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PubMed1988

The effect of zinc on iron-induced lipid peroxidation in different lipid systems including liposomes and micelles.

The effect of zinc on FeSO4/ascorbic acid-induced lipid peroxidation was measured by the thiobarbituric acid assay in various lipid systems including small unilamellar liposomes prepared from egg phosphatidylcholine (EPC), ionic micelles prepared from arachidonic acid (C20:4), non-ionic monocomponent micelles prepared from EPC-derived, methylated fatty acids, and an eicosatetrene emulsion. With the exception of C20:4 micelles, zinc inhibited lipid peroxidation in each of the above systems in a similar dose-related fashion, with 0.5 mM zinc having maximal effect. Gas-chromatographic fatty acid analysis too indicated a protective effect of zinc against FeCl3-induced lipid peroxidation in soybean PC vesicles, which do not contain C20:4 moieties. These findings, in particular the inhibition of lipid peroxidation in eicosatetrene emulsion, suggest that the presence of uncharged polar head groups, or packing of lipid molecules into ordered self-assemblages (membranes and micelles) have no critical influence on the antioxidant effect of zinc. The results with Fe2+ are compatible with the concept that zinc interferes with the formation of Fe2+-oxygen-enoic complexes. This mechanism, however, cannot account for the inhibition by zinc of the Fe#+-induced lipid peroxidation, suggesting the involvement of other types of zinc effects in these systems.

Ascorbic Acid↗
PubMed1980

Effect of lipid A-associated protein and lipid A on the expression of lipopolysaccharide activity. I. Immunological activity.

A detailed investigation has been made of the contribution of the various chemical moieties of bacterial endotoxins, namely lipid A-associated protein (LAP), lipid A and O-antigen polysaccharide to a number of the immunological activities of these active bacterial products. Advantage was taken of the availability of antigenically identical endotoxin preparations from Escherichia coli 0111:B4 which differed greatly in their content of LAP and/or lipid A. The capacity to initiate in vitro proliferative responses in murine splenocytes was in a large part related to the presence of LAP with a less potent, although still critical, dependence upon lipid A. On the other hand, the in vivo polyclonal antibody response was dependent only upon lipid A. In this respect, the presence of LAP had no apparent effect on the stimulation of nonspecific low affinity antibody. All preparations, regardless of LAP and lipid A content, stimulated similar in vivo enhancement of antibody responses to a protein antigen (adjuvanticity) and specific immune responses to the endotoxin polysaccharide antigen. The results emphasize the lack of correlation between in vitro B lymphocyte proliferative responses and in vivo immunostimulatory responses of bacterial endotoxin preparations. These data also suggest a minimal contribution of LAP to in vivo responses and an extremely limited contribution of lipid A to the adjuvant activity and the primary immune response to O-antigen polysaccharide.

Adjuvants, Immunologic↗
PubMed1994

NMR lipid profiles of cells, tissues, and body fluids: proton NMR analysis of human erythrocyte lipids.

One- and two-dimensional high resolution NMR spectroscopy was applied to determine quantitatively and qualitatively the lipids extracted from human erythrocyte membranes. The relative amounts of the major lipids were determined from the spectra of unfractionated lipid extracts. After HPLC fractionation of the lipid extracts and NMR analysis of the fractions, it was possible to determine the features of the component lipids of each lipid class and to compare, especially, the fatty acid types and composition of the individual major glycerophospholipids. The results of this proton NMR analysis were compared to those obtained elsewhere using classical lipid analytical techniques and found to be in substantial agreement.

Cholesterol↗
PubMed1994

Serum lipid screening to identify high-risk individuals for coronary death. The results of the Lipid Research Clinics prevalence cohort.

