signal transduction. To investigate the possible functional significance of EET and DHET incorporation into cell lipids, we examined the capacity of EETs and DHETs to relax porcine coronary arterial rings and determined responses to bradykinin (which potently activates endothelial phospholipases) before and after incubating the rings with these eicosanoids. 14,15-EET and 11,12-EET (5 mumol/L) produced 75 +/- 9% and 52 +/- 4% relaxation, respectively, of U46619-contracted rings, whereas 8,9-EET and 5,6-EET did not produce significant relaxation. The corresponding DHET regioisomers produced comparable relaxation responses. Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated. Pretreatment with 2 mumol/L triacsin C (an inhibitor of acyl coenzyme A synthases) inhibited [3H]14,15-EET incorporation into endothelial phospholipids and blocked 11,12-EET- and 14,15-DHET-induced potentiation of relaxation to bradykinin. Exposure of [3H]14,15-EET-labeled endothelial cells to the Ca2+ ionophore A23187 (2 mumol/L) resulted in a 4-fold increased release of EET and DHET into the medium. We conclude that incorporation of EETs and DHETs into cell lipids results in potentiation of bradykinin-induced relaxation in porcine coronary arteries, providing the first evidence that incorporated EETs and DHETs are capable of modulating vascular function.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Arachidonic acid diols produced by cytochrome P-450 monooxygenases are incorporated into phospholipids of vascular endothelial cells.

Epoxyeicosatrienoic acids (EETs) are synthesized by cytochrome P-450 monooxygenases and released into the blood. When taken up by vascular endothelial and smooth muscle cells, the EETs are primarily esterified to phospholipids or converted to dihydroxyeicosatetraenoic acids (DHETs) and released. In the present studies, radiolabeled 8,9-, 11,12-, and 14,15-DHETs released into the medium from vascular smooth muscle cells were isolated and incubated for 4-16 h with cultured bovine aortic endothelial cells. The uptake ranged from 2 to 50% for the three regioisomers. Hydrolysis of the endothelial lipids and gas chromatographic-mass spectral analyses of the products indicated that all three DHET regioisomers were incorporated intact into phosphatidylcholine and phosphatidylinositol. Similar incubations with EETs confirmed that small amounts of DHETs were also esterified to endothelial phospholipids. These studies indicate that DHETs are incorporated into phospholipids either at the time of EET conversion to DHET or upon release and re-uptake of DHETs. Beside demonstrating for the first time that fatty acid diols are incorporated intact into endothelial lipids, these studies raise the possibility that both EETs and DHETs remain long enough in the vascular wall to produce chronic vasoactive effects.

Animals↗
PubMed1996

The fatty acid composition of human gliomas differs from that found in nonmalignant brain tissue.

To compare the fatty acid composition of tumor tissue from glioma patients with that of normal brain tissue, tissue samples were obtained from 13 glioma patients and from 3 nonmalignant patients. Following lipid extraction, total fatty acid composition was measured using gas-liquid chromatography. samples were further separated into phospholipids and neutral lipids. Representative samples were then separated into phospholipid classes by thin-layer chromatography and the fatty acid composition assayed. Levels of the polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA), were significantly reduced (P = 0.029) in the glioma samples compared with normal brain samples; mean values were 4.8 +/- 2.9% and 9.2 +/- 1.0%, respectively. This reduction in glioma DHA content was also observed in terms of phospholipids (4.6 +/- 2.1% vs. 9.6 +/- 0.8%, P = 0.002). The phosphatidylserine and phosphatidylethanolamine phospholipid classes were reduced in the glioma samples. Differences were also noted in the n-6 PUFA content between glioma and normal brain samples. The glioma content of the n-6 PUFA linoleic acid was significantly greater (P < 0.05) than that observed in the control samples in terms of total lipids. Thus, the fatty acid composition of human gliomas differs from that found in nonmalignant brain tissue.

Adolescent↗
PubMed1996

Functional implications of a newly characterized pathway of 11,12-epoxyeicosatrienoic acid metabolism in arterial smooth muscle.

