Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PHOSPHOLIPIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,531 records · Page 85Linked to original sources

Content of phospholipids in human diets studied by the duplicate-portion technique.

1. The phospholipid intake by eight healthy women was studied by the duplicate-portion technique, i.e. chemical analyses of duplicates of the food consumed. Their intake of phospholipids was 1.5-2.5 mmol lipid-phosphorus/d, which corresponds to 0.023-0.059 mmol lipid-P/g dietary fat and 0.24-0.45 mmol lipid-P/MJ respectively. 2. Choline phosphoglyceride constituted 480-700 mmol/mol and ethanolamine phosphoglyceride 170-240 mmol/mol total lipid-P. Most of the choline in nature occurs as choline phospholipids, the intake of which ranged between 0.91-1.85 mmol/d or 0.15-0.33 mmol/MJ. 3. Palmitate, stearate, oleate, and linoleate ere the four major fatty acids both in choline phosphoglyceride and ethanolamine phosphoglyceride. Significant amounts of highly unsaturated, C20 and C22 fatty acids were also observed. It was calculated that 13-33 mg/g total dietary fatty acids was consumed as phospholipids. Together with bile phospholipids, dietary phospholipids and their degradation products may be important in the digestion and absorption processes.

Adult↗

Membrane phospholipid composition and membrane fluidity of human brain tumour: a spin label study.

Membrane fluidity in membrane phospholipids of brain tumours was investigated and compared with those of white and grey matter. Fifteen brain tumours including 5 gliomas, 5 meningiomas and 5 metastatic cancers were examined. These samples were frozen immediately after extirpation in liquid nitrogen. After extraction of total lipids from the tumour tissues, membrane phospholipids were separated and analysed by thin-layer and gas-liquid chromatography. The fluidity of the phospholipid membrane was studied by electron spin resonance (ESR) spectroscopy, using a stearate spin probe. The fatty acid composition of total phospholipid of brain tumours was characterized by an increase in linoleic and arachidonic acids when compared to the control brain. The percentage of palmitoleic acid was higher in gliomas and metastatic tumours than in meningiomas. Furthermore, in the brain tumour tissues, the decreases of phosphatidylethanolamine and phosphatidylserine and the increase of phosphatidylcholine were observed when compared with grey or white matter with the exception of meningioma. There was some difference in phospholipid membrane fluidity between brain tumour and control brain tissue. The order parameter calculated from ESR spectra became higher in the following order: metastatic brain tumour, less than meningioma, less than grey matter, less than glioma, less than white matter. These results suggest that the phospholipid metabolism in the brain tumour is different from that of the normal brain, and this difference may affect the alteration of membrane physical properties which exhibit in part the character of the transformation.

Brain Chemistry↗

Plasma free, phospholipid-bound and urinary free choline all decrease during a marathon run and may be associated with impaired performance.

BACKGROUND: Previous investigations have shown that plasma free choline decreases during long distance running. OBJECTIVE: This study was undertaken to determine if body choline status changes during a marathon run and whether performance is thereby adversely affected. DESIGN: Twenty-three accomplished marathon runners 25 to 49 years of age were studied before and after the 1997 Houston-Methodist Marathon. Fasting blood and five-hour urine samples were obtained in the morning, 14 days prior to the race, immediately after the race and approximately 48 hours after completion of the race. Runners were asked to predict their finish times two weeks prior to the race. Performance was indicated by the ratio of predicted to actual time. RESULTS: Both plasma free and phospholipid-bound choline concentrations as well as urinary free choline concentration decreased immediately following the race (19.2+/-4.5 to 14.6+/-4.2 nmol/mL, p=0.005, and 2565.2+/-516.4 to 2403.4+/-643.0 nmol/mL, p=0.068, respectively) and, except for the phospholipid-bound choline, rebounded towards baseline after 48 hours (15.6+/-3.2 and 2299.9+/-426.7 nmol/mL), although plasma concentrations remained significantly below baseline. Plasma free and phospholipid-bound choline concentrations were significantly correlated (r=0.46, p=0.0001), although urinary free choline concentration was not correlated with either. There was no correlation between plasma free, phospholipid-bound or urinary free choline concentration and actual finish time or the ratio of predicted to actual finish time. However, the percent decrease in urinary free choline concentration was significantly correlated with the ratio of predicted to actual time (r=0.47, p=0.036). No relationship was seen between this ratio and the percent decrease in either plasma free or phospholipid-bound choline concentrations immediately after the race. CONCLUSION: Our finding of both decreased free and phospholipid-bound choline suggests the decrease in choline status is related to accelerated choline metabolism or enhanced choline uptake by tissues rather than decreased hepatic choline release. The role of choline supplementation during endurance running requires further investigation.