OBJECTIVE: To assess the accuracy of specific plasma lipid fractions in predicting coronary heart disease (CHD) mortality among adults. METHODS: Follow-up data for a random sample of 30- to 79-year-old men and women recruited into the Lipid Research Clinics Prevalence and Follow-up Studies were included in this analysis (n = 4499). Baseline measurements of total plasma cholesterol and lipoprotein fractions were compared with subsequent CHD mortality after a mean follow-up of 12.3 years. The areas under receiver operating characteristics curves for specific serum lipids were compared for individuals aged 30 to 59 and 60 to 79 years. MAIN RESULTS: For the younger cohort, the ratio of total cholesterol to high-density lipoprotein cholesterol was a better predictor (P < .05) of CHD mortality (receiver operating characteristic curve area, 0.80 +/- 0.03) than was total cholesterol level alone (receiver operating characteristic curve area, 0.73 +/- 0.03) or any other single lipoprotein measurement. Among the older cohort, the same screening strategies performed poorly, with receiver operating characteristic curve areas ranging from 0.51 +/- 0.05 for total cholesterol to 0.64 +/- 0.05 for the ratio of low-density to high-density lipoprotein cholesterol levels. CONCLUSION: Plasma lipid levels are poor predictors of coronary death among those aged 60 to 79 years without known CHD. These data indicate the need to define better lipid screening strategies for older, asymptomatic adults. Among younger adults aged 30 to 59 years, high-density lipoprotein cholesterol measurement should be included as part of any lipid screening program, as the ratio of total to high-density lipoprotein cholesterol levels is the best lipid screening test to identify those at high risk for subsequent CHD mortality.

Adult↗
PubMed2005

Functional lipidomics: the roles of specialized lipids and lipid-protein interactions in modulating neuronal function.

Lipids fulfill multiple specialized roles in neuronal function. In brain, the conduction of electrical impulses, synaptic function, and complex signaling pathways depend on the temporally and spatially coordinated interactions of specialized lipids (e.g., arachidonic acid and plasmalogens), proteins (e.g., ion channels, phospholipases and cyclooxygenases) and integrative lipid-protein interactions. Recent technical advances in mass spectrometry have allowed unparalled insight into the roles of lipids in neuronal function. Through shotgun lipidomics and multidimensional mass spectrometry, in conjunction with the identification of new classes of phospholipases (e.g., calcium dependent and calcium independent intracellular phospholipases), new roles for lipids in cerebral function have been accrued. This review summarizes the advances in our understanding of the types of lipids and phospholipases in the brain and the role of functional lipidomics in increasing our chemical understanding of complex neuronal processes.

Animals↗
PubMed1999

Action of methanolic extract of mung bean hulls as inhibitors of lipid peroxidation and non-lipid oxidative damage.

The antioxidant effects of methanolic extract of mung bean hulls (MEMBH) on lipids and non-lipids, including liposome, carbohydrate, protein and 2'-deoxyguanosine (2'-dG), were investigated. MEMBH exhibited a remarkable antioxidant effect in a liposome model system, indicating that the extract was an inhibitor of lipid peroxidation. The inhibitory effect of MEMBH on deoxyribose damage was amount-dependent and it afforded considerable protection against damage to deoxyribose. In addition, MEMBH at low amounts was more effective in protecting protein oxidation. Furthermore, the oxidation of 2'-dG to 8-hydroxy-2'-deoxyguanosine (8-OH-2'dG) was inhibited by MEMBH. These results show that the extract also was an inhibitor of non-lipid oxidation damage. The extract exhibited metal binding ability and scavenging activity for hydrogen peroxide and hydroxyl radical, which may explain the mechanism of their protecting lipids and non-lipids from oxidative damage.

Antioxidants↗
PubMed1995

Dietary lipid and iron status modulate lipid peroxidation in rats with induced adjuvant arthritis.

