bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peroxidase‐catalyzed oxidation of β‐carotene in HL‐60 cells and in model systems: Involvement of phenoxyl radicals
Authors: Tyurin Vladimir A. , Carta Gianfranca , Tyurina Yulia Y. , Banni Sebastiano , Day Billy W. , Corongiu Francesco P. , Kagan Valerian E. 
Published: November 2006

AbstractRecent studies provide extensive evidence for the importance of carotenoids in protecting against oxidative stress associated with a number of diseases. In particular, reactions of carotenoids with phenoxyl radicals generated by peroxidasecatalyzed one‐electron metabolism of phenolic compounds may represent an important antioxidant function of carotenoids. To further our understanding of the antioxidant mechanisms of carotenoids, we used in the present work two different phenolic compounds, phenol and a polar homologue of vitamin E (2,2,5,7,8‐pentamethyl‐6‐hydroxychromane, PMC), as representatives of two different types of phenols to study reactions of their respective phenoxyl radicals with carotenoids in cells and in model systems. We found that phenoxyl radicals of PMC did not oxidize β‐carotene in either HL‐60 cells or in model systems with horseradish peroxidase (HRP)/H2O2. In contrast, the phenoxyl radicals generated from phenol (by native myeloperoxidase in HL‐60 cells or HRP/H2O2 in model systems) effectively oxidized β‐carotene and other carotenoids (canthaxanthin, lutein, lycopene). One‐electron reduction of the phenoxyl radical by ascorbate (assayed by electron spin resonance‐detectable formation of semidehydroascorbyl radicals) prevented HRP/H2O2‐induced oxidation of β‐carotene. PMC, but not phenol, protected β‐carotene against oxidation induced by a lipid‐soluble azo‐initiator of peroxyl radicals. No adducts of peroxidase/phenol/H2O2‐induced β‐carotene oxidation intermediates with phenol were detected by high‐performance liquid chromatography‐mass spectrometry analysis of the reaction mixture. Since carotenoids are essential constituents of the antioxidant defenses in cells and biological fluids, their depletion through the reaction with phenoxyl radicals formed from endogenous, nutritional and environmental phenolics, as well as phenolic drugs, may be an important factor in the development of oxidative stress.
Stearic acid modifies very low density lipoprotein lipid composition and particle size differently from shorter‐chain saturated fatty acids in cultured rat hepatocytes
Authors: Pai Tonkun , Yeh Yu‐Yan 
Published: November 2006

AbstractStearic acid as compared to myristate, palmitate, or oleate is poorly incorporated into triacylglycerol, a major lipid component of very low density lipoprotein (VLDL). The present study investigated the effects of these fatty acids on VLDL metabolism in cultured rat hepatocytes. All fatty acids stimulated [2‐3H] glycerol incorporation into VLDL lipids and secretion of [3H]‐labeled VLDL by hepatocytes. However, the rate of [3H]‐labeled VLDL secretion in the presence of nonlabeled stearate (12.8±0.7 pmol/mg protein/4h) was 46, 59, and 22% of that observed for those treated with myristate, palmitate, and oleate, respectively. [1‐14C]Stearate as a substrate was also less effective than other labeled fatty acids to be incorporated into VLDL lipids. Of total VLDL lipids synthesized from [1‐14C] stearate, triacylglycerol accounted for 78% as compared to 88–97% of that derived from palmitate, myristate, and oleate. The amounts of apoB100 and apoB48 were the same in hepatocytes treated with or without exogenous fatty acids. Similarly, the rate of apoB synthesis from [35S] methionine was not affected by exogenous fatty acids. The treatment of cells with various saturated fatty acids increased the particle size of VLDL to different extents. The largest particles of VLDL, with a mean diameter of 79.3±11.9 nm, were seen in the cells treated with stearate, followed by those treated with palmitate and myristate (45.5±9.8 and 38.6±6.8 nm, diameter, respectively). Clearly, hepatocytes treated with stearate secrete less VLDL and produce larger VLDL particles than those treated with shorter‐chain saturated fatty acids.
Impaired cholesterol esterification in the plasma in patients with breast cancer
Authors: Subbaiah Papasani V. , Liu Ming , Witt Thomas R. 
Published: November 2006

