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At least 757 records · Page 42Linked to original sources
PubMed2002

Lipid compositional differences of small, dense low-density lipoprotein particle influence its oxidative susceptibility: possible implication of increased risk of coronary artery disease in subjects with phenotype B.

An increased susceptibility of low-density lipoprotein (LDL) to lipid peroxidative modification may be a key factor in the higher risk of coronary artery disease (CAD) among subjects with phenotype B. Compositional differences in the LDL particle may also be implicated in its atherogenicity and, in particular, may be associated with varying degrees of oxidative susceptibility of LDL, although this remains unclear. We hypothesized that the oxidative susceptibility of small, dense LDL was directly influenced by its lipid composition, which may lead to an increased risk of CAD in subjects with phenotype B. To test this hypothesis, we compared the differences in lipid compositions of LDL particles from subjects with phenotype A and those with phenotype B, and investigated the direct association of lipid composition with susceptibility to lipid peroxidative modification in 102 subjects who underwent a coronary angiographic examination. Subjects with phenotype B (n = 52) had a significantly higher incidence of CAD than subjects with phenotype A (77% v 44%; P <.005). In comparing the oxidative susceptibility of LDL, the lag time was significantly reduced in subjects with phenotype B compared to phenotype A (48.7 +/- 8.6 v 41.5 +/- 5.5 minutes; P <.0001). In addition, the lag time showed a positive correlation with LDL-peak particle diameter (PPD) (r = 0.324, P <.005). Lipid composition per LDL particle was expressed as the ratio of lipid content to apolipoprotein B (apoB) content (wt/wt). Subjects with phenotype B showed a significant depletion in the contents of free-cholesterol (FC), cholesterol ester (CE), and phospholipid (PL) per particle compared to subjects with phenotype A, although there was no significant difference in the triglyceride (TG) content per LDL particle. Except for TG, the lipid content per LDL particle showed a significant positive correlation with lag time in all subjects. Moreover, increased susceptibility of small, dense LDL to lipid peroxidative modification was most strongly associated with a depleted FC content per LDL particle. In conclusion, the greater risk of CAD in subjects with phenotype B may result, in part, from increased susceptibility to lipid peroxidative modification of LDL that is depleted in lipid contents, especially FC content per LDL particle.

Aged↗
PubMed1979

Physical modifications of rhodopsin boundary lipids in lecithin-rhodopsin complexes: a spin-label study.

The microviscosity of rhodopsin boundary lipids was studied with a spin-labeled fatty acid covalently attached to rhodopsin, in rhodopsin-egg lecithin vesicles. When the lipid-to-protein ratio was high (500:1, mole to mole), only narrow peaks were visible in electron paramagnetic resonance spectrum at 37 degrees C. This enabled us to show that, under these conditions, not more than 10% of the probes have their motion strongly restricted by the proximity of the protein. When the temperature was reduced, a second component characteristic of strong immobilization appeared. It corresponds to 50% of the signal at -5 degrees C. At all temperatures reduction of the lipid-to-protein ratio also resulted in an increase of the amount of immobilized lipid. These results show that the rhodopsin boundary layer under physiological conditions is associated with low microviscosity. However, low temperatures, low lipid-to-protein ratios, or combinations of the two can induce dramatic modifications of the physical state of the boundary lipids, which under these conditions may no longer be representative of the functional biological system. These results are relevant to the general theory of lipid-protein interaction.

Animals↗
PubMed2003

Chemical modification of proteins by lipids in diabetes.

Advanced glycation and lipoxidation end-products (AGE/ALE) increase in tissue proteins with age and at an accelerated rate in diabetes. This Review focuses on the nature and source of AGEs/ALEs and the factors affecting their formation in tissue and plasma proteins. Lipids are identified as an important source of chemical modification of proteins in diabetes, and the role of diabetes, dyslipidemia and renal disease in formation of AGEs/ALEs is reviewed. The article concludes with a discussion of ELISA assays for AGEs/ALEs and the merits of measuring AGEs/ALEs in the clinical laboratory.