Adult↗

Proton and 31-phosphorus neurospectroscopy in the study of membrane phospholipids and fatty acid intervention in schizophrenia, depression, chronic fatigue syndrome (myalgic encephalomyelitis) and dyslexia.

Neurospectroscopy allows biochemical processes in the brain to be studied non-invasively. At magnetic field strengths of 1.5 T or higher, cerebral proton neurospectroscopy allows the ascertainment of values of myo-inositol, choline-containing compounds, creatine, glutamate, glutamine, and N-acetyl aspartate. At similar field strengths, cerebral 31-phosphorus neurospectroscopy allows the ascertainment of values of phosphomonoesters, inorganic phosphate, phosphodiesters, phosphocreatine, and the gamma, alpha and beta nucleotide triphosphate (mainly adenosine triphosphate) resonances. Since choline is a common polar head group at the Sn3 position of membrane phospholipid molecules, a raised level of free choline, as indexed by proton neurospectroscopy, can indicate relatively low anabolism of membrane phospholipid molecules. Furthermore, the choline peak includes phosphorylcholine and glycerophosphorylcholine and even ethanolamine. The phosphomonoesters peak measured using 31-phosphorus spectroscopy includes major contributions from phosphocholine, phosphoethanolamine and L-phosphoserine, which are important precursors of membrane phospholipids, while the phosphodiesters peak includes contributions from glycerophosphocholine and glycerophosphoethanolamine, which are important products of membrane phospholipid catabolism. Hence proton neurospectroscopy and 31-phosphorus neurospectroscopy can yield important information relating to the metabolism of cerebral membrane phospholipids. The application of these techniques to the investigation of membrane phospholipid metabolism in schizophrenia, depression, chronic fatigue syndrome (myalgic encephalomyelitis or M.E.) and dyslexia is described.

Brain↗

Passive transmembrane redistributions of phospholipids as a determinant of erythrocyte shape change. Studies on electroporated cells.

Echinocytes formed from discocytic erythrocytes by electric field pulses at 0 degree C return to the discoytic shape upon incubation at 37 degrees C and subsequently turn into stomatocytes. Active and passive components of phospholipid translocation are involved in this shape recovery. Following low-field-strength pulses (5 kV cm-1), shape recovery is fully suppressed by ATPase inhibitors, such as vanadate. When vanadate is only added after stomatocyte formation has been completed, the cells return to the stage of echinocytosis prevailing before recovery. At higher field strength (7 kV cm-1) and in particular after repetitive field pulses, the subsequent incubation at 37 degrees C results in partial shape recovery even in the presence of vanadate. On the basis of the enhanced passive transmembrane mobilities of phospholipid probes observed previously following electroporation, the shape changes in the presence of vanadate are proposed to be due to a passive net movement of phospholipids from the outer to the inner membrane leaflet, as a consequence of the different mobilities of the various membrane phospholipids. Repetitive pulses at higher field strengths lead to a progressively more discocytic stationary shape during subsequent resealing. This phenomenon is explained by the progressively increased transbilayer mobility of the normally almost immobile phospholipid sphingomyelin and a consecutive progressive symmetrization of all membrane phospholipids.

