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PubMed1994

Cholesterol, phospholipid and phospholipase activity of ampullary and isthmic fluid from the bovine oviduct.

Cholesterol and phospholipid concentrations and phospholipase activity were measured in fluid from cannulae collected from the bovine oviductal isthmus and ampulla at different stages of the oestrous cycle. The cholesterol concentration and cholesterol normalized by protein were significantly (P = 0.03) greater in isthmic oviductal fluid (224.3 +/- 42.7 micrograms ml-1 over all stages) than in ampullary oviductal fluid (164.5 +/- 11.3 micrograms ml-1), and maximal concentrations (284.5 +/- 25.5 micrograms ml-1) were found during the luteal stage (serum progesterone concentration > or = 1.5 ng ml-1). The concentrations of the phospholipids sphingomyelin and lysophosphatidylcholine increased at different stages of the cycle and in different regions. In the ampulla, the concentration of sphingomyelin was significantly (P < 0.05) greater in oviductal fluid collected during the luteal phase (12.1 +/- 2.7% of total phospholipids) than in fluid collected near oestrus and ovulation (7.5 +/- 1.5% and 6.9 +/- 1%, respectively). The concentration of lysophosphatidylcholine was greater (P < 0.01) in ampullary (19.2 +/- 1.6% of total phospholipids) than in isthmic oviductal fluid (9.9 +/- 1.1%) collected near ovulation. The ratio of cholesterol to total phospholipid was highest in oviductal fluid collected from the isthmus during all stages (2.3 micrograms ml-1:% total phospholipid), while the minimal ratio was found in ampullary fluid collected near ovulation (1.5). Phospholipase activity was higher (P = 0.03) in isthmic oviductal fluid (20.4 +/- 3.2% product formed) than in ampullary oviductal fluid (14.6 +/- 1.4%); the lowest activity (12.6 +/- 1.7% product formed) was in fluid collected during the phase of the oestrous cycle immediately before ovulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Phospholipid methylation in canine cardiac membranes. Relations to beta-adrenergic receptors and digitalis receptors.

Phospholipid methylation of canine cardiac membranes was studied in vitro to determine its relationship to the regulation and function of beta-adrenergic and digitalis receptors. Cardiac membranes were prepared from the left ventricle of mongrel dogs. Phospholipid methylation was assayed by measuring [3H] methyl incorporation after incubation with methyl donor S-adenosyl-L-[methyl-3H] methione at 37 degrees C. The reaction of phospholipid methylation had an optimum pH around 9 and a linear time course of up to 60 min. The reaction was inhibited by the addition of S-adenosyl-L-homocysteine, a known antagonist of biological transmethylation. L-isoproterenol enhanced phospholipid methylation markedly, but ouabain had no effect. On the other hand, after phospholipid methylation in cardiac membranes was stimulated by pre-incubation with S-adenosyl-L-methionine for 60 min at 37 degrees C, [125I] iodohydroxybenzylpindolol binding to the membranes was increased. The number of the beta-adrenergic receptor binding sites (Bmax), calculated from Scatchard analysis in cardiac membranes of 3 dogs significantly increased. On the other hand, [3H] ouabain binding and Na+, K+, Mg2+-ATPase activity were not increased. The increase in [125I] iodohydroxybenzylpindolol binding was inhibited by the addition of S-adenosyl-L-homocysteine. These binding suggest that phospholipid methylation is closely related to beta-adrenergic receptors, but not digitalis receptors in cardiac membranes.

Animals↗
PubMed2003

Quantitative trait locus analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels in the (SM/J x A/J)F2 mice.