Albumins↗
PubMed1985

Postischemic cerebral lipid peroxidation in vitro: modification by dietary vitamin E.

Using an in vitro system, we studied the effect of postischemic reoxygenation on cerebral lipid peroxidation in relation to the dietary intake of vitamin E (VE) in rats. Homogenates prepared from VE-deficient, -normal, and -supplemented brains, which were previously rendered ischemic for 30 min by decapitation, were incubated under air or nitrogen gas for 60 min. The extent of peroxidation in brain tissue was estimated by a thiobarbituric acid (TBA) test and by diene conjugation in total lipid extracts. The brain levels of alpha-tocopherol and of total and free fatty acids (FAs) were also determined. Aerobic incubation increased TBA reactants in all dietary groups; the effect was largest in the VE-deficient group, intermediate in the VE-normal group, and smallest in the VE-supplemented group. In contrast, nitrogen incubation did not alter the basal levels of TBA reactants except for a small rise associated with VE deficiency. Conjugated dienes changed in parallel with TBA reactants. alpha-Tocopherol decreased after aerobic incubation and also, to a lesser degree, after nitrogen incubation in each dietary group. Only in the reoxygenated samples of the VE-deficient group was there a significant fall in total polyunsaturated FAs. The levels of free FAs continuously increased throughout ischemia and subsequent incubation. However, the level of free polyunsaturated FAs was similar after aerobic and nitrogen incubation in each dietary group, and was not affected by VE. Thus, cerebral reoxygenation after ischemia propagates peroxidative reactions within esterified polyunsaturated FAs. The modification by VE of reoxygenation-induced lipid peroxidation suggests free radical mediation.

Aerobiosis↗
PubMed2003

A novel lipid hydroperoxide-derived modification to arginine.

The guanidine group present in the amino acid arginine was found to react with the lipid hydroperoxide-derived bifunctional electrophile, 4-oxo-2-nonenal. The reaction between N(alpha)-tert-butoxycarbony-l-arginine and 4-oxo-2-nonenal resulted in the formation of an adduct (adduct A) that subsequently dehydrated on heating to adduct B. Liquid chromatography/mass spectrometry and nuclear magnetic resonance spectroscopy were used to assign the structure of adduct B as (N(delta),N(omega)(')-etheno-2'-heptanon-2' '-one)-N(alpha)-t-Boc-arginine. The reaction proceeded from initial reaction of the primary N(omega)-amino group at the C-1 aldehyde of 4-oxo-2-nonenal. Subsequently, an intramolecular Michael addition of a secondary N(delta)-amino group occurring at C-3 resulted in formation of the cyclic carbinolamine adduct A. Dehydration and rearrangement of the exocyclic imine resulted in the formation of adduct B, which contained a stable imidazole ring. The tetra peptide LRDE reacted with 4-oxo-2-nonenal primarily at arginine rather than at the amino terminus. This suggests that arginine-containing proteins can react with lipid hydroperoxide-derived 4-oxo-2-nonenal to form a novel imidazole modification.

Aldehydes↗
PubMed2006

Protective effect of black tea against ethanol-induced oxidative modifications of liver proteins and lipids.