4-Chloro-7-nitrobenzofurazan↗

Phospholipid and nucleic acid gradients in the developing amphibian embryo.

Rana pipiens embryos at the end of the blastula stage were dissociated and the cell suspension was separated into presumptive ectoderm, mesoderm, light endoderm, and heavy endoderm cells by a discontinuous density gradient centrifugation technique. The isolated germ layers were analyzed for total lipid, lipid phosphorus, plasmalogen, RNA, and DNA. Per gram dry weight, DNA showed a threefold decrease from ectoderm to heavy endoderm. On the same basis, the RNA content of the mesoderm was 34 per cent higher than that of ectoderm, and 320 and 570 per cent higher than that of light and heavy endoderm, respectively. In addition to the RNA and DNA gradients, there were at least two superimposed lipid gradients: a neutral lipid gradient decreasing from ectoderm to endoderm, and a total phospholipid gradient increasing from ectoderm to endoderm. In contrast to total phospholipid, a specific phospholipid class, ethanolamine plasmalogen, decreased from ectoderm to endoderm. The total lipid content per gram dry weight was the same in all the germ layers. Total phospholipids were analyzed quantitatively by thin layer chromatography. Phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and inositol phospholipid constituted 34, 13, 12, and 34 per cent, respectively, of the total lipid phosphorus. The phospholipid composition was different in each germ layer. The possible role of specific lipids in embryonic induction and differentiation is discussed.

Animals↗

Assembly of lipids into membranes in Acanthamoeba palestinensis. II. The origin and fate of glycerol- 3 H--labeled phospholipids of cellular membranes.

The membranes of Acanthamoeba palestinensis were studied by examination in fixed cells, and then by following the movements of glycerol-(3)H-labeled phospholipids by cell fractionation. Two previously undescribed structures were observed: collapsed cytoplasmic vesicles of cup shape, and plaques in food vacuole and plasma membrane similar in size to the collapsed vesicles. It appeared that the plaques formed by insertion of collapsed vesicles into membranes and/or that collapsed vesicles formed by pinching off of plaques. Fractions were isolated, enriched with nuclei, rough endoplasmic reticulum (RER), plasma membrane, Golgi-like membranes, and collapsed vesicles. The changes in specific activity of glycerol-(3)H-labeled phospholipids in these membranes during incorporation, turnover, and after pulse-labeling indicated an ordered sequence of appearances of newly synthesized phospholipids, first in nuclei and RER, then successively in Golgi membranes, collapsed vesicles, and finally, plasma membrane. In previous work we had found no large nonmembranous phospholipid pool in A. palestinensis. These observations are consistent with the hypothesis that membrane phospholipids are synthesized, perhaps as integral parts of membranes, in RER and nuclei. Subsequently, some of the newly synthesized phospholipids are transported to the Golgi complex to become integrated into the membranes of collapsed vesicles, which are precursors of the plasma membrane. Collapsed vesicles from the plasma membrane by inserting into it as plaques. When portions of the plasmalemma from food vacuoles, collapsed vesicles pinch off from their membranes and are recycled back to the cell surface.

Amoeba↗

Effects of antiglaucoma drugs on [32P]orthophosphate incorporation into phospholipids of cat iris and ciliary process.