AbstractAn important factor which determines the movement of cholesterol in and out of the cells is the free cholesterol (FC)/esterified cholesterol (EC) ratio in the plasma. Although this ratio has been shown to be increased in several types of malignancies in humans as well as experimental animals, it is not known whether such an abnormality is found in breast cancer patients. Furthermore, the reasons for such an increase in cancer patients are unknown. We studied the plasma lipid composition and the activity of lecithin‐cholesterol acyltransferase (LCAT), the enzyme responsible for the formation of most of EC in human plasma, in 12 women with breast cancer and 9 agematched control women. The plasma EC concentration was found to be significantly decreased in cancer patients, whereas the FC concentration was unchanged, leading to increased FC/EC ratios (P<0.05). The concentration of phosphatidylcholine, the acyl donor in the LCAT reaction, was decreased significantly, whereas all other phospholipids were unaffected. The cholesterol‐esterifying activity of LCAT was significantly lower in cancer patients, whether assayed with endogenous substrates (P<0.05), or with an exogenous substrate (P<0.01). However, another function of the enzyme, namely the lysolecithin acyltransferase activity, was increased (P<0.02), indicating that the enzyme concentration in plasma may not be decreased. These results show that the increase in the FC/EC ratio in cancer patients is due to an impaired esterification of cholesterol by plasma LCAT, probably due to an alteration in the composition of substrate lipoproteins, or the presence of an inhibitory factor.
Early dietary intervention with structured triacylglycerols containing docosahexaenoic acid. Effect on brain, liver, and adipose tissue lipids
Authors: Christensen Merete Myrup , Høy Carl‐Erik 
Published: November 2006

AbstractNewborn rats were fed liquid diets containing 7 wt% fat in which 3.8% of the total fatty acids were 22:6n‐3. The fats were either a specific structured oil with 22:6n‐3 mostly located in the sn‐2 position or a randomized oil with 22:6n‐3 equally distributed in the triacylglycerol (TAG) molecules. The oils were manufactured by interesterification of fish oil TAG with free fatty acids from butterfat. The pups were tube‐fed three times a day and stayed with their dams during the night. After 14 d they were fed solid diets containing the same oils for the next 7 d. A reference group stayed with the dams and received ordinary rat chow at weaning. In general no significant differences between the two dietary treatments were observed in the tissues examined except for adipose tissue. The levels of 22:6n‐3 were significantly increased in brain phosphatidylcholines (PC) and phosphatidylserines (PS) of both experimental groups compared with the reference group after three weeks, whereas no differences were found in brain phosphatidylethanolamines (PE) and phosphatidylinositols (PI). In all groups and all phospholipids examined, the levels of 20:4n‐6 generally decreased from 1 to 3 wk and were significantly lower in the experimental groups compared with the reference group at 3 wk except for PI. In liver, PC and PE 22:6n‐3 remained constant in the experimental groups but decreased significantly in the reference group, whereas in liver PS 22:6n‐3 increased in all groups, but reached significantly higher levels in the experimental groups than in the reference group. In adipose tissue, 22:6n‐3 increased in the experimental groups during the study period, but decreased in the reference group, suggesting that a surplus of dietary 22:6n‐3 was stored.
Phospholipid fatty acid composition in type I and type II rat muscle
Authors: Blackard William G. , Li Jing , Clore John N. , Rizzo William B. 
Published: November 2006

AbstractThe fatty acid composition of the membrane phospholipids phosphatidylcholine (PC) and phosphatidylethanolamine in insulin‐sensitive Type I (soleus) and insulin‐resistant Type II (EDL) muscle is not known. In the present studies, soleus and EDL muscles were removed from 250–300 g Sprague‐Dawley rats, and the fatty acid composition of total and individual phospholipid (PL) species was quantitated. As expected, triglyceride content was increased twofold in soleus muscle. No quantitative differences in the individual PL species or cholesterol content were found between the two muscles. However, a striking difference in PL fatty acid composition was observed in the PC fraction. An increase in 16∶0 with decreases in 18∶0, 18∶1, 22∶5n‐3, and 22∶6n‐3 (P<0.001 for each) was observed in the PC fraction of EDL compared to that from soleus, consistent with reduced elongation of PC fatty acids. Inhibition of fatty acid oxidation with the carnitine palmitoyl transferase‐1 inhibitor, etomoxir, did not alter the fatty acid pattern in either muscle. We conclude that an alteration in PL fatty acid composition consistent with reduced elongation of both saturated and unsaturated fatty acids is observed in Type II muscle. The restriction of these alterations to the PC fraction has important implications.
Conjugated linoleic acid modulates hepatic lipid composition in mice
Authors: Belury Martha A. , Kempa‐Steczko Anna 
Published: November 2006