Quantitative trait locus (QTL) analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels at 10 weeks of age was performed in 321 F2 offspring from SM/J and A/J mice. Interval mapping revealed a total of 22 suggestive QTLs affecting the four traits: two insulin QTLs on Chromosomes (Chrs) 6 and 8; six triglyceride QTLs on Chrs 4, 8, 9, 11, 12 and 19; six total-cholesterol QTLs on Chrs 1, 3, 4, 14, 17 and 19; and eight phospholipid QTLs on Chrs 2, 3, 4, 6, 8, 10 and 19. Gender influenced the expression of eight of the suggestive QTLs. The total-cholesterol QTLs on Chrs 4, 14 and 17, the triglyceride QTL on Chr 9 and the phospholipid QTL on Chr 4 were specific to females. The phospholipid QTLs on Chrs 2 and 6 and the insulin QTL on Chr 8 were specific to males. In addition, common QTLs involved in the regulation of some of the traits were identified. The female-specific QTL on Chr 4 appeared to be involved in the regulation of total cholesterol and phospholipid levels. The QTL on Chr 8 affected insulin and phospholipid levels, whereas the Chr 19 QTL was common to the three lipid parameters.

Animals↗
PubMed1983

Characteristics of phospholipids associated with fibrins in partial thromboplastin test.

With the aim to obtain information on the role of individual phospholipids in the coagulation process, lipids associated with fibrins formed with partial thromboplastin reagents were examined. In the absence of the partial thromboplastin reagents, phosphatidylethanolamine and phosphatidylserine plus phosphatidylinositol in citrated plasma were incorporated preferentially into fibrin, although the main phospholipid associated with the fibrin was phosphatidylcholine. In the presence of the partial thromboplastin reagents, most phospholipids unseparable from the corresponding fibrins appeared to be derived from the reagents with little selectivity for individual phospholipids, except for lysophosphatidylcholine. These results suggest that phospholipids other than thromboplastic phospholipids may play some role in the coagulation process. The incorporation of lysophosphatidylcholine in the reagent into fibrins was significantly enhanced by the addition of activating agents (celite and ellagic acid), suggesting one role of the activating agents in fibrin formation.

Blood Coagulation↗
PubMed1999

In vitro thermogenesis and phospholipid fatty acid composition of brown adipose tissue in fasted and refed rats.

Membrane phospholipids are known for their role in the regulation of membrane structures and functions. Membrane phospholipid fatty acid docosahexaenoic acid (DHA) has been recently indicated to be important for the regulation of cellular activities, including metabolic regulation. Our previous studies have indicated the involvement of DHA in the regulation of brown adipose tissue (BAT) thermogenesis. The objective of the present study is to examine the changes in BAT phospholipid fatty acid composition including DHA and thermogenic activity in fasted and refed rats. Phospholipid content per microgram DNA was decreased in rats fasted for 72 h and it was not restored to the control level by refeeding for 72 h. Phospholipid fatty acid composition of BAT, as expressed by mol%, was modified in the fasted rats. Most notably, DHA, which constituted about 89% of the n-3 polyunsaturated fatty acids, was decreased concomitant with the increase in the n-6 polyunsaturated fatty acid arachidonic acid. The monounsaturated to saturated fatty acid ratio, which is an index of Delta(9)-desaturase activity and membrane fluidity, was decreased. Thermogenesis, as measured by the in vitro oxygen consumption of BAT, was suppressed in the fasted rats. All of the above changes were restored to normal levels after refeeding the fasted rats for 72 h. In vitro oxygen consumption correlated with the level of DHA and monounsaturated to saturated fatty acid ratio. These results indicate that the modification of phospholipid fatty acid composition, especially the modification of n-3 polyunsaturated fatty acid DHA, and membrane fluidity are related to BAT thermoregulation in fasted and refed rats.

Adipose Tissue, Brown↗
PubMed2003

Phospholipid analogs against HIV-1 infection and disease.

Phospholipid analogs are a new class of compounds with potent activity against HIV infection when used alone or conjugated with other therapeutic agents. When conjugated to the nucleoside analog AZT, the resulting phospholipid-AZT conjugate can double target the virus replication cycle by inhibiting the viral reverse transcriptase (by AZT) and inducing the production of defective virus particles that lack functional gp120 expression on the virus surface resulting in reduced capacity to bind to CD4+ cells and inhibition of infected cell-cell fusion (by phospholipid). Of great interest are data indicating that selected phospholipids are active against drug resistant variants, a current major problem in treating HIV/AIDS and controlling the epidemic occurring in various parts of the world. The purpose of this review is to provide current information on the design and synthesis of various types of phospholipids and phospholipid conjugates, in-vitro and in-vivo antiviral activity, tissue distribution, intracellular metabolism, and mechanism of action. The future development of this novel class of compounds offers an exciting approach for reducing the toxicity and enhancing the distribution of therapeutic drugs to the lymphatics and central nervous system and suppressing the emergence of drug resistant variants of HIV.