OBJECTIVE: Black tea has been recently ascertained as a source of water-soluble antioxidants that may enhance cellular antioxidant abilities. The present study was designed to investigate the efficacy of the preventive effect of black tea on oxidative modifications of liver lipids and proteins of 2-month-old rats intoxicated chronically (28 days) with ethanol. METHOD: Lipid peroxidation was estimated by measurement of lipid hydroperoxides, malondialdehyde, and 4-hydroxynonenal by high-performance liquid chromatography (HPLC) and by spectrophotometric determination of conjugated dienes. The markers of protein oxidative modification products-bistyrosine and tryptophan-were quantified by spectrofluorimetry, whereas levels of amino, sulfhydryl, and carbonyl groups were estimated spectrophotometrically. RESULTS: Ethanol intoxication caused changes in liver antioxidant abilities that led to the generation of oxidative stress and, consequently, to the significant increase in products of lipid and protein oxidative modification. Enhanced lipid peroxidation was confirmed by assessment of the concentration of lipid peroxidation products measured at all examined levels. Protein modifications were evidenced by increase in levels of bistyrosine and carbonyl groups and by decrease in concentration of tryptophan and levels of sulfhydryl and amino groups. The metabolic consequences of oxidative modifications of lipids and proteins were reduced by cathepsin B activity and translocation of this lysosomal protease into cytosol as well as markers of liver damage-alanine aminotransferase (ALT) and aspartate aminotransferase (AST)-into the blood serum. Administration of black tea to ethanol-intoxicated rats partially protected antioxidant parameters and, remarkably, prevented the significant increase in concentrations of all measured lipid peroxidation products. Moreover, the levels of markers of the protein-modification process were similar to those of the control group. Protection of biological membranes by black tea prevents changes in the permeability of these membranes and translocation of the examined enzymes. CONCLUSIONS: Our findings indicate that black tea protects proteins and lipids against oxidative modification induced by chronic ethanol intoxication, which preserves changes in redox and proteolytic homeostasis.

Alanine Transaminase↗
PubMed2000

Iron-induced lipid peroxidation and protein modification in endoplasmic reticulum membranes. Protection by stobadine.

Treatment with FeSO(4)/EDTA (0.2 micromol Fe(II) per mg of protein) was used to study the effect of oxidative stress on lipid peroxidation and structural properties of endoplasmic reticulum (ER) membranes isolated from rabbit brain. Oxidative stress resulted in conjugated diene formation and a decrease of 1-anilino-8-naphthalenesulfonate (ANS) fluorescence in a time-dependent manner. In contrast, fluorescence anisotropy of 1, 6-diphenyl-1,3,5-hexatriene was increased early after the initiation of lipid peroxidation and no further increase was observed after 1, 2 and 3 h of peroxidation. FeSO(4)/EDTA treatment was accompanied by formation of conjugates of lipid peroxidation products with membrane proteins, as detected by the increase in fluorescence excitation (350-360 nm) and emission (440-450 nm) maximum. Oxidative stress also induced a marked decrease of the intrinsic fluorescence of aromatic amino acids, suggesting modification or changes in the environment of these amino acid residue(s). The lipid antioxidant, stobadine, completely prevented the changes of ANS fluorescence and production of peroxidized lipid-protein conjugates whereas tryptophan fluorescence was only partially protected. These results suggest that Fe(II) induces both lipid-mediated- and lipid peroxidation independent-modification of ER membrane proteins. The study also demonstrates that stobadine is a potent inhibitor of Fe(II)-induced protein modification.

Amino Acids↗
PubMed1986

Dietary n-3 polyunsaturated fatty acids: modification of rat cardiac lipids and fatty acid composition.

The effects of 5, 10 and 20% dietary menhaden oil (MO) on the composition of heart lipid classes and fatty acids were studied. Male Sprague-Dawley rats were fed ad libitum 0, 5, 10 and 20% MO for 3 wk. The heart phosphoglyceride content and composition and cholesterol were unchanged by dietary MO. A nonlinear dose-response relationship was observed between dietary MO levels and fatty acid compositional changes. Cardiolipin, choline (PC), ethanolamine (PE) and serine/inositol (PS/PI) phosphoglycerides showed an incorporation of n-3 fatty acids, eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3), between the control and 5% MO group, a plateau between the 5 and 10% MO groups and a further increase at the 20% MO level. The initial reduction in 20:4n-6 content remained unchanged as dietary MO increased except in PE where a further reduction was found at the 20% MO level. Dietary MO did not significantly change the 20:4n-6 content in neutral lipids. Linoleic acid content was most resistant to dietary MO removal. The level of 18:2n-6 was significantly lowered in heart PC when rats were fed 10% MO. No significant differences were found in PS/PI. In PE and NL significant differences occurred only when rats were fed 20% MO. The significant fatty acid modifications of heart lipid and PL found between the control and lowest level of dietary MO (5%) suggest that dietary fish oil supplementation in human diets may not be required for this effect.