The effects of antiglaucoma drugs on [32P]-orthophosphate incorporation into phospholipids of iris and ciliary process were investigated. Both iris and ciliary process rapidly incorporated 32Pi into the major phospholipids, with the acidic phosphoinositides demonstrating a greater labelling than phosphatidylcholine, indicating a greater turnover. The muscarinic agonists, carbachol and pilocarpine, stimulated 32Pi-labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in both iris and ciliary process. These effects were blocked by atropine, suggesting that the response was mediated through muscarinic receptors. The beta blocking ocular hypotensive drugs, propranolol, timolol and atenolol, produced varying effects on 32P incorporation into phospholipids of iris and ciliary process. Propranolol stimulated 32Pi-labelling into phosphatidylinositol 4', 5' bisphosphate (PIP2), phosphatidylinositol 4' phosphate (PIP), PI and PA. Timolol decreased 32Pi-incorporation into PIP2 and PI, whereas atenolol, a selective beta 1 antagonist, had no significant effect on 32Pi-labelling of phospholipids. The above findings on propranolol agree with previous observations which demonstrated that propranolol redirects glycerolipid metabolism through multiple effects on the enzymes in phospholipid biosynthesis, particularly in stimulating phosphatidylinositol kinases. The results with timolol suggest that this drug may decrease phosphoinositide hydrolysis. The effects of these ocular hypotensive, non-selective beta blocking drugs on phospholipid turnover may ultimately limit the accumulation of breakdown products which could serve as cellular messengers.

Animals↗

c-Fos activated phospholipid synthesis is required for neurite elongation in differentiating PC12 cells.

We have previously shown that c-Fos activates phospholipid synthesis through a mechanism independent of its genomic AP-1 activity. Herein, using PC12 cells induced to differentiate by nerve growth factor, the genomic effect of c-Fos in initiating neurite outgrowth is shown as distinct from its nongenomic effect of activating phospholipid synthesis and sustaining neurite elongation. Blocking c-Fos expression inhibited differentiation, phospholipid synthesis activation, and neuritogenesis. In cells primed to grow, blocking c-Fos expression determined neurite retraction. However, transfected cells expressing c-Fos or c-Fos deletion mutants with capacity to activate phospholipid synthesis sustain neurite outgrowth and elongation in the absence of nerve growth factor. Results disclose a dual function of c-Fos: it first releases the genomic program for differentiation and then associates to the endoplasmic reticulum and activates phospholipid synthesis. Because phospholipids are key membrane components, we hypothesize this latter phenomenon as crucial to support membrane genesis demands required for cell growth and neurite elongation.

Animals↗

Altered phospholipid fatty acid content and metabolism in heart cell cultures from newborn spontaneously hypertensive rats.

Genetic hypertension has been proposed to be associated with impaired lipid metabolism. To investigate whether lipid metabolism is altered in young rats of the spontaneously hypertensive Okamoto strain (SHR), we have compared the phospholipid fatty acid content and metabolism in cultured heart myocytes and fibroblasts from SHR and normotensive Wistar-Kyoto (WKY) newborn rats. The phospholipid-bound fatty acid profile and metabolism were altered in SHR cardiomyocytes and unchanged in SHR fibroblasts. In SHR myocytes, the fatty acid composition of the phospholipid fraction was modified, with a lowered proportion of linoleic (P < .05) and eicosapentaenoic acid (P < .001), resulting in a decreased polyunsaturated to saturated fatty acid ratio (1.16 +/- 0.08 in SHR v 1.44 +/- 0.08 in WKY, P < .02). The metabolism of radioactive arachidonate (C20:4) and linoleate (C18:2) also differed between SHR and WKY myocytes. Their release was increased (P < .004 and .05 for C20:4 and C18:2, respectively). The labeled phospholipid species also differed between the two strains, suggesting an altered phospholipid turnover in SHR. This study demonstrates modifications of phospholipid fatty acid profile and metabolism in spontaneously contractile cardiac cells from newborn prehypertensive SHR, in the absence of neural, hormonal, and hemodynamic influences.

Animals↗

Cholesterol and phospholipid uptake by mycoplasmas.