Anti-HIV Agents↗
PubMed1992

Specificity of antibodies to single-stranded (ss) DNA in SLE patients with anti-phospholipid syndrome.

Although the concept of anti-phospholipid syndrome has been proposed in patients with SLE and other rheumatic diseases, the immunological mechanism is still controversial. Recently, the crossreactivity between anti-cardiolipin antibody and anti-ssDNA antibodies has been discussed in relation to this syndrome. In the present study, the specificity such as the avidity and the crossreactivity of anti-ssDNA antibodies was examined to find a clue to clarify the question why all of anti-cardiolipin antibody positive patients do not have any specific clinical features, thrombosis and spontaneous abortion. The avidity of IgG anti-ssDNA antibodies was examined by salt elution studies in solid phase ELISA. The avidity of anti-ssDNA antibodies tended to be lower in 10 patients with specific features than in other 10 patients without those features. The crossreactivity of affinity purified IgG anti-ssDNA antibodies was investigated by competitive ELISA. Purified anti-ssDNA antibodies from 4 patients without specific features were slightly inhibited by negatively charged phospholipids, cardiolipin and phosphatidylserine, whereas purified anti-ssDNA antibodies from 2 patients with specific features, who were considered to have anti-phospholipid syndrome, were little inhibited by these phospholipids. The above results suggest that the specificity of anti-ssDNA antibodies appears, at least partly, in different manners whether specific features are present or absent in anti-cardiolipin antibody positive patients. Moreover, anti-ssDNA antibodies and anti-phospholipid antibodies may form separate groups of antibodies in patients with anti-phospholipid syndrome.

Antibody Specificity↗
PubMed1984

The mechanism of action of insulin on phospholipid metabolism in rat adipose tissue. Requirement for protein synthesis and a carbohydrate source, and relationship to activation of pyruvate dehydrogenase.

We studied certain metabolic requirements for insulin-induced increases in phospholipids, and the relationship of phospholipid changes to the insulin-induced activation of pyruvate dehydrogenase, in rat adipocytes and fat pads in vitro. Increases in the contents of phosphatidylinositol and phosphatidylserine mass were maximal in rat fat pads within 10 min of incubation with insulin, and preceded or accompanied measurable increases in pyruvate dehydrogenase activity. In dose-response studies, the contents of these phospholipids and pyruvate dehydrogenase activity increased in parallel in response to increasing concentrations of insulin. Cycloheximide and puromycin inhibited insulin-induced increases in the mass of both of these phospholipids, as well as (in confirmation of previous reports) pyruvate dehydrogenase activity. Effects of insulin on phospholipid metabolism and pyruvate dehydrogenase were found to require an exogenous carbohydrate source, and fructose was nearly as effective as glucose in this regard. Insulin-induced increases in phosphatidylinositol and phosphatidylserine were demonstrated in the mitochondrial fraction, which is also the subcellular locus of pyruvate dehydrogenase. The present findings suggest that there is a relationship between insulin-induced increases in phospholipids and pyruvate dehydrogenase activity, but the nature of this relationship remains to be defined.

Adipose Tissue↗
PubMed1992

Drug-phospholipid interactions: role in aminoglycoside nephrotoxicity.