Epoxyeicosatrienoic acids (EETs) are potent vasodilators derived from cytochrome P-450 metabolism of arachidonic acid. The rapid conversion of EETs to their corresponding dihydroxyeicosatrienoic acids (DHETs) has been proposed as a process whereby EETs are rendered biologically inactive. However, the vascular metabolism of EETs and the vasoactivities of EET metabolites have not been extensively studied. Accordingly, 11,12-EET metabolism was characterized in porcine aortic smooth muscle cells. The cells converted [3H]11,12-EET to 11,12-DHET and to a newly identified metabolite, 7,8-dihydroxy-hexadecadienoic acid (DHHD). 11,12-DHET accumulation in the medium reached a maximum in 2 to 4 hours and then declined, whereas 7,8-DHHD accumulation increased continuously and exceeded the amount of 11,12-DHET by 8 hours. [3H]11,12-EET conversion to radiolabeled 7,8-DHHD was reduced in the presence of unlabeled 11,12-DHET, indicating that 11,12-DHET is an intermediate in the conversion of 11,12-EET to 7,8-DHHD. This is consistent with a pathway whereby 11,12-EET is converted by an epoxide hydrolase to 11,12-DHET, which then undergoes two beta-oxidations to form 7,8-DHHD. In porcine coronary artery rings contracted with a thromboxane mimetic, 11,12-DHET produced relaxation similar in magnitude to that produced by 11,12-EET (77% versus 64% relaxation at 5 mumol/L, respectively). 7,8-DHHD also produced vasorelaxation. Thus, the vasoactivity of 11,12-EET is not eliminated by conversion to 11,12-DHET and 7,8-DHHD. These results suggest that 11,12-DHET and its metabolite, 7,8-DHHD, may contribute to the regulation of vascular tone in the porcine coronary artery and possibly other vascular tissues.

8,11,14-Eicosatrienoic Acid↗
PubMed1995

Functional and ultrastructural effects of essential fatty acid deficiency in kidney epithelial cells.

Madin-Darby canine kidney (MDCK) epithelial cells were grown in culture medium supplemented with 1% fetal bovine serum (FBS) to provide a cell culture model of essential fatty acid deficiency (EFAD). 5,8,11-Eicosatrienoic acid (20:3n-9) accumulated in cellular phospholipids, and arachidonic acid (20:4) decreased. A large increase in cellular cholesterol/phospholipid ratio was observed. Hemicyst formation was greatly reduced from normal levels in the EFAD-MDCK cells. Scanning and transmission electron microscopy revealed that EFAD-MDCK were much flatter than their normal counterparts. They had much less dense surface microvilli, mitochondria and other organelles were very sparse, except in the perinuclear area, and much of the peripheral cytoplasm was amorphous. The EFAD was rapidly reversed by the addition of as little as 10 microM linoleic or arachidonic acid to the medium. Cells supplemented with 10% FBS, the usual culture condition, displayed borderline EFAD, with intermediate levels of 20:3n-9 and 20:4 and hemicyst formation. These studies suggest that EFAD reduces water and electrolyte transport in renal tubular epithelium.

8,11,14-Eicosatrienoic Acid↗
PubMed1995

Epoxyeicosatrienoic acid metabolism in arterial smooth muscle cells.

Epoxyeicosatrienoic acids (EETs) are eicosanoids synthesized from arachidonic acid by the cytochrome P450 eposygenase pathway. The present studies demonstrate that 8,9-, 11,12-, and 14,15-EET are rapidly taken up by porcine aortic smooth muscle cells. About half of the uptake is incorporated into phospholipids, and saponification indicates that most of this remains in the form of EET. The EETs also are converted to the corresponding dihydroxyeicosatrienoic acids (DHETs) and during prolonged incubations, additional metabolites that do not retain the EET carboxyl group are formed. Most of these products are released into the medium. However, some DHET and metabolites less polar than EET are incorporated into the phospholipids, and a small amount of unesterified EET is also present in the cells. The incorporation of 14,15-EET and its conversion to DHET did not approach saturation until the concentration exceeded 10-20 microM, indicating that vascular smooth muscle has a large capacity to utilize this EET. These findings suggest that certain vasoactive effects of EETs may be due to their incorporation by smooth muscle cells. Furthermore, through conversion to DHET and other oxidized metabolites, smooth muscle apparently has the capacity to inactivate EETs that are either formed in or penetrate into the vascular wall.