AbstractConjugated linoleic acid (CLA) is a chemoprotective fatty acid that inhibits mammary, colon, forestomach, and skin carcinogenesis in experimental animals. We hypothesize that the ubiquitous chemoprotective actions of dietary CLA in extrahepatic tissues are dependent upon its role in modulating fatty acid composition and metabolism in liver, the major organ for lipid metabolism. This study begins to evaluate the role of CLA in lipid metabolism by determining the modulation of fatty acid composition by CLA. Female SENCAR mice were fed semipurified diets containing 0.0% (Diet A), 0.5% (Diet B), 1.0% (Diet C), or 1.5% (Diet D) CLA (by weight) for six weeks. Mice fed Diets B, C, and D exhibited lower body weights and elevated amounts of extractable total lipid in livers compared with mice fed diets without CLA (Diet A). Analyses of the fatty acid composition of liver by gas chromatography revealed that dietary CLA was incorporated into neutral and phospholipids at the expense of linoleate in Diets B, C, and D; oleate increased and arachidonate decreased in neutral lipids of CLA diet groups. In addition, increasing dietary CLA was associated with reduced linoleate in hepatic phospholipids. In an in vitro assay, CLA was desaturated to an unidentified 18:3 product to a similar extent as linoleate conversion to γ‐linolenate (9.88, and 13.63%, respectively). These data suggest that CLA may affect metabolic interconversion of fatty acids in liver that may ultimately result in modified fatty acid composition and arachidonate‐derived eicosanoid production in extrahepatic tissues. In addition to determining how dietary CLA modulates eicosanoid synthesis, further work is needed to identify enzymatic products that may result from desaturation of CLA.
Effects of cationic liposome‐DNA complexes on pulmonary surfactant function in vitro and in vivo
Authors: Boncuk Pinar , Kaser Matthew , Yu Yip , Taeusch H. William 
Published: November 2006

AbstractCationic liposome‐DNA complexes are being evaluated as potential gene therapy agents for the lung. Cations have strong effects on the biophysical functions of lung surfactant. Therefore, we assessed whether cationic liposomes [composed of N‐(1‐(2,3‐dioleyloxy) propyl)‐N,N,N‐trimethyl‐ammonium chloride and dioleylphosphatidylethanolamine] with or without DNA affect behavior of four types of surfactant in vitro. Experiments were carried out using a modified Wilhelmy surface balance. The ability of surfactants that contain protein and anionic lipids to lower surface tension was inhibited in the presence of cationic liposomes. Inactivation was less when DNA was preincubated with cationic liposomes. Surfactant that contained neither protein nor anionic lipids was not inactivated. Mechanical properties of the lung were studied to assess in vivo surfactant function after intratracheal instillation of a cationic liposome‐DNA complex into adult rats. Pressure‐volume deflation curves were shifted by 18% compared with those from normal (untreated) animals, but this effect was transient and not different from that observed in animals who received a similar volume of saline. These findings indicate that cationic liposomes alone may have deleterious effects on behavior of some surfactants possibly by disrupting charge interactions between negatively charged phospholipids and surfactant proteins. When DNA is added to liposomes before exposure to surfactants, the adverse charge interactions may be obviated by charge neutralization of liposomes by DNA.
Simvastatin impairs mitogen‐induced proliferation of malignant B‐lymphocytes from humans—in vitro and in vivo studies
Authors: Vitols S. , Angelin B. , Juliusson G. 
Published: November 2006

AbstractChronic lymphocytic leukemia (CLL) cells express lower low density lipoprotein (LDL) receptor activity and higher 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) reductase activity than normal mononuclear blood cells indicating that CLL cells may depend on cholesterol synthesis for their proliferation. We studied the effects of competitive inhibitors of HMG‐CoA reductase on malignant lymphocyte proliferation in vitro and in vivo. Tumor B‐cells from 13 patients with CLL, hairy cell leukemia, or immunoblastic B‐cell lymphoma were cultured for 4 d in the presence of B‐cell mitogens and cholesterol synthesis inhibitors. Simvastatin and lovastatin suppressed, in a concentration‐dependent manner, the mitogen‐induced cellular thymidin uptake in medium with 10% human AB‐serum or lipoprotein‐deficient serum. Pravastatin was active only in medium with lipoprotein‐deficient serum. Ten previously untrated patients with CLL received simvastatin orally, 40 mg daily for 12 wk. Mean reductions in total plasma and LDL cholesterol were 30% (range 9–46%) and 37% (range 16–63%), respectively. Cells from four patients showed moderate to minor increases in the degradation rate of 125I‐LDL suggesting that the need for exogenous cholesterol had increased, three patients showed an increase in HMG‐CoA reductase activity, and the cells from one patient showed both. There was no significant change in the clinical disease status during medication. However, four of the ten patients developed a therapy‐demanding progressive disease during the subsequent year. Further clinical studies with cholesterol synthesis inhibitors in leukemia are warranted.
Polyunsaturated fatty acids increase the sensitivity of 36B10 rat astrocytoma cells to radiation‐induced cell kill
Authors: Vartak Sujata , Robbins Mike E. C. , Spector Arthur A. 
Published: November 2006