Aminoglycoside antibiotics are known to be transported and accumulated within lysosomes of renal proximal tubular cells and to cause proximal tubular cell injury and necrosis. The pathogenesis of aminoglycoside nephrotoxicity is postulated to be related to the capacity of these organic polycations to interact electrostatically with membrane anionic phospholipids and to disrupt membrane structure and function. Aminoglycoside antibiotics have been shown to bind to anionic phospholipids of model membranes and to alter membrane permeability and promote membrane aggregation. In vivo these drugs induce phospholipiduria and a renal cortical phospholipidosis. The latter reflects the accumulation of phospholipid-containing myeloid bodies within the lysosomal compartment consequent to aminoglycoside-induced inhibition of lysosomal phospholipases. The mechanism of drug-induced inhibition of phospholipases has been shown to be secondary to the binding of these cationic drugs to anionic phospholipids. As the lysosomes became progressively distended with myeloid bodies, they become unstable and eventually rupture, which results in the release of acid hydrolases as well as high concentrations of aminoglycosides into the cytoplasm where they interact with and disrupt the function of other membranes and organelles including mitochondria and microsomes. It is postulated that the redistribution of drug from the lysosomal compartment to organellar membranes is the critical event which triggers the irreversible injury cascade. Polyaspartic acid is a polyanionic peptide which when administered in vitro or in vivo forms electrostatic complexes with aminoglycoside antibiotics and prevents these drugs from interacting with anionic phospholipids, from perturbing phospholipid metabolism and from causing cell injury and necrosis.

Aminoglycosides↗
PubMed1988

[Fatty acid composition of platelet phospholipids and plasma lipids in obese Zucker rats].

The purpose of this work was to see whether hyperlipaemia observed in genetically obese Zucker rats (fa/fa) was associated with differences in fatty-acid composition of plasma triacylglycerols, plasma phospholipids and of platelet phospholipids, in comparison with the control lean rats (Fa/-). Results showed that plasma triacylglycerols and phospholipids were increased in obese rats. In triacylglycerols, the amount of saturated and monounsaturated fatty acids was highly increased whereas the amount of the n-6 and n-3 polyunsaturated fatty acids was little modified. In plasma phospholipids, saturated and monounsaturated fatty acids were also increased, as were the n-3 fatty acids (except C 18:3 n-3); the n-6 fatty acids were little increased except C 20:3 n-6 which was markedly increased. These results concerning the amounts of fatty acids have their counterpart in their relative proportions of fatty acids. Data thus obtained suggest that conversion of linoleic acid (C 18:2 n-6) into arachidonic acid (C 20:4 n-6) was decreased in obese rats, particularly the delta 5 desaturation step. On the contrary, conversion of linolenic acid (C 18:3 n-3) into higher polyenes seemed increased. Thrombocytosis was not modified in the obese rat, but the volume of the platelets was increased. Platelet phospholipids exhibited the same modifications as plasma phospholipids but with different magnitude. Saturated and monounsaturated fatty acids were little augmented, n-3 fatty acids were more augmented (except C 18:3 n-3 acid which was unchanged); n-6 fatty acids were not modified except C 20:3 n-6 acid which was highly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A method for separation and quantification of phospholipid classes in human milk.

A simple, isocratic method for separating the major phospholipid classes of human milk by HPLC is described. Resolution of phosphatidylinositol, phosphatidylserine, phosphatidylethanolamine, lysophosphatidylethanolamine, phosphatidylcholine, and spingomyelin from human milk phospholipids was achieved in 30 min on a silica column. Total phospholipids were injected in 50 microliter of chloroform:diethyl ether (1:2, vol/vol) and eluted with a solvent mixture of acetonitrile:methanol:sulfuric acid (100:3:.05, vol/vol/vol) at a flow rate of 2.5 ml/min. Fractions were collected and each phospholipid class quantified by analysis of inorganic phosphorus after sulfuric acid digestion. A repeatability study with 19 samples had a coefficient of variation of 5.3%. The analytical recoveries of phospholipid standards averaged 98%. Recoveries varied with phospholipid class; variation was greatest with spingomyelin.

Chromatography, High Pressure Liquid↗
PubMed1988

Alterations in phospholipid composition of egg yolks from laying hens fed choline and methionine-supplemented diets.