We studied the effect of dietary lipids on iron metabolism and lipid peroxidation during induced adjuvant arthritis and/or iron overload in rats. We compared a control diet containing corn oil and rapeseed oil with a diet devoid of polyunsaturated fatty acids containing only tripalmitin as lipids. Four subgroups of rats were used with each diet: without further treatment, with induction of adjuvant arthritis, with iron overload, and with induction of adjuvant arthritis and iron overload. The profile of fatty acids present in plasma and in microsomes changed in rats fed the tripalmitin diet. The level of tetra- and pentaunsaturated fatty acids was reduced, and the level of monounsaturated fatty acids and iron stores was increased with respect to control rats. Thus, ingestion of a tripalmitin diet reduced the substrate for lipid peroxidation, as shown by the decrease in thiobarbituric acid-reactive substances in plasma and conjugated dienes in hepatic microsomal fraction. Adjuvant arthritis and iron overload had a synergistic effect on lipid peroxidation and iron storage in liver. Further, in the hepatic microsomal fraction, tripalmitin reduced the levels of cytochrome P-450, and arthritis reduced the levels of cytochrome P-450 and Ca2+ sequestration. Our results suggest that rats fed tripalmitin showed a reduction of lipid peroxidation induced by inflammation or by iron overload, because of the lack of polyunsaturated fatty acids in the diet, although tripalmitin usually increases the iron stores in the body and causes hepatic alterations.

Animals↗
PubMed2003

Attenuated lipid peroxidation in preterm infants during subsequent doses of intravenous lipids.

The aim of this study was to determine whether the administration of a lipid emulsion containing less polyunsaturated fatty acids but rich in monounsaturated fatty acids causes less in vivo lipid peroxidation in preterm infants. The prospective intervention study included 13 infants with birth weights and gestational ages ranging between 1,100 and 2,660 g and from 28.4 to 32.9 weeks. All were in a stable condition and randomly allocated for a 3-hour infusion (0.16 g/kg/h) of an olive oil-based and a soybean oil + medium chain fatty acid (MCT) emulsion on 2 consecutive days. Expired pentane and plasma triglycerides (TGs) were measured before, during, and after the 3-hour infusion. Basal exhaled pentane averaged 9.4 +/- 7.0 pmol/kg/min (mean +/- SD). During the olive oil-based emulsion, exhaled pentane increased to 95.2 +/- 56.7, and during soybean oil + MCT it increased to 110 +/- 93.9 pmol/kg/min (p < 0.05 both from basal, n.s. between preparations). One hour after discontinuation of the infusion, exhaled pentane returned to 21.1 +/- 12.6 pmol/kg/min (p < 0.05 vs. basal). Combined data on expired pentane measurements demonstrated that on day 1 pentane peaked at 124 +/- 87.0 pmol/kg/min which was significantly attenuated to 57.5 +/- 24.4 pmol/kg/min after an identical dose of lipid on day 2 (p < 0.05). No difference in peak TGs was detected between the two preparations or the study days. Infusion of a constant dose of intravenous lipids on 2 subsequent days to the newborn infants is associated with a reduction in lipid peroxidation. This finding may be dependent on normal postnatal maturation or may represent an appropriate adaptive response aiming at a reduction in oxidative stress. Peroxidation of soybean oil + MCT and olive oil-based lipid emulsions was similar in the newborn infants.

Fatty Acids, Monounsaturated↗
PubMedDate not supplied

[The effect of cadmium chloride and hydrogen peroxide on the lipid peroxidation and fractional composition of lipids in hepatocytes of rats].

The isolated hepatocytes were incubated in the medium, containing cadmium chloride or hydrogen peroxide. Influence of the latter on the intensity of lipid peroxidation and contents of some lipids fractions, as well as viability of hepatocytes in these conditions has been studied. It is shown that under such cultivation conditions the activation of lipid peroxidation in the hepatocytes takes place. Its activation in presence of cadmium chloride was one of the factors of the membranes damage. The changes in the content of some fractions of lipids were similar both under the incubations of the cells with cadmium chloride and hydrogen peroxide. This allows one to suppose that cadmium chloride causes changes in the lipid composition of membranes as a result of intensification of lipid peroxidation.

Animals↗
PubMed2005

Non-HDL cholesterol, apolipoproteins A-I and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women.

