bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lipid composition and peroxide levels of mucosal cells in the rat large intestine in relation to dietary fat
Authors: Turini M. E. , Thomson A. B. R. , Clandinin M. T. 
Published: November 2006

AbstractTo examine whether dietary fat alters membrane lipid composition and peroxidation of polyunsaturated fatty acids in “non‐proliferative” and “proliferative” cells in the large intestine, Sprague‐Dawley rats were fed diets providing a polyunsaturated‐to‐saturated fatty acid ratio of 1.2 or 0.3 at a high or low level of fat intake for a 25‐day period. Cell populations were isolated and the effect of dietary fat on membrane polyunsaturated fatty acid content and peroxide levels was determined. Neither fat level nor fatty acid composition of diet influenced total cholesterol, total phospholipids, and percentage of phospholipid classes in membrane phospholipids. Feeding the high fat and/or high polyunsaturated‐to‐saturated fatty acid ratio diet increased polyunsaturated fatty acid content of mucosal cell phospholipids. Increase in polyunsaturated fatty acid content was paralleled by a decrease in the monounsaturated fatty acid content of mucosal cell phospholipids. Membrane content of total saturated fatty acids was not significantly affected by diet. Variation in phospholipid fatty acid composition between “non‐proliferative” and ”proliferative” cells was observed. Lipid peroxide levels in mucosal cell lipid fractions were altered by dietary fat treatment. Animals fed high fat diets, compared to groups fed low fat diets, exhibited higher membrane peroxide levels when results are expressed as nmol/mg protein. Higher peroxide levels were observed in mucosal cells for rats fed high polyunsaturated‐to‐saturated fatty acid ratio diets when results were expressed per nmol of phospholipid. It is concluded that changes in fat level and fatty acid composition of the diet alters the mucosal cell membrane lipid composition in the rat large intestine and influences susceptibility of mucosal cell lipid to peroxidation. Further research is required to delineate which dietary factors—fat level, polyunsaturated‐to‐saturated fatty acid ratio, or both—have a primary influence on the degree of lipid peroxidation.
Effect of dietary fat on diabetes‐induced changes in liver microsomal fatty acid composition and glucose‐6‐phosphatase activity in rats
Authors: Venkatraman J. T. , Pehowich D. , Singh B. , Rajotte R. V. , Thomson A. B. R. , Clandinin M. T. 
Published: November 2006

AbstractExperimental diabetes may manifest itself in a defect in liver microsomal fatty acid desaturation and increased activity of glucose‐6‐phosphatase (G‐6‐Pase). The present study was designed to determine whether these changes could be normalized by a change in the dietary fat consumed. Control and streptozotocin‐induced diabetic rats were fed nutritionally adequate diets which varied in fatty acid composition. Fatty acid analysis of liver microsomal phospholipids revealed that non‐diabetic control animals fed saturated fat (beef tallow) or a diet high in ω3 fatty acids (fish oil) exhibited a significantly higher level of 18∶2ω6 and a lower level of 20∶4ω6 in the phosphatidylcholine and phosphatidylethanolamine fractions compared with diabetic animals. Control and diabetic animals fed the high linoleic acid diet had similar levels of 18∶2ω6 in the microsomal phosphatidylcholine and phosphatidylserine fractions. Microsomal G‐6‐Pase activity was higher in diabetic than in control animals. Activity of G‐6‐Pase was lower in microsomes of control animals fed the soybean oil or the fish oil diet, but was not significantly reduced in diabetic animals fed high polyunsaturated fats. Blood glucose levels were similar in control groups fed the different diets, but the plasma hemoglobin A1c level was lower in diabetic animals fed the soybean oil diet. Cholesterol and triglyceride levels were lower in diabetic animals fed the fish oil‐based diet. The results suggest that dietary fat manipulation has the potential to change at least some of the abnormalities in the microsomal membrane in experimental diabetes.
The effect of dietary linoleic acid on the fatty acid composition of individual phospholipid and lipoxygenase products from gills and leucocytes of Atlantic salmon (Salmo salar)
Authors: Gordon Bell J. , Raynard Robert S. , Sargent John R. 
Published: November 2006