Mycoplasma offer several unique advantages for investigating the mechanism controlling transfer and uptake of exogenous cholesterol and phospholipids by biomembranes, as their plasma membrane interacts directly with exogenous lipid donors and their endogenous lipid synthesis is restricted. Growing cells of five species of Mycoplasma were found to take up significant quantities of phosphatidylcholine and sphingomyelin as well as free and esterified cholesterol. In contrast, growing cells of three species of Acholeplasma failed to take up any of the exogenous phospholipids and incorporated only low amounts of free cholesterol and no esterified cholesterol. It is hypothesized that Mycoplasma species have receptors for serum lipoproteins and phospholipid-cholesterol vesicles that facilitate the transfer of cholesterol and phospholipids to the growing cell membrane. Our finding that gentle trypsin treatment of growing Mycoplasma capricolum cells decreased their cholesterol uptake ability by about 50% but did not affect cholesterol uptake by growing Acholeplasma laidlawii cells appears to support the existence of protein receptors for lipoproteins on the surface of Mycoplasma but not on Acholeplasma species. Digestion of membrane phospholipids by phospholipase A2 decreased the cholesterol-binding capacity of isolated A. laidlawii and M. capricolum membranes, roughly in proportion to the amount of phospholipid digested. The total removal of phosphatidylglycerol and diphosphatidylglycerol from A. laidlawii membranes by phospholipase A2 only decreased but did not abolish cholesterol uptake, an indication that glycolipids also participate in cholesterol uptake.

Acholeplasma↗

Mutations in DnaA protein suppress the growth arrest of acidic phospholipid-deficient Escherichia coli cells.

Cell growth arrests when the concentrations of anionic phospholipids drop below a critical level in Escherichia coli, with the insufficient amounts of acidic phospholipids adversely affecting the DnaA-dependent initiation of DNA replication at the chromosomal origin (oriC). Mutations have been introduced into the carboxyl region of DnaA, including the portion identified as essential for productive in vitro DnaA-acidic phospholipid interactions. Expression of DnaA proteins possessing certain small deletions or substituted amino acids restored growth to cells deficient in acidic phospholipids, whereas expression of wild-type DnaA did not. The mutations include substitutions and deletions in the phospholipid-interacting domain as well as some small deletions in the DNA-binding domain of DnaA. Marker frequency analysis indicated that initiation of replication occurs at or near oriC in acidic phospholipid- deficient cells rescued by the expression of DnaA having a point mutation in the membrane-binding domain, DnaA(L366K). Flow cytometry revealed that expression in wild-type cells of plasmid-borne DnaA(L366K) and DnaA(Delta363-367) reduced the frequency with which replication was initiated and disturbed the synchrony of initiations.

Amino Acid Substitution↗

Effect of dietary phospholipids and their constituent bases on serum lipids and apolipoproteins in rats.

To evaluate alterations of serum lipoproteins, liver lipids and fecal sterol excretion caused by feeding a crude soybean phospholipid preparation, the effect of purified phospholipids and phospholipid bases were studied in rats. Soybean phosphatidylcholine preparations showed no effect on serum lipoproteins and liver lipids. Egg yolk phospholipid, which contained phosphatidylethanolamine and phosphatidylcholine, caused a decrease in serum cholesterol and apoprotein A-I and an increase in serum apoprotein B and liver cholesterol. Ethanolamine, but not choline and inositol, showed an effect on serum lipoproteins similar to egg yolk phospholipid. All phospholipids tested increased fecal excretion of neutral sterols. It is suggested that phosphatidylethanolamine exerts marked influence on serum lipoprotein levels.

Animals↗

Meats and fish consumed in the American diet contain substantial amounts of ether-linked phospholipids.

The primary goal of this study was to determine the amounts of ether-containing phospholipids, along with their concentration of certain polyunsaturated acyl groups, from selected, commonly consumed foods of animal origin (salmon, catfish, pork, beef, turkey and chicken). Levels of ether-linked glycerolipids in the samples were of particular interest, because ingestion of ether lipids could contribute to the production of platelet-activating factor (PAF; 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine), one of the most potent biological mediators known. Alkylacyl-sn-glycero-3-phosphocholine was found in all of the meats, with pork loin having the highest levels (0.9 mumol/g tissue) and chicken breasts the lowest (0.1 mumol/g tissue). Although choline plasmalogens were not as evident as the ubiquitous ethanolamine plasmalogens, substantial amounts (1.0 mumol/g tissue) of alk-1-enylacyl-sn-glycero-3-phosphocholine were found in tissues from beef and turkey. Triacylglycerols contained greater proportions of saturated fatty acids than phospholipids, and the ether-linked phospholipids were generally more unsaturated than diacyl species of the same phospholipid. Our data indicate that in addition to the phospholipid fraction of commonly eaten animal tissues supplying substantial amounts of polyunsaturated fatty acids, they are also a rich source of ether-linked lipids. Dietary ether-linked phospholipids could influence the lipid composition of host tissues to the extent that biological responses produced by ether lipid mediators would be affected.