CONTEXT: Current guidelines for cardiovascular risk detection are controversial with regard to the clinical utility of different lipid measures, non-high-density lipoprotein cholesterol (non-HDL-C), lipid ratios, apolipoproteins, and C-reactive protein (CRP). OBJECTIVE: To directly compare the clinical utility of total cholesterol, low-density lipoprotein cholesterol (LDL-C), HDL-C, non-HDL-C, apolipoproteins A-I and B(100), high-sensitivity CRP, and the ratios of total cholesterol to HDL-C, LDL-C to HDL-C, apolipoprotein B(100) to apolipoprotein A-I, and apolipoprotein B(100) to HDL-C as predictors of future cardiovascular events in women. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of 15,632 initially healthy US women aged 45 years or older (interquartile range, 48-59 years) who were enrolled between November 1992 and July 1995. All participants were followed up over a 10-year period for the occurrence of future cardiovascular events. MAIN OUTCOME MEASURE: Hazard ratios (HRs) and 95% confidence intervals (CIs) for first-ever major cardiovascular events (N = 464) according to baseline levels of each biomarker. RESULTS: After adjustment for age, smoking status, blood pressure, diabetes, and body mass index, the HRs for future cardiovascular events for those in the extreme quintiles were 1.62 (95% CI, 1.17-2.25) for LDL-C, 1.75 (95% CI, 1.30-2.38) for apolipoprotein A-I, 2.08 (95% CI, 1.45-2.97) for total cholesterol, 2.32 (95% CI, 1.64-3.33) for HDL-C, 2.50 (95% CI, 1.68-3.72) for apolipoprotein B(100), 2.51 (95% CI, 1.69-3.72) for non-HDL-C, and 2.98 (95% CI, 1.90-4.67) for high-sensitivity CRP (P<.001 for trend across all quintiles). The HRs for the lipid ratios were 3.01 (95% CI, 2.01-4.50) for apolipoprotein B(100) to apolipoprotein A-I, 3.18 (95% CI, 2.12-4.75) for LDL-C to HDL-C, 3.56 (95% CI, 2.31-5.47) for apolipoprotein B(100) to HDL-C, and 3.81 (95% CI, 2.47-5.86) for the total cholesterol to HDL-C (P<.001 for trend across all quintiles). The correlation coefficients between high-sensitivity CRP and the lipid parameters ranged from -0.33 to 0.15, and the clinical cut points for CRP of less than 1, 1 to 3, and higher than 3 mg/L provided prognostic information on risk across increasing levels of each lipid measure and lipid ratio. CONCLUSIONS: Non-HDL-C and the ratio of total cholesterol to HDL-C were as good as or better than apolipoprotein fractions in the prediction of future cardiovascular events. After adjustment for age, blood pressure, smoking, diabetes, and obesity, high-sensitivity CRP added prognostic information beyond that conveyed by all lipid measures.

Apolipoproteins↗
PubMed1997

Incorporation and Antibody Recognition of a Lipid-Anchored Membrane Protein in Supported Lipid Layers

The formation of supported lipid layers incorporating promastigote surface protease (PSP), a glycosylphosphatidylinositol-anchored protein, is investigated using surface plasmon resonance. Both hydrophilic and hydrophobic substrates are used for the formation of lipid layers, and results are consistent with the formation of lipid bilayers and monolayers, respectively. Specific antibody binding to layers containing PSP is observed, whereas nonspecific binding of the antibody to the surface is effectively suppressed by the phosphatidylcholine lipid layer. Phosphatidylinositol-specific phospholipase C is used to remove the lipid moieties from the membrane-incorporated PSP, releasing it into solution in a hydrophilic form and demonstrating that a large fraction of the protein is anchored in the lipid layer via the lipid moieties. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗
PubMed1991

Dietary supplementation with ether-linked lipids and tissue lipid composition.