AbstractDiets containing either fish oil or sunflower oil, both of which supplied the minimum required level of n−3 fatty acids, were given to Atlantic salmon (Salmo salar) postsmolts for a period of 16 weeks. In fish fed sunflower oil, the phospholipids of gills showed increased 18∶2n−6 (2–13‐fold), 20∶2n−6 (4.5–12‐fold) and 20∶−6 (2–8‐fold). In addition, phosphatidylethanolamine had increased 20∶4n−6 (1.5‐fold). Changes of a similar magnitude were observed in the phospholipids of blood leucocytes except that, in addition, 20∶4n−6 was elevated in phosphatidylserine (1.7‐fold) and phosphatidylinositol (1.4‐fold). Both tissues showed a general decrease in phospholipid 20∶5n−3 (up to 3‐fold), which caused an increase in 20∶4n−6/20∶5n−3 ratio (1.3–6‐fold). The elongation and desaturation products of 20∶4n−6, 22∶4n−6 and 22∶5n−6 were not increased as a result of feeding sunflower oil. When isolated gill cells were stimulated with the calcium ionophore A23187, 12‐hydroxy‐8,10,14,17‐eicosapentaenoic acid (12‐HEPE) was the major lipoxygenase product from salmon given fish oil. 12‐HEPE was significantly reduced in salmon given sunflower oil. When stimulated with A23187, the lipoxygenase products derived from whole blood of fish given sunflower oil showed decreased levels of leukotriene B5, 12‐HEPE and 12‐hydroxy‐5,8,10,14‐eicosatetraenoic acid.
Effect of chronic glucagon administration on lipoprotein composition in normally fed, fasted and cholesterol‐fed rats
Authors: Guettet Catherine , Rostaqui Najmuddin , Mathe Denis , Lecuyer Bernard , Navarro Nicole , Jacotot Bernard 
Published: November 2006

AbstractMale adult Wistar rats received daily (at 9 a.m. and 5 p.m.) 10 μg of zinc‐protamine glucagon by subcutaneous injection for 8 days. Plasma cholesterol levels were decreased by 36% in fed rats, 33% in cholesterol‐fed rats and by 55% in fasted rats. Lipoproteins were separated into 22 fractions by ultracentrifugation using a density gradient. Glucagon administration decreased the cholesterol content in all lipoproteins except low density lipoprotein (LDL1) (1.006–1.040) and very low density lipoprotein (VLDL) from cholesterol‐fed rats. The main decrease (−57 to −81%) was observed in 1.050–1.100 g/mL lipoproteins (LDL2 and HDL2), which contained a large amount of apo E, while HDL3 cholesterol was not affected. Triacylglycerol levels were decreased only in chylomicrons and VLDL (−70%) of fed and cholesterol‐fed rats, while plasma and lipoprotein triacylglycerol levels were not changed in fasted rats treated with glucagon. In normally fed rats glucagon administration increased by 42% the fractional catabolic rate of [125I]HDL2 while the absolute catabolic rate appeared to be unchanged. Glucagon seems to be a potent hypolipidemic agent affecting mainly the apo E‐rich lipoproteins. Its chronic administration limits lipoprotein accumulation which occurs upon cholesterol feeding.
The effect of dietary zinc deficiency on the lipid composition of the rat erythrocyte membrane
Authors: Driscoll Eric R. , Bettger William J. 
Published: November 2006

AbstractThe effect of dietary zinc deficiency in the rat on the lipid composition of the erythrocyte membrane was determined. Weanling male Wistar rats were fed an egg whitebased diet containing <1.0 mg Zn/kg dietad libitum. Control rats were either pair‐fed orad libitum‐fed the basal diet suppelemented with 100 mg Zn/kg diet. A zinc refed group was fed the −Zn diet until day 18 and then pairfed the +Zn diet until day 21. The voluntary feed restriction associated with dietary zinc deficiency resulted in erythrocyte membranes that had depressed phospholipid/protein and elevated cholesterol/phospholipid ratios. Similarly, all feed restricted groups had elevated 22‐carbon n−3 polyunsaturated fatty acid (PUFA) and depressed 22‐carbon n−6 PUFA concentrations in alkenylacyl and diacyl glycerophosphoethanolamine, phosphatidylserine and phosphatidylcholine; they also had depressed 24∶2n−6 levels in sphingomyelin. The relative concentrations of phospholipids in the membrane was similar between −Zn and +Zn (ad libitum) groups; however, the −Zn group had significantly less phosphatidylserine relative to +Zn (pair‐fed) controls.
Effect of dietary α‐linolenate/linoleate balance on endotoxin‐induced hepatitis in mice
Authors: Watanabe Shiro , Okuyama Harumi 
Published: November 2006