Animals↗
PubMed1993

Analysis of plasma lipids by NMR spectroscopy: application to modifications induced by malignant tumors.

Lipid extracts of plasma were studied by 31P and 1H NMR spectroscopy at 9.4 T. Signals recorded on lipid mixtures were assigned to different lipid classes using a data base built with two-dimensional 1H COSY spectra of seven standard lipids. Signals unique to glycerophospholipids, sphingolipids, and triacylglycerols were identified. 31P and 1H NMR spectroscopy was used to study qualitative and quantitative modifications induced in plasma by malignant tumors. The results show a significant increase in triglyceride/phospholipid ratio and a concomitant decrease of total phospholipids in patients with cancer. In order to check for the possible presence of particular lipids such as glycolipids in these patients, 1H COSY spectra were recorded on the intact plasma and on extracts of plasma lipids in patients with cancer and in healthy subjects. Only in one case of ovarian cancer, a cross-peak at 1.35 and 4.15 ppm, corresponding to fucose residue in glycolipids, was detected.

Databases, Factual↗
PubMedDate not supplied

Nutritional control of lipid synthesis.

Dietary modification for the manipulation of lipid biosynthetic pathways has currently become a major direction for improving health status. Certainly changing dietary constituents can alter lipogenic processes and blood lipid parameters. However, the extremes of such modifications are often impractical, and the impact of major changes are not without consequence. For example, high carbohydrate diets are hyperlipemic and increased fish oil intake prolongs blood clotting time. Thus, no dietary fat modifications can be undertaken without considering the organism as a whole and the complexity of interactions within the individual. Such definition requires appreciation of human individuality and greater understanding of the regulation of lipogenic pathways.

Acetyl-CoA Carboxylase↗
PubMed2005

Purification and characterization of deacylated and/or palmitoylated lipid A species unique to Salmonella enterica serovar Typhimurium.

The Salmonella enterica serovar Typhimurium virulence gene products PhoP/PhoQ sense host microenvironments to regulate the expression of a lipid A 3-O-deacylase, PagL, and a lipid A palmitoyltransferase, PagP. Therefore, deacylation and/or palmitoylation of lipid A could occur in Salmonellae adapted to host environments. The PhoP/PhoQ-regulated modification of lipid A alters host recognition and signaling, and may play an important role in host defense against Salmonellae infection. Here we report the purification and characterization of modified lipid A species. Deacylated lipid A, deacylated and palmitoylated lipid A, and palmitoylated lipid A species were generated in Escherichia coli cells heterologously expressing salmonellae PagL and/or PagP, and then purified by sequential thin-layer chromatography. The purified lipid A species showed m/z values that correspond to single lipid A species on mass spectrometry analysis. The modified lipid A species showed reduced ability to induce cellular signaling through Toll-like receptor 4, suggesting a specific function of the lipid A modifications in the pathogenesis of salmonellae infection.

Acylation↗
PubMed1999

Lipid A mutant Salmonella with suppressed virulence and TNFalpha induction retain tumor-targeting in vivo.

Systemically administered tumor-targeted Salmonella has been developed as an anticancer agent, although its use could be limited by the potential induction of tumor necrosis factor alpha (TNFalpha)-mediated septic shock stimulated by lipid A. Genetic modifications of tumor-targeting Salmonella that alter lipid A and increase safety must, however, retain the useful properties of this bacteria. We report here that disruption of the Salmonella msbB gene reduces TNFalpha induction and increases the LD50 of this pathogenic bacteria by 10,000-fold. Notwithstanding this enormous difference, Salmonella retains its tumor-targeting properties, exhibiting tumor accumulation ratios in excess of 1000:1 compared with normal tissues. Administration of this bacteria to mice bearing melanoma results in tumors that are less than 6% the size of tumors in untreated controls at day 18. Thus, the antitumor activity previously demonstrated using tumor-targeting Salmonella with normal lipid A is retained. Lipid modification of tumor-specific bacterial vectors provides a means for reducing septic shock and further suggests that the antitumor activity of these bacteria may be independent of TNFalpha.