The goal of this investigation was to determine the effect of an alkylglycerol dietary supplement on the lipid composition of several major organs. Lipids from kidney, liver, and lung tissues of rats on a laboratory chow diet (controls) were compared to lipids from the same tissues of rats that had received oral supplements (300-600 mg/day) of 1-O-alkyl-2,3-diacetyl-sn-glycerol (alkyl groups were 65% 18:1 and 17% 16:1) for six days. Incorporation of the alkylglycerol into tissue lipids was indicated by both the presence of a neutral lipid in liver that had the same chromatographic migration as alkyldiacylglycerols and by a substantial increase (approximately 150% of controls) in the octadecenyl group of the alk-1-enyl- and alkyl-glycerol side chains derived from total phospholipids of all three tissues. Compared to controls, there was a significant increase in the amount of alkylacylglycerophosphocholine in all three tissues of the alkylglycerol supplemented group. Total lipids, total phospholipid phosphorus, or the distribution of phospholipid classes (except for small differences in lung tissue) were not affected by the dietary supplement. The increase in ether lipids was offset by a corresponding decrease in the diacyl subclass in tissues from animals on the alkyldiacetylglycerol supplement. Our results indicate that the amount of ether-linked glycerolipids in rat tissues can be easily increased with dietary supplements of alkylglycerols.

Animals↗
PubMed1990

Lipid transfer between human plasma low-density lipoprotein and a triolein/phospholipid microemulsion catalyzed by insect hemolymph lipid transfer particle.

Lipid transfer between human plasma low-density lipoprotein (LDL) and an LDL-size microemulsion of triolein and phosphatidylcholine stabilized with human apolipoprotein A-I was catalyzed by the lipid transfer particle from hemolymph of the tobacco hornworm (Manduca sexta). Net transfer of phospholipid and triacylglycerol from the emulsion to LDL was observed and the apparent initial rates of transfer were dependent on the amount of catalyst. Net transfer of phospholipid mass was twice as much as that of triacylglycerol with respect to both the initial rate and the final equilibrium state. The final amount of net transfer of both lipids was dependent upon the initial ratio of LDL: microemulsion present in the incubation mixture up to 1:1 on the basis of phospholipid. The microemulsion lipid composition was maximally altered from an initial weight ratio of 1.09 +/- 0.08 (phospholipid/triolein) to 0.90 +/- 0.03 by this reaction. Further increase of LDL in the incubation caused neither further net transfer nor further change in the lipid composition of the microemulsion. The catalyst neither affected spontaneous transfer of free cholesterol between the emulsion and LDL nor enhanced cholesteryl ester transfer in this reaction system. As a result of the facilitated reaction, LDL gained a significant amount of phospholipid and triacylglycerol causing up to an 8% increase in core lipids and 14% in phospholipid. Some free cholesterol is recovered in the emulsions via spontaneous exchange. Transfer or exchange of apolipoproteins during the course of facilitated lipid transfer did not occur.

Animals↗
PubMed1995

Cycling of apolipoprotein A-I between lipid-associated and lipid-free pools.

It has been shown previously that the reduction in particle size of HDL which follows incubation with the cholesteryl ester transfer protein (CETP) plus very-low-density lipoproteins (VLDL) or low-density lipoproteins (LDL) is accompanied by the dissociation of lipid-free apolipoprotein A-I (apo A-I) from HDL. In the present study, we demonstrate that this dissociation of apo A-I is reversible in a process dependent on the activity of lecithin:cholesterol acyltransferase (LCAT). The lipoprotein fraction (d < 1.21 g/ml) of human plasma was mixed with CETP and incubated under conditions such that the HDL decreased in size and there was a dissociation of about 30% of the apo A-I. Following this incubation, the d < 1.21 g/ml fraction was reisolated, supplemented with lipid-free apo A-I and reincubated in the presence and absence of LCAT, either as a component of lipoprotein-deficient plasma or as purified enzyme. In the absence of LCAT, HDL size did not increase and there was no incorporation of lipid-free apo A-I into the HDL density range. In contrast, when LCAT was present, the particle size of HDL increased and lipid-free apo A-I was incorporated into the HDL such that the HDL apo A-I content was comparable to that of the original, unmodified particles. The incorporation of lipid-free apo A-I into the HDL density range was dependent on both the presence of pre-existing HDL and an increase in their size. Thus, just as a reduction in HDL size is accompanied by the dissociation of lipid-free apo A-I, we have now shown that a subsequent increase in HDL size is accompanied by the reincorporation of lipid-free apo A-I into the particle.