A trial was conducted to assess the effects of choline and methionine supplementation of the diets of hens on phospholipid composition of egg yolk. By chemical analysis, the basal diet contained 16.6% protein, 1,041 parts per million (ppm) of choline, and .53% TSAA. The energy level was 2,899 kcal ME/kg diet, with no added fat. A rapid isocratic HPLC procedure using a Waters mu Bond-NH2 column (Waters Associates, Milford, MA) was developed to quantify phospholipid components. Analysis of egg samples at peak production (36 wk of age) showed significant (P less than .05) elevations in total phospholipids, phosphatidylcholine (PC), and the ratio of PC to phosphatidylethanolamine (PE), when choline was added at 500 or 1,000 ppm. Phosphatidylethanolamine, in contrast, showed a decline with choline supplementation. Methionine supplementation (125 to 250 ppm) also caused elevations in the total phospholipid composition of the egg yolk but had only modest effects on PC and PE. There was a significant (P less than .05) correlation between the yolk weight and total phospholipid concentration, PC, and the PC:PE ratio. There was a relationship between phospholipid content and weight of eggs when diets of laying hens were supplemented with choline.

Animals↗
PubMed2001

Lupus antibody bivalency is required to enhance prothrombin binding to phospholipid.

Lupus anticoagulants (LA) are a family of autoantibodies that are associated with in vitro anticoagulant activity but a strong predisposition to in vivo thrombosis. They are directed against plasma phospholipid-binding proteins including prothrombin. We have proposed that LA propagates coagulation in flowing blood by facilitating prothrombin interaction with the damaged blood vessel wall. A murine monoclonal anti-prothrombin Ab and three of three LA IgGs enhanced prothrombin binding to 75:25 phosphatidyl choline:phosphatidyl serine vesicles measured by either ultracentrifugation or right-angle light scattering. The assembly of prothrombin and LA IgG on phospholipid vesicles was estimated by surface plasmon resonance. The on rates for prothrombin and LA IgG were approximately the same as the on rate for prothrombin alone. In contrast, the off rates for prothrombin and LA IgG were 2- to 3-fold slower than the off rate for prothrombin. LA IgG bivalency was required for enhanced prothrombin binding to phospholipid vesicles, as Fab of the LA IgGs did not influence prothrombin binding at concentrations up to 40 microM. Modeling of the interactions of prothrombin, LA IgG and phospholipid vesicles indicated that augmentation of prothrombin binding to phospholipid vesicles by LA IgG could be accounted for by the bivalency of the LA IgG and the elevated microenvironmental concentration of prothrombin on the surface of phospholipid vesicles.

Adjuvants, Immunologic↗
PubMed2005

Prevalence and clinical correlation of anti-phospholipid-binding protein antibodies in anticardiolipin-negative patients with systemic lupus erythematosus and women with unexplained recurrent miscarriages.