AbstractMice were fed diets with three different ratios of α‐linolenate (18∶−3) to linoleate (18∶2n−6), and the severity of hepatitis during endotoxic shock was compared. Dietary enrichment with α‐linolenate increased the severity of hepatitis and the mortality induced by lipopolysaccharide (LPS) in combination with D‐galactosamine (GalN). Differences in the dietary α‐linolenate/linoleate balance were mainly reflected in the levels of arachidonate and eicosapenatenoate in liver phospholipids. Pretreatement of mice with indomethacin was found to also enhance the severity of GalN/LPS‐hepatitis. This indicated that cyclooxygenase products of arachidonate may suppress the development of GalN/LPS‐hepatitis. The enhancement by high α‐linolenate diets was not observed when a lethal dose of LPS in the absence of GalN was given. Our results indicate that there are pathophysiological conditions of endotoxin‐induced hepatitis under which cyclooxygenase products of arachidonate play protective roles.
Headspace gas chromatography of volatile lipid peroxidation products from human red blood cell membranes
Authors: Frankel E. N. , Tappel A. L. 
Published: November 2006

AbstractAn improved headspace capillary gas chromatographic (GC) method was developed to measure the oxidative susceptibility of human red blood cell (RBC) membranes. This method analyzed volatile peroxidation products of both n−6 (hexanal and pentane) and n−3 (propanal) polyunsaturated fatty acids. Oxidative susceptibility tests were standardized by incubating in a sealed 10‐mL headspace bottle 0.25 or 1 mL of human RBC membrane in 40 mM phosphate buffer for 1 hr at 37°C with a mixture of Fe++, ascorbic acid and H2O2. Sodium dodecyl sulfate increased significantly the amount of hexanal measured by headspace GC. By this standard headspace method, in one series of red blood cell membranes (RBCM) samples a four‐fold variation in oxidative susceptibility was observed in RBCM from blood freshly drawn from six healthy subjects. In another series of RBCM samples a sixteen‐fold variation in oxidative susceptibility was noted in frozen RBCM from blood freshly drawn from five healthy subjects. Correlation between hexanal formation and polyunsaturated fatty acids (PUFA) depletion provided good evidence that under these standard conditions hexanal is exclusively derived from the oxidation of arachidonic acid. Hydroperoxides of arachidonic acid are more readily formed and decomposed than those of linoleic acid in the presence of Fe++, ascorbic acid and H2O2 to produce hexanal as the main product that can be readily analyzed by headspace GC. This method may provide a useful tool to study susceptibility toward lipid peroxidative damage in human RBC membranes.
Transformation of fatty acid hydroperoxides by alkali and characterization of products
Authors: Gardner Harold W. , Simpson Thomas D. , Hamberg Mats 
Published: November 2006

AbstractIt has previously been determined that (13S,9Z,11E)‐13‐hydroperoxy‐9,11‐octadecadienoic acid was mainly converted into (13S,9Z,11E)‐13‐hydroxy‐9,11‐octadecadienoic acid by 5 N KHO with preservation of the stereochemistry of the reactant [Simpson, T.D., and Gardner, H.W. (1993)Lipids 28, 325–330]. In addition, about 20–25% of the reactant was converted into several unknown by‐products. In the present work it was confirmed that the stereochemistry was conserved during the hydroperoxy‐diene to hydroxydiene transformation, but also, novel by‐products were identified. It was found that after only 40 min reaction (9Z)‐13‐oxo‐trans‐11,12‐epoxy‐9‐octadecenoic acid accumulated to as much as 7% of the total. Later, (9Z)‐13‐oxo‐trans‐11,12‐epoxy‐9‐octadecenoic acid began to disappear, and several other compounds continued to increase in yield. Two of these compounds, 2‐butyl‐3,5‐tetradecadienedioic acid and 2‐butyl‐4‐hydroxy‐5‐tetradecenedioic acid, were shown to originate from (9Z)‐13‐oxo‐trans‐11,12‐epoxy‐9‐octadecenoic acid, and they accumulated up to 2–3% each after 4 to 6 h. Some other lesser products included 11‐hydroxy‐9,12‐heptadecadienoic acid, 3‐hydroxy‐4‐tridecenedioic acid, 13‐oxo‐9,11‐octadecadienoic acid and 12,13‐epoxy‐11‐hydroxy‐9‐octadecenoic acid. Except for the latter two, most or all of the compounds could have originated from Favorskii rearrangement of the early product, (9Z)‐13‐oxo‐trans‐11,12‐epoxy‐9‐octadecenoic acid, through a cyclopropanone intermediate.
Dynamics of iron‐ascorbate‐induced lipid peroxidation in charged and uncharged phospholipid vesicles
Authors: Fukuzawa Kenji , Seko Takayuki , Minami Kazushi , Terao Junji 
Published: November 2006