Apolipoprotein A-I↗
PubMed2005

Halting the progression of atherosclerosis with intensive lipid lowering: results from the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial.

Intravascular ultrasonography is a catheter-based technique used to provide 3-dimensional views of the vessel lumen as well as the size and distribution of atherosclerotic plaques. This imaging technique was used in the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) study, an 18-month, randomized, controlled, multicenter trial comparing the effects of intensive versus moderate lipid-lowering therapy on plaque progression in patients requiring coronary angiography. A total of 253 patients were randomized to atorvastatin 80 mg/day (intensive lipid lowering) and 249 patients were randomized to pravastatin 40 mg/day (moderate lipid lowering). Low-density lipoprotein (LDL) cholesterol levels decreased from a baseline mean of 150 mg/dL (3.9 mmol/L) in both groups to 79 mg/dL (2.0 mmol/L) in the atorvastatin group and 110 mg/dL (2.9 mmol/L) in the pravastatin group. High-sensitivity C-reactive protein (hs-CRP) levels decreased by 36.4% in the atorvastatin group versus 5.2% in the pravastatin group (P <0.001). For the primary end point of percent change in total atheroma volume, a significantly lower rate of progression from baseline was observed with atorvastatin (-0.4%) than with pravastatin (2.7%) (P = 0.02). Linear regression analysis showed an inverse relation between lipid reduction and plaque progression for both groups; however, at any given level of LDL cholesterol, the progression rate was lower with atorvastatin compared with pravastatin. Both regimens were well tolerated. The results show that intensive lipid lowering with atorvastatin 80 mg/day for 18 months halted the progression of coronary atherosclerosis, whereas more moderate lipid lowering with pravastatin 40 mg/day was associated with progression. The differences in the progression rate are likely to be a result of greater reduction in atherogenic lipoproteins and hs-CRP with intensive therapy.

Atherosclerosis↗
PubMed2006

Lipidized dermatofibromas and their relationship to serum lipids.

BACKGROUND: Lipidized dermatofibromas represent a rare variant of dermatofibroma that has been regarded as an incidental finding with no particular clinical significance. OBJECTIVE: The goal of this study was to investigate the relationship between lipidized dermatofibromas and patient age, anatomic location, and serum total cholesterol. METHODS: A retrospective case control format was used with an experimental group containing patients with biopsy-proven lipidized dermatofibromas and a control group containing patients with nonlipidized dermatofibromas. RESULTS: Ages in the experimental group ranged from 35 to 75 years with a mean value of 53 years whereas ages in the control group ranged from 27 to 72 years with a mean value of 48 years. A comparison between the mean of the ages between the two groups using the t test method showed no statistically significant difference (P = .09). Lesion location on the body was grouped into 4 sites: leg, thigh, trunk, and upper extremity. Of the 23 patients in the experimental group, 10 had lesions on the legs, 5 had lesions on the thighs, 2 had lesions on the trunk, and 5 had lesions on the upper extremities. Of the 41 patients in the control group, 15 had lesions on the legs, 7 had lesions on the thighs, 9 had lesions on the trunk, and 10 had lesions on the upper extremities. A comparison between the two groups showed no statistically significant difference (P = .60). In all, 16 of the 23 patients in the experimental group and 24 of the 41 patients in the control group were considered to have high cholesterol. A comparison showed no statistically significant difference between the cholesterol levels of the two groups (P = .38). LIMITATIONS: Limitations that we encountered during the study included the relative infrequency of lipidized dermatofibromas, limiting the number of patients in the study. In addition, medication histories and lipid levels on patients were not always available. In addition, we formed a control group from people who had their cholesterol checked often, which may cause them to have a higher average cholesterol than that of the general population. CONCLUSIONS: Our data show that lipidized dermatofibromas do not differ clinically from nonlipidized dermatofibromas in age distribution of patients, tumor location, or underlying serum lipid levels.