CONTEXT: Anti-phospholipid antibodies (aPL) are a heterogeneous group of autoantibodies, the presence of which is associated with thrombotic events and miscarriage. OBJECTIVE: To establish whether antibodies directed against phospholipid-binding plasma proteins such as beta(2)-glycoprotein I (beta(2)GPI), prothrombin (PT), and annexin V (Anx V) constitute a risk factor for thromboembolism in patients with systemic lupus erythematosus (SLE) and for miscarriage in women with recurrent pregnancy loss (RPL), independently of the presence of the classic anticardiolipin (aCL) antibodies, and whether their determination together with that of aCL would help to increase the diagnostic sensitivity of aPL tests. DESIGN: The prevalence of various antibodies directed toward phospholipids (CL and other anionic phospholipids [APL]) and phospholipid-binding proteins (beta(2)GPI, PT, and Anx V) was determined by immunoenzymatic methods in 311 serum samples. PATIENTS: Twenty-five patients with aCL-positive primary anti-phospholipid syndrome (pAPS); 89 patients with SLE, 23 of whom had thrombotic complications (SLE/APS) and 66 of whom had no thrombosis; and 77 women with unexplained recurrent pregnancy loss comprised our study group. One hundred twenty healthy subjects matched for age and sex were studied as the control group. RESULTS: Immunoglobulin (Ig) G and/or IgM aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 25 (100%), 20 (80%), 15 (60%), and 6 (24%), respectively, of the 25 aCL-positive pAPS patients; IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 33 (37%), 42 (47%), 31 (35%), 40 (45%), and 12 (13%) of the 89 SLE patients, respectively. Of the 56 SLE patients who proved to be aCL negative, anti-beta(2)GPI was present in 3 patients (5%), anti-PT in 13 (23%) patients, and anti-Anx V in 5 (9%) patients. In the subset of 23 SLE/APS patients, IgG anti-PT prevalence was higher than that of the other autoantibodies (87% vs 70% aCL, 66% aAPL, 57% anti-beta(2)GPI, and 4% anti-Anx V), and in 26% of cases, IgG anti-PT was the only antibody present. Anti-PT had a slightly lower specificity than aCL (46% vs 49%); however, the occurrence of both antibodies brought the specificity to 92.4%. The highest risk for thrombosis in SLE patients was associated with the presence of IgG anti-PT antibody (odds ratio [OR] 15.3, P < .001, vs 6.5 aCL, 3.5 aAPL, 3.4 anti-beta(2)GPI, 0.2 anti-Anx V). Fifty-one of the 77 women with recurrent pregnancy loss were negative for all antibodies investigated; the prevalence of IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies was 6% (5), 12% (9), 6% (5), 16% (12), and 17% (13), respectively. Of the 67 aCL-negative women, none had anti-beta(2)GPI antibodies, 7 (11%) were anti-PT positive, and 13 (19%) were anti-Anx V positive. In the subgroup of 26 recurrent pregnancy loss patients who had at least one antibody, anti-Anx V was present in 50% of cases (in 42% as the sole antibody) and was the only antibody significantly associated with miscarriage (P = .02). CONCLUSIONS: The results of this study indicate that it is useful to measure anti-PT antibodies in addition to the more widely used aCL and anti-beta(2)GPI antibodies in the prognostic evaluation of SLE patients for the risk of thrombosis, and the results also confirm that anti-Anx V antibodies may play an important role in recurrent pregnancy loss.

Abortion, Spontaneous↗
PubMed1976

[Incorporation of 32P-orthophosphate in aortic phospholipids in chronic lathyrims in the rat].

Study of 32P orthophosphate incorporation into rat aortic phospholipids after B.A.P.N. treatment, which was followed or not by a lipid-supplemented diet (4.5 p. 100 cholesterol and 37 p. 100 butter). The 32P orthophosphate turnover in the total phospholipid was twice as slow among B.A.P.N.-treated rat than among control-rat. Such a decrease of the 32P orthophosphate turnover could be found as well in phosphatidylethanolamines, phosphatidylcholines and lysophosphatidylcholines. Sphingomyelins showed a very weak metabolic activity among two groups of rats. 32P orthophosphate incorporation into inositolphosphatides was slowed down by B.A.P.N. treatment. Maximal specific activity of inositolphosphatides after injection of 32P orthophosphate was reached within 4 hours in control rats, and 8 hours in B.A.P.N.-treated rats. Three months after the end of B.A.P.N. treatment, no difference in specific activity could be found between control-rats and B.A.P.N.-treated rats. Lipid supplemented diet modified the metabolic activity of phospholipids equally in control rats and B.A.P.N.-treated rats. Specific activity decrease in total phospholipids, phosphatidylcholines, phosphatidylethanolamines, and increase in lysophosphatidylcholines were noted in both groups of animals under a high rat diet. These modifications of the metabolic activity of different phospholipids were most marked fourteen hours after 32P orthophosphate injection. B.A.P.N. treatment only slowed the incorporation of 32P phosphate into phospholipids. Administration of a single lipid supplemented diet or a diet associated with B.A.P.N. treatment induced a slower turnover of phosphatidylcholines and phosphatidylethanolamines, and a faster turnover of lysophosphatidylcholines.