8,11,14-Eicosatrienoic Acid↗
PubMed1995

Docosahexaenoic acid synthesis in human skin fibroblasts involves peroxisomal retroconversion of tetracosahexaenoic acid.

The purpose of this study was to determine whether the formation of docosahexaenoic acid in human cells occurs through a pathway that involves 24-carbon n-3 fatty acid intermediates and retroconversion. Normal human skin fibroblasts synthesized radiolabeled docosahexaenoic acid from [1-(14)C]18:3n-3, [3-(14)C]22:5n-3, [3-(14)C]24:5n-3, and [3-(14)C]24:6n-3. The amount of docosahexaenoate formed was reduced in fibroblasts defective in peroxisomal biogenesis, by 90-100% in Zellweger's syndrome and by 50-75% in infantile Refsum's disease. Fatty acid elongation and desaturation were intact in these mutant cells. No decrease in radiolabeled docosahexaenoic acid production occurred in mutant fibroblasts defective in peroxisomal alpha-oxidation or mitochondrial beta-oxidation, or in normal fibroblasts treated with methyl palmoxirate to inhibit mitochondrial beta-oxidation. Therefore, the retroconversion step in docosahexaenoic acid formation occurs through peroxisomal beta-oxidation in normal human cells. These results demonstrate that the pathway for docosahexaenoic acid synthesis in human cells involves 24-carbon intermediates. The limited ability to synthesize docosahexaenoic acid may underlie some of the pathology that occurs in genetic diseases involving peroxisomal beta-oxidation.

Cells, Cultured↗
PubMed1994

Formation and release of a peroxisome-dependent arachidonic acid metabolite by human skin fibroblasts.

Human skin fibroblasts labeled with [5,6,8,9,11,12,-14,15-3H]arachidonic acid produce a radioactive metabolite that has a shorter retention time on reverse-phase high-performance liquid chromatography than arachidonic acid. This product is not retained in the cells; it is released entirely into the extracellular fluid in a time-dependent manner. The metabolite does not cochromatograph with any of the eicosanoid standards, and its formation is not prevented by the addition of cyclooxygenase, lipoxygenase, or cytochrome P-450 inhibitors. The compound is not produced by fibroblasts labeled with [1-14C]arachidonic acid, suggesting that it is formed through an oxidative process. Chemical analyses indicated that the metabolite is 4,7,10-hexadecatrienoic acid (16:3). Peroxisome-deficient human skin fibroblasts did not produce 16:3, indicating that it probably is formed through peroxisomal beta-oxidation. Human umbilical vein endothelial cells and porcine pulmonary artery smooth muscle cells also release radioactive 16:3 following labeling with [3H]arachidonic acid. Therefore, the production of this metabolite is not limited only to fibroblasts. The fact that 16:3 is released into the extra-cellular fluid suggests that it may be a new type of lipid mediator derived from arachidonic acid, formed through a peroxisome-dependent oxidative process.

Animals↗
PubMed1994

15-HETE: selective incorporation into inositol phospholipids of MDCK cells.

The interaction of 15-hydroxyeicosatetraenoic acid (15-HETE) and cultured MDCK renal tubular epithelial cells was investigated to determine whether incorporation of this lipoxygenase product will affect polyphosphoinositide formation. MDCK cells were incubated with 1 microM [3H]-15-HETE for 15 to 120 minutes. Maximum uptake occurred between 15 and 30 minutes, and after 60 minutes, 70% of the incorporated 15-HETE was present in the phosphatidylinositol (PI) fraction. Some 15-HETE was also incorporated into phosphatidylinositol-4-monophosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2). However, even though more 15-HETE than arachidonic acid was incorporated into PI, the fractional amount of 15-HETE present in the polyphosphoinositides was smaller than arachidonic acid. Therefore, although 15-HETE is selectively channeled into PI, conversion of PI species containing 15-HETE to PIP and PIP2 is relatively impaired. This suggests that either PI containing 15-HETE is a less effective substrate for phosphorylation, or PI containing arachidonic acid is a preferred substrate. MDCK cells converted 15-HETE to polar metabolites that were released into the extracellular fluid. This process may constitute a renal tubular mechanism for the clearance of 15-HETE and related lipoxygenase products.

Animals↗
PubMed1994

13-HODE increases intracellular calcium in vascular smooth muscle cells.