Adult↗
PubMed1990

Surface dipole moments of lipids at the argon-water interface. Similarities among glycerol-ester-based lipids.

Surface potential-surface pressure-area isotherms at the argon-buffer interface have been determined for 38 lipid species comprising 19 chemical classes. These lipids all exhibited a finite range of liquid-expanded surface pressure-area behavior. For most species, the linearity of surface potential with reciprocal area was excellent, but nonzero intercepts were obtained. This suggests a lipid-induced reorganization of interfacial water molecules which is area independent. The linearity of the data permits calculation of the surface dipole moment, mu perpendicular, for each lipid. The values of mu perpendicular for a series of oleoyl-containing acylglycerols, dioleoyl phosphatidylcholine, and dioleoyl phosphatidylethanolamine exhibit acylglycerol ester group mu perpendicular's which are generally consistent with known conformational properties of such lipids. The values are 132 mD for the perpendicular oleoyl glycerol-ester group and 252 mD for that in the kinked-chain conformation. Comparison of mu perpendicular's calculated using these values with homologues confirms the approximate independence of mu perpendicular from aliphatic chain length and permits identification of exceptions with possible conformational or orientational differences. Notably, diphytanoyl phosphatidylcholine shows a 45% larger mu perpendicular than predicted. Differences in mu perpendicular among lipid classes allow estimation of the electrical consequences of lipid metabolism and exchange. Calculations show that reactions such as the generation of 1,2-diacylglycerol from diacyl glycerophosphocholine or diacyl glycerophosphoinositol should produce surface potential changes of -127 and +42 mV, respectively. Thus, the two phospholipids are not simply alternative sources of diacylglycerol with respect to processes dependent on surface potential.

Argon↗
PubMedDate not supplied

Lipid and lipid-free total parenteral nutrition: differential effects on macrophage phagocytosis in rats.

Lipid emulsions provided with total parenteral nutrition (TPN) have been associated with mononuclear phagocytic system functional changes. The aim of the present investigation was to assess the influence of TPN with added lipid emulsions on macrophage (M phi) phagocytosis. Wistar rats (n = 70) with external jugular vein cannulation were randomized into seven groups. The rats received an oral diet or six different isocaloric (1.16 kcal/mL), isonitrogenous (1.5 g/mL), and isolipidic (30% non-protein calories) TPN regimens: (a) an oral diet with intravenous infusion of saline (OS); (b) non-lipid TPN (glucose); (c) TPN with 10% long chain triacylglycerol emulsions (LCT); (d) TPN with 90% LCT and 10% fish oil (FO) emulsion; (e) TPN with 50% LCT and 50% FO; (f) TPN with 10% lipid emulsion with 50% medium chain triacylglycerol (MCT) and 50% LCT; and (g) TPN with 45% MCT, 45% LCT, and 10% FO. After 96 h of TPN or saline infusion, colloidal carbon (Pelikan, Germany) was injected intravenously at 1.0 mL/kg body weight, and the rats were killed after 3 h. Liver, spleen, and lung were weighed and prepared by immunohistochemistry analyses with the HAM-56 anti-M phi antibody. Under light microscopy, the total M phi number (MT) and the colloidal carbon phagocytic M phi number (MP) were established, and the phagocytic index was calculated as MP/MT x 100. There were no statistical (P < 0.05) differences in liver, spleen, or lung weights among the seven groups in comparison with the OS group. Non-lipid TPN inhibited spleen and lung M phi phagocytosis when compared with the OS and lipid-TPN groups. Lipid TPN supplemented with fish oil emulsion increased total liver and lung M phi number and phagocytosis. These results indicate that TPN supplemented with fish oil increases M phi phagocytosis in rats.

Animals↗