Aminopropionitrile↗
PubMed2000

Phospholipid supplementation reverses behavioral and biochemical alterations induced by n-3 polyunsaturated fatty acid deficiency in mice.

This study investigated the effects of a diet deficient in alpha-linolenic acid followed or not by supplementation with phospholipids rich in n-3 polyunsaturated fatty acids (PUFA) on behavior and phospholipid fatty acid composition in selected brain regions. Three weeks before mating, two groups of mice were fed a semisynthetic diet containing both linoleic and alpha-linolenic acid or a diet deficient in alpha-linolenic acid. Pups were fed the same diet as their dams. At the age of 7 weeks, a part of the deficient group was supplemented with n-3 PUFA from either egg yolk or pig brain phospholipids for 2 months. In the open field, rearing activity was significantly reduced in the deficient group. In the elevated plus maze (anxiety protocol), the time spent on open arms was significantly smaller in deficient mice than in controls. Using the learning protocol with the same task, the alpha-linolenic acid deficiency induced a learning deficit. Rearing activity and learning deficits were completely restored by supplementation with egg yolk or cerebral phospholipids, though the level of anxiety remained significantly higher than that of controls. There were no differences among the 4 diet groups for either the Morris water maze or passive avoidance. In control mice, the level of 22:6 n-3 was significantly higher in the frontal cortex compared to all other regions analysed. The frontal cortex and the striatum were the most markedly affected by the deficiency. Supplementation with phospholipids restored normal fatty acid composition in brain regions except for frontal cortex. Egg yolk or cerebral phospholipids are an effective source of n-3 PUFA for reversing behavioral changes and altered fatty acid composition induced by a diet deficient in n-3 PUFA.

Animals↗
PubMed2000

Effect of triiodothyronine on phospholipid metabolism in skeletal muscles of the rat.

The aim of the present study was to examine the effect of treatment with triiodothyronine (T3) on certain aspects of phospholipid metabolism in skeletal muscles. Rats were injected with triiodothyronine (T3) daily (10 microg x 100 g(-1) b.w., s.c.) for six days. Saline-treated rats served as controls. 24 h after the last dose of T3, 14C palmitic acid suspended in the serum of a donor rat, was administered intravenously. Thirty min later, samples of the soleus, white and red section of the gastrocnemius and blood from the abdominal aorta were taken. The muscle phospholipids were extracted and separated into different fractions by means of thin layer chromatography. The following fractions were obtained: shingomeylin, phosphatidylcholine phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and cardiolipin. The phospholipids were quantified and their radioactivity was measured. The plasma free fatty acid concentration and radioactivity was also determined. Treatment with T3 reduced the content of phosphatidylinositol and phosphatidylserine in each muscle type, whereas the concentration of other phospholipids remained stable. T3 increased markedly incorporation of the blood-borne fatty acids into each phospholipid fraction in the muscles. It is concluded that an excess of T3 influences the metabolism of phospholipids in skeletal muscles.

Animals↗
PubMed2000

Phospholipid distribution in murine mammary adenocarcinomas induced by activated neu oncogene.

The aim of this study was to analyze possible changes in the total phospholipid distribution in murine mammary adenocarcinomas induced in transgenic mice by the tissue-specific expression of the neu oncogene, as compared with normal tissues. To understand whether the altered phospholipid profile might be specifically tissue-related to the oncogene expression, phospholipid composition also has been analyzed in liver, kidney, lung, and spleen. The data indicate that only tumor mammary tissues show a drastic increase of the total phospholipid content (P < 0.0001) associated with a significant increment of phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin (P < 0.05). Moreover, gas-chromatography analysis of total phospholipid-derived fatty acids shows a decrease in the percentage content of linoleic acid in tumor tissues, suggesting an altered metabolism of this fatty acid related to the enhanced epithelial proliferation. We conclude that neu transgenic mice provide a good model to clarify the involvement of phospholipids in neu-induced neoplastic transformation and to study in vivo the metabolic pathways related to the intracellular signaling.

Adenocarcinoma↗