13-Hydroxyoctadecadienoic acid (HODE) (2 microM) consistently increased porcine aortic and pulmonary artery smooth muscle cell calcium concentrations ([Ca2+]i), whereas 9-HODE and linoleic acid had no significant effect in the aortic cells and a much lesser effect in the pulmonary artery cells. A transient increase in [Ca2+]i occurred with as little as 50 nM 13-HODE. Structural specificity for elevation of [Ca2+]i also was seen with the monohydroxyeicosatetraenoic acids (HETEs), with 12-HETE but not 5- or 15-HETE increasing [Ca2+]i. 13-HODE, but not 9-HODE, increased smooth muscle cell guanosine 3',5'-cyclic monophosphate (cGMP) levels. The [Ca2+]i increase produced by 13-HODE was dependent on extracellular calcium and was inhibited by the calcium channel blockers verapamil and nifedipine and by KT-5823, a cGMP-dependent kinase inhibitor. A similar increase in [Ca2+]i was produced by 8-bromo-cGMP. These results suggest that 13-HODE, a 15-lipoxygenase product formed from linoleic acid, can act as a lipid mediator in vascular smooth muscle. It raises smooth muscle cGMP, causing a secondary increase in [Ca2+]i due to Ca2+ influx through a cGMP kinase-dependent L-type channel.

Animals↗
PubMed1994

Cell fatty acid composition affects free radical formation during lipid peroxidation.

Lipid-derived free radicals generated from intact human U937 monocytes exposed to iron-induced oxidative stress were detected by electron paramagnetic resonance (EPR) with the spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN). Lipid radical formation was enhanced when the cells were enriched with n-3 or n-6 polyunsaturated fatty acids. Computer simulation indicated that at least two POBN spin adducts were formed, having spectral characteristics consistent with carbon-centered radicals (aN = 15.9 G and aH = 2.6 G; aN = 15.1 G and aH = 2.8 G). These alkyl radicals are probably formed by beta-scission of alkoxyl radicals. POBN spin adduct formation correlated with ethane generation. Addition of ascorbate to the assay medium greatly increased the radical signal intensity. Although radical generation was cell dependent and POBN spin adducts were observed in cell homogenates, the adducts formed by the intact cells were detected only in the extracellular medium. These findings indicate that the extent of lipid radical formation in response to oxidative stress can be influenced by changes in the polyunsaturated fatty acid composition of the cell lipids and suggest the possibility that carbon-centered lipi radicals may interact with extracellular structures.

Ascorbic Acid↗
PubMed1994

Regulation of CTP:choline-phosphate cytidylyltransferase by polyunsaturated n-3 fatty acids.

Disaturated phosphatidylcholine (DSPC) is the most distinctive surface-active lipid in pulmonary surfactant. The feeding of docosahexanoic acid (DHA) 22:6 n-3 has recently been described to elevate the levels of DSPC in rodent lung. The purpose of the present study was to determine the mechanisms by which this n-3 fatty acid might regulate CTP:choline-phosphate cytidylyltransferase, a key enzyme required for phosphatidylcholine (PC) synthesis. Cytidylyltransferase exists in lung cytosol as a large lipid-associated aggregate (H form) which is active, and as an inactive, low-molecular-weight species (L form). Fatty acids in vitro stimulate and aggregate the inactive L form to the active H form. Short-term (2-h) and long-term (24-h) exposure of fetal lung explants to DHA (150 microM) stimulated choline incorporation into PC by 54 and 64%, respectively. The fatty acid also enhanced DSPC synthesis by 88%. These changes were associated with an increase in the activity of cytidylyltransferase by 63% after addition of DHA to the explant medium. In vitro, DHA (50 microM) stimulated L form nearly 15-fold and appeared to be a more potent activator and aggregator of the enzyme than either linoleic 18:2 n-6 or arachidonic 20:4 n-6 acids. The effect of DHA on L-form activation was comparable, however, with other members of the n-3 family. Kinetic studies revealed that DHA increased the maximum velocity of enzyme reaction for cytidylyltransferase, although it did not alter the Michaelis constant of the enzyme for CTP. These observations provide in vitro evidence that n-3 fatty acids may play an important role in the regulation of surfactant PC biosynthesis.

Animals↗