AbstractPolyunsaturated fatty acids (PUFA) such as γ‐linolenic acid (GLA, 18:3n‐6), eicosapentaenoic acid (EPA, 20: 5n‐3), and docosahexaenoic acid (DHA, 22:6n‐3) have been shown to be cytotoxic to tumor cells. The objective of this work was to study the effect of PUFA on the radiation response of a 36B10 rat astrocytoma cell line. Supplementation of the astrocytoma cells with 15–45 μM GLA, EPA, or DHA produced marked changes in the fatty acid profiles of their phospholipids and neutral lipids. The methylene bridge index of these lipids increased significantly. These PUFA also exerted cytotoxic effects, as determined using the clonogenic cell survival assay. While GLA and DHA produced a moderate cell‐killing effect, EPA was extremely cytotoxic, especially at a concentration of 45 μM. The monounsaturated oleic acid (OA, 18:1n‐9) did not affect cell survival. Further, all three PUFA, and particularly GLA, increased the radiation‐induced cell kill; OA did not enhance the effect of radiation. α‐Tocopherol acetate blocked the enhanced radiation sensitivity of GLA‐ and DHA‐supplemented cells. In conclusion, GLA, EPA, and DHA supplementation prior to, during, and after irradiation can enhance the radiation‐induced cytotoxicity of rat astrocytoma cells. GLA and DHA supplementation post‐irradiation also enhanced the radiation response of the 36B10 cells. Because GLA maximally increases the radioresponsiveness of a rat astrocytoma, this PUFA might prove useful in increasing the therapeutic efficacy of radiation in the treatment of certain gliomas.
Oryzanol decreases cholesterol absorption and aortic fatty streaks in hamsters
Authors: Rong Ni , Ausman Lynne M. , Nicolosi Robert J. 
Published: November 2006

AbstractOryzanol is a class of nonsaponifiable lipids of rice bran oil (RBO). More specifically, oryzanol is a group of ferulic acid esters of triterpene alcohol and plant sterols. In experiment 1, the mechanisms of the cholesterol‐lowering action of oryzanol were investigated in 32 hamsters made hypercholesterolemic by feeding chow‐based diets containing 5% coconut oil and 0.1% cholesterol with or without 1% oryzanol for 7 wk. Relative to the control animals, oryzanol treatment resulted in a significant reduction in plasma total cholesterol (TC) (28%, P<0.01) and the sum of IDL‐C, LDL‐C, and VLDL‐C (NON‐HDL‐C) (34%, P<0.01). In addition, the oryzanol‐treated animals also exhibited a 25% reduction in percent cholesterol absorption vs. control animals. Endogenous cholesterol synthesis, as measured by the liver and intestinal HMG‐CoA reductase activities, showed no difference between the two groups. To determine whether a lower dose of oryzanol was also efficacious and to measure aortic fatty streaks, 19 hamsters in experiment 2 were divided into two groups and fed for 10 wk chow‐based diets containing 0.05% cholesterol and 10% coconut oil (w/w) (control) and the control diet plus 0.5% oryzanol (oryzanol). Relative to the control, oryzanol‐treated hamsters had reduced plasma TC (44%, P<0.001), NON‐HDL‐C (57%, P<0.01), and triglyceride (TG) (46%, P<0.05) concentrations. Despite a 12% decrease in high density lipoprotein cholesterol (HDL‐C) (P<0.01), the oryzanol‐treated animals maintained a more optimum NON‐HDL‐C/HDL‐C profile (1.1±0.4) than the contorl (2.5±1.4; P<0.0075). Aortic fatty streak formation, so defined by the degree of accumulation of Oil Red O‐stained macrophage‐derived foam cells, was reduced 67% (P<0.01) in the oryzanol‐treated animals. From these studies, it is concluded that a constituent of the nonsaponifiable lipids of RBO, oryzanol, is at least partially responsible for the cholesterol‐lowering action of RBO. In addition, the cholesterol‐lowering action of oryzanol was associated with significant reductions in aortic fatty streak formation.
Effect of nicotine on lipoprotein metabolism in rats
Authors: Ashakumary L. , Vijayammal P. L. 
Published: November 2006