Animals↗

Diet-induced changes in liver and bile but not brain fatty acids can be predicted from differences in plasma phospholipid fatty acids in formula- and milk-fed piglets.

The fatty acid composition of plasma phospholipids differs between infants fed formula and infants fed human milk, but the extent to which this is accompanied by differences in tissue phospholipid fatty acids is unclear. This paper describes analysis of plasma, liver and brain fatty acids from piglets fed one of seven formulas, varying in saturated, monounsaturated, (n-6) and (n-3) fatty acids or sow milk from birth for 18 d. Bile fatty acids were analyzed because they are secreted from liver and may be an important source of fatty acids for intestinal lipoprotein synthesis. The results were used to determine the relation between diet-related differences in plasma phospholipid fatty acids and those in brain, liver and bile. Where significant associations were found, prediction limits were constructed to assess the usefulness of analysis of plasma phospholipid fatty acids to predict diet-induced changes in tissue fatty acids. The proportions (g/100 g fatty acids) of 16:0, 18:0, 18:1, 18:2(n-6) and 20:4(n-6) in plasma phospholipids were significantly associated with the proportions of the same fatty acids in liver and bile, but not brain. The results show a reasonably precise, predictable association between plasma and liver, and plasma and bile fatty acids. Brain 20:4(n-6) and 22:6(n-3), in contrast, were not reliably associated with plasma phospholipid 20:4(n-6) and 22:6(n-3) for piglets fed milk or formula providing about 1.5% energy as 18:3(n-3).

Animal Feed↗

Amelioration of gentamicin nephrotoxicity by phospholipids.

The effect of phospholipids on gentamicin-induced nephrotoxicity was studied in Sprague-Dawley rats. Group 1a (5 rats) were given daily intraperitoneal injections of 100 mg/kg of gentamicin and sacrificed on day 7. Group 1b (10 rats) were similarly treated but were sacrificed on day 14. Group 2a (5 rats) were given 30 mg/kg of phospholipids for 6 days and sacrificed on day 7, serving as phospholipid controls. Group 2b (5 rats) were similarly treated, and from day 7 onwards daily intraperitoneal injections of 100 mg/kg of gentamicin were given while oral phospholipids were continued until the rats were sacrificed 7 days after gentamicin treatment. Group 2c (10 rats) were treated in the same manner as group 2b but the animals were sacrificed on day 28 after gentamicin treatment. Group 3 (10 rats) were given 30 mg/kg of phospholipids concurrently with intraperitoneal gentamicin injections and were sacrificed on day 28. Protein concentrations, N-acetyl-beta-glucosaminidase (NAG) activities and creatinine were measured in 24-h urine samples. Serum creatinine concentrations were measured in blood samples and 24-h creatinine clearance calculated. Gentamicin concentrations were determined in kidney tissues from which sections were also taken for light- and electron-microscopy. Results showed that gentamicin induced a marked increase in NAG and protein excretion, and a marked decrease in creatinine clearance with six rats succumbing to uraemia. Phospholipid treatment, whether started before or concurrently with gentamicin injections, reduced gentamicin-induced nephrotoxicity. The rats did not lose weight. Urinary excretion of NAG and protein was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗

Ethanol-mediated promotion of oesophageal carcinogenesis: association with lipid peroxidation and changes in phospholipid fatty acid profile of the target tissue.