Acyltransferases↗
PubMed1993

Lipid advanced glycosylation: pathway for lipid oxidation in vivo.

To address potential mechanisms for oxidative modification of lipids in vivo, we investigated the possibility that phospholipids react directly with glucose to form advanced glycosylation end products (AGEs) that then initiate lipid oxidation. Phospholipid-linked AGEs formed readily in vitro, mimicking the absorbance, fluorescence, and immunochemical properties of AGEs that result from advanced glycosylation of proteins. Oxidation of unsaturated fatty acid residues, as assessed by reactive aldehyde formation, occurred at a rate that paralleled the rate of lipid advanced glycosylation. Aminoguanidine, an agent that prevents protein advanced glycosylation, inhibited both lipid advanced glycosylation and oxidative modification. Incubation of low density lipoprotein (LDL) with glucose produced AGE moieties that were attached to both the lipid and the apoprotein components. Oxidized LDL formed concomitantly with AGE-modified LDL. Of significance, AGE ELISA analysis of LDL specimens isolated from diabetic individuals revealed increased levels of both apoprotein- and lipid-linked AGEs when compared to specimens obtained from normal, nondiabetic controls. Circulating levels of oxidized LDL were elevated in diabetic patients and correlated significantly with lipid AGE levels. These data support the concept that AGE oxidation plays an important and perhaps primary role in initiating lipid oxidation in vivo.

Adult↗
PubMed2004

Esterified lipid hydroperoxide-derived modification of protein: formation of a carboxyalkylamide-type lysine adduct in human atherosclerotic lesions.

We have recently identified Nepsilon-azelayllysine (AZL) as a carboxyalkylamide-type novel lysine adduct in the reaction of linoleic acid hydroperoxides with the lysine derivative. To examine the formation of AZL in vivo, a novel monoclonal antibody (mAb19D5) specific to AZL moiety was prepared. The mAb19D5 scarcely recognized oxidized low-density lipoprotein (oxLDL), whereas the treatment of oxLDL with alkali or phospholipase A2 significantly increased the immunoreactivity. Similarly, the immunopositive materials were detected in alkali- or phospholipase A2-treated sections from human atherosclerotic aorta but not in untreated sections. These results suggest that esterified lipid hydroperoxide-derived modification of protein may serve as one mechanism for the oxidative modification of LDL and subsequent formation of atherosclerotic lesions in vivo.

Alkalies↗
PubMedDate not supplied

Facile functionalization of lipid bilayer vesicles by titania: the use of cerasome-forming lipids for surface and core modification.

Two kinds of functionalization of a lipid bilayer vesicle by titania were achieved by utilizing a cerasome-forming lipid, which is the starting material to prepare a cerasome, a morphologically stable lipid bilayer vesicle having an atomic layer of siloxane networks on its surface. One system is the preparation of the titania-coated cerasomes by immobilizing nanaometer-sizes of titania onto the surface siloxane network of cerasomes. The other is the creation of an asymmetric lipid bilayer structure on the surface of the colloidal titania particles. The characteristics of these surface- and core-functionalized vesicles were investigated, and it was found that these conjugates showed photocatalytic activity as evaluated by photolysis experiments of the cationic dye methylene blue.

Catalysis↗
PubMed2005

Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities.