AbstractNicotine, a major component of cigarette smoke, plays an important role in the development of cardiovascular disease and lung cancer in smokers. The effect of nicotine on lipoprotein metabolism was studied using rats as the experimental animal. There was a significant increase in the total cholesterol, phospholipids, and triglycerides as well as the amount of lipids associated with very low density lipoprotein (VLDL) and low density lipoprotein (LDL) in sera of nicotine‐treated rats. The incorporation of 3H labeled leucine into the apo B was found to be increased both in the medium and associated cells in the hepatocytes isolated from nicotine‐treated rats indicating an increased synthesis and secretion of the apo B containing lipoproteins. This was further confirmed by the higher incorporation of 14C acetate into total and individual lipids of LDL and VLDL secreted into the medium as well as that associated with different lipids in the cell layer. The activity of lipoprotein lipase in extrahepatic tissues and plasma lecithin cholesterol acyltransferase activity were significantly lower in nicotine‐treated rats. These results indicate that nicotine exerts hyperlipidemic effects particularly by increasing the synthesis and secretion of triglyceride‐rich lipoproteins. Since nicotine is one of the major hazardous components present in cigarette smoke and tobacco, one can extrapolate that the deleterious effect exerted by nicotine on rats extends to cigarette smokers and those who use other forms of tobacco.
A rapid method for the determination of vitamin E forms in tissues and diet by high‐performance liquid chromatography using a normal‐phase diol column
Authors: Kramer John K. G. , Blais Lisa , Fouchard Robert C. , Melnyk Roman A. , Kallury Krishna M. R. 
Published: November 2006

AbstractThis paper describes a simple method for the analysis of tocopherols in tissues by which frozen tissues −70°C were pulverized at dry ice temperatures (−70°C) and immediately extracted with hexane. There was no need to remove the coeluting lipids from tissues by saponification, since at that level of neutral lipids in the sample, there was no reduction in fluorescence response. For the analysis of oil, in which large amounts of neutral lipids were coextracted, a 20% reduction of fluorescence response was observed, but the response was equal for all tocopherol forms, and was appropriately corrected. Saponification was used only when tocopherol esters were present, and only after an initial hexane extraction to remove the free tocopherols in order to avoid their loss by saponification, particularly non α‐tocopherol and tocotrienols. All the tocopherols and tocotrienols were separated on a normal‐phase diol (epoxide) column that gave consistent and reproducible results, without the disadvantages of nonreproducibility with silica columns, or the lack of separation with reversed‐phase columns. The tocopherols were quantitated by using a tocopherol form not present in the sample as an internal tocopherol standard, or using an external tocopherol standard if all forms were present, or when the sample was saponified. Piglet heart and liver samples showed the presence of mainly α‐tocopherol, with minor amounts of β‐ and γ‐tocopherol and α‐tocotrienol, but no δ‐tocopherol. Only small amounts of tocopherol esters were present in the liver but not in the heart.
Analysis of lipoxygenase‐derived fatty acid hydroperoxides by electrospray ionization tandem mass spectrometry
Authors: Schneider Claus , Schreier Peter , Herderich Markus 
Published: November 2006

AbstractA rapid method is described for the identification of fatty acid hydroperoxides by electrospray ionization‐tandem mass spectrometry coupled to liquid chromatography without any derivatization required prior to analysis. Localization of fatty acid hydroperoxides in complex mixtures was achieved by monitoring the loss of hydrogen peroxide using constant neutral loss scanning. In the presence of 5 mM NH4OAc in methanol‐water, adductions [M+NH4]+ were formed almost exclusively, directly revealing the molecular mass of the thermolabile hydroperoxides. In addition, low energy collision‐induced dissociation of precursor ions [M+NH4]+ led to characteristic product ions from both the 9‐ and 13‐regioisomers. Thus, electrospray ionization‐tandem mass spectrometry provides a straightforward approach for the study of the regioselectivity of lipoxygenase catalysis without any derivatization step required prior to analysis.