Ethanol consumption is a high risk factor for oesophageal carcinoma and studies indicate that it acts as a promoter of N-nitrosomethylbenzylamine (NMBzA)-induced oesophageal carcinogenesis. The studies described here indicate that ethanol-induced promotion was related with an increase in indices of lipid peroxidation in the target oesophageal tissue and that such an increase was associated with significant changes in the fatty acid profile of phospholipids. Young Sprague-Dawley rats were treated with NMBzA, 2.5 mg/kg body weight, three times a week for 3 weeks, and a week afterwards fed a 7% ethanolic diet that was continued until their death at 10 months. Cumulative ethane exhaled by rats was measured a week before their death and was found to increase significantly with NMBzA treatment but more so when followed by ethanol consumption. Cholesterol, phospholipids, and some indices of lipid peroxidation were measured in the oesophagus and liver. Whereas the levels of cholesterol and phospholipids were not affected in control-fed rats with or without the NMBzA treatment, ethanol consumption by either the untreated or NMBzA-treated rats caused a significant increase in the targeted oesophagus as well as the liver, the major site of ethanol and carcinogen metabolism. Ethanol consumption also increased all the indices of lipid peroxidation, i.e. malondialdehyde, lipid fluorescence, diene- and triene-conjugates; the largest increases were observed in rats that received both NMBzA and ethanol. A comparison of the fatty acid profile of phospholipids from the oesophagus and liver indicated significant alterations both with the NMBzA treatment and ethanol consumption. However, the fatty acid profile with regard to its peroxidability was significantly modified only with ethanol consumption and only in the oesophagus of the NMBzA-treated or untreated rats. Also, hepatic phospholipids showed a substantial increase in linolenate and no change in arachidonate, but the oesophageal phospholipids exhibited a pronounced increase in the levels of C18:3, C20:2, C20:3, C20:3' and C22:6 with a significant increase in arachidonate when use of ethanol followed the NMBzA treatment, suggesting a disorder in lipid and eicosanoid metabolism. We propose that ethanol may promote carcinogenesis through excessive cell proliferation induced by disordered lipid and eicosanoid metabolism that may cause a selective outgrowth of the initiated cells.

Alcoholism↗

Oxidation of rat liver phospholipids: comparison of pathways in homogeneous solution, in liposomal suspension and in whole tissue homogenates.

The oxidation of equivalent concentrations of phospholipids in homogeneous solution, in multilamellar liposomal suspension, and in rat liver homogenate was carried out under aerobic conditions at 37 degrees C in order to examine the biochemical fate of oxidized phospholipids. Rat liver phospholipids were extracted with chloroform and methanol, and oxidation in this homogeneous solution was initiated with a lipid-soluble radical initiator. The oxidation products were phosphatidylcholine hydroperoxide (PC-OOH) and phosphatidylethanolamine hydroperoxide (PE-OOH), which were quantified by HPLC separation using a hydroperoxide-specific chemiluminescence detector. Co-extracted alpha-tocopherol and ubiquinol-9 suppressed the formation of PC-OOH and PE-OOH until oxidatively exhausted. The oxidation of extracted rat liver phospholipids in multilamellar liposomal suspension initiated with the lipid-soluble initiator gave similar results, but with slower rates of antioxidant depletion and phospholipid hydroperoxide formation due to a lower efficiency of free radical production in liposomal membranes. In contrast, the oxidation of rat liver homogenate containing active tissue enzymes initiated by the addition of either free radical initiators or tert-butyl hydroperoxide gave phosphatidylcholine hydroxide, phosphatidylethanolamine hydroxide, and free fatty acid hydroxides as oxidation products. Exogenous PC-OOH added to the rat liver homogenate was reduced to phosphatidylcholine hydroxide with subsequent hydrolysis to its free fatty acid hydroxide. These results suggest that peroxidase and phospholipase enzymes play important roles in the repair of oxidatively damaged phospholipids in biomembranes.

Animals↗