Oxidative stress induced by chronic ethanol consumption, particularly in aging subjects, has been implicated in the pathophysiology of many neurodegenerative diseases. Antioxidants with polyphenol structures, such as those contained in green tea, given alone for 5 weeks in liquid Lieber de Carli diet followed by administration with ethanol for 4 weeks with ethanol have been investigated as potential therapeutic antioxidant agents in the brain in rats of three ages (2, 12, and 24 months). Ethanol consumption caused age-dependent decreases in brain superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities. In addition, ethanol consumption caused age-dependent decreases in the levels of GSH, selenium, vitamins, E, A and C, and beta-carotene and increases in the levels of oxidized glutathione (GSSG). Changes in the brain's antioxidative ability were accompanied by enhanced oxidative modification of lipids (increases in lipid hydroperoxides, malondialdehyde, and 4-hydroxynonenal levels) and proteins (increases in carbonyl groups and bistyrosine). Reduced risk of oxidative stress and protection of the central nervous system, particularly in young and adult rats, after green tea supplementation were observed. Green tea partially prevented changes in antioxidant enzymatic as well as nonenzymatic parameters induced by ethanol and enhanced by aging. Administration of green tea significantly protects lipids and proteins against oxidative modifications in the brain tissue of young and adult rats. The beneficial effect of green tea can result from the inhibition of free radical chain reactions generated during ethanol-induced oxidative stress and/or from green tea-induced increases in antioxidative abilities made possible by increases in the activity/concentration of endogenous antioxidants.

Aging↗
PubMed1993

Lipid metabolism by the intestinal mucosa in malnourished subjects following enteral nutrition supplemented with omega3 fatty acids.

UNLABELLED: Chronic malnutrition results in severe metabolic imbalance in man as the body modifies its modes of regulation of different nutrients, and in particular lipids. This study of the modifications in lipid metabolism induced by 15 days of enteral renutrition include: 12 malnourished patients (global nutritional deficit (GND) <20%) were given a cyclical enteral diet for 15 days under two conditions: ternary diet (Sondalis) or a similar diet whose lipid concentration was enriched by 5.3 g omega3 fatty acid per day. On Day 0 and Day 15, the serum lipid values were assayed and duodenal biopsies were taken to measure HMG-CoA reductase and (14)C acetate incorporation in the various classes of lipids. After 15 days of refeeding, the GND had been corrected by an average of 27% and HMG-CoA reductase activity had increased by 37% (60.2 +/- 7.46 vs 82.88 +/- 14.8 pmol/min/mg protein; p < 0.05). In 7 12 patients, the serum cholesterol values had increased (p < 0.01). No difference was observed in synthesis of FA, DG or cholesterol. Synthesis of phosphatidylcholines (PC) and phosphatidylglycerols (PG) was reduced by 12% and 23% respectively. Triglyceride synthesis (TG) increased by 20% (p < 0.05). The only difference between the two diets was in TG synthesis in organ-specific culture, which was increased only by the standard diet. IN CONCLUSION: (i) refeeding is accompanied by an increase in intestinal HMG-CoA reductase activity, a decrease in PC and PG synthesis, and an increase in TG synthesis; (ii) a diet enriched in omega3 FA increases TG synthesis less than the standard diet.

Journal Article↗
PubMed2004

Green tea protection against age-dependent ethanol-induced oxidative stress.

Ethanol intoxication leads to oxidative stress, which may be additionally enhanced by aging. The aim of this study was to investigate the influence of green tea as a source of water-soluble antioxidants on the ability to prevent oxidative stress in aged rats sub-chronically intoxicated with ethanol. Two-, 12-, and 24-mo-old male Wistar rats were divided into 4 experimental groups: (1) control, (2) green tea, (3) ethanol, and (4) ethanol and green tea. Ethanol intoxication produced age-dependent decrease in the activity of serum superoxide dismutase, glutathione peroxidase, and reductase and in levels of glutathione (GSH), vitamins C, E, and A, and beta-carotene. Changes in the serum antioxidative ability were accompanied by enhanced oxidative modification of lipid (increase in lipid hydroperoxides, malondiadehyde, and 4-hydroxynonenal levels) and protein (rise in carbonyl group levels). Green tea partially protected against changes in antioxidant enzymatic as well as nonenzymatic parameters produced by ethanol and enhanced by aging. Administration of green tea significantly protects cellular components such as lipids and proteins against oxidative modification. Results indicate that green tea effectively protects blood serum against oxidative stress produced by ethanol as well as aging.

Aging↗