AbstractPeroxidation of egg yolk phosphatidylcholine (egg PC) liposomes was induced by addition of ascorbic acid (AsA) and Fe(II) in the presence of a trace of autoxidized egg PC (PC−OOH), but not in the absence of PC−OOH. PC−OOH was degraded upon addition of AsA and Fe(II) but not of either one alone. The results suggest that PC−OOH is necessary to initiate lipid peroxidation by AsA/Fe(II). AsA oxidation in the bulk water phase was also associated with an increase in lipid peroxidation by AsA/Fe(II) in the presence of PC−OOH, but not in the absence of PC−OOH. Furthermore, the spin probe 12‐NS [12‐(N‐oxyl‐4,4′‐dimethyloxazolidin‐2‐yl)stearic acid], which labels the hydrophobic region of dimyristoyl phosphatidylcholine (DMPC) liposomal membranes, was degraded upon addition of AsA and Fe(II) in the presence of PC−OOH, but not in the absence of PC−OOH. These results indicate that the “induction message” that is associated with decreases of PC−OOH and AsA in the initiation step of lipid peroxidation must be transferred from the membrane surface to the inner hydrophobic membrane region. AsA in the bulk phase was oxidized faster and more extensively upon its addition together with Fe(II) to egg PC liposomes than to DMPC liposomes, though the initial content of PC−OOH in the former was 5–10 times lower than in the latter. This suggests that, in egg PC liposomes, the OOH‐groups of new PC−OOH generated in the inner membrane regions must become accessible from the surface, enabling reaction with AsA/Fe(II) which in turn would result in an extensive decrease in AsA. By contrast, in DMPC liposomes, that do not generate PC−OOH, AsA is only oxidized slightly in connection with the degradation of the PC−OOH initially present. The effect of surface charges on the membrane surface was also studied to obtain further information on the initiation step of lipid peroxidation. The rate of lipid peroxidation by AsA/Fe(II) or Fe(III) decreased in the order, egg PC liposomes ≫negatively charged egg PC liposomes containing dicetylphosphate>positively charge egg PC liposomes containing stearylamine. The rate of associated AsA oxidation was in the order, egg PC liposomes≫egg PC/stearylamine liposomes>egg PC/dicetylphosphate liposomes. However, in DMPC liposomes that do not generate PC−OOH, the rates of AsA oxidation associated with the reductive cleavage of PC−OOH by AsA/Fe(II) and coupled with the reduction of Fe(III) to Fe(II) were in the order, DMPC liposomes =DMPC/stearylamine liposomes≫DMPC/dicetylphosphate liposomes. These differences in the rates of lipid peroxidation, depending on differences in membrane charge, are discussed in relation to two properties of AsA: (i) its antioxidant property through trapping of lipid radicals and (ii) its prooxidant properties (a) by being an effective iron chelator thus altering the reactivity of iron with oxygen and peroxides and (b) by being an iron reductant and providing a source of Fe(II).
Role of lipid structure in the activation of phospholipase A2 by peroxidized phospholipids
Authors: McLean Larry R. , Hagaman Karen A. , Davidson W. Sean 
Published: November 2006

AbstractThe time course of hydrolysis of a mixed phospholipid substrate containing bovine liver 1,2‐diacyl‐sn‐glycero‐3‐phosphocholine (PC) and 1,2‐diacyl‐sn‐glycero‐3‐phosphoethanolamine (PE) catalyzed byCrotalus adamanteus phospholipase A2 was measured before and after peroxidation of the lipid substrate. The rate of hydrolysis was increased after peroxidation by an iron/adenosine diphosphate (ADP) system; the presence of iron/ADP in the assay had a minimal inhibitory effect. The rate of lipid hydrolysis was also increased after the substrate was peroxidized by heat and O2. Similarly, peroxidation increased the rate of hydrolysis of soy PC liposomes that did not contain PE. In order to minimize interfacial factors that may result in an increase in rate, the lipids were solubilized in Triton X‐100. In mixtures of Triton with soy PC in the absence of PE, peroxidation dramatically increased the rate of lipid hydrolysis. In addition, the rate of hydrolysis of the unoxidizable lipid 1‐palmitoyl‐2‐[1‐14C]oleoyl PC incorporated into PC/PE liposomes was unaffected by peroxidation of the host lipid. These data are consistent with the notions that the increase in rate of hydrolysis of peroxidized PC substrates catalyzed by phospholipase A2 is due largely to a preference for peroxidized phospholipid molecules as substrates and that peroxidation of host lipid does not significantly increase the rate of hydrolysis of nonoxidized lipids.
Effect of age and α‐linolenic acid deficiency on Δ6 desaturase activity and liver lipids in rats
Authors: Dinh T. K. L. , Bourre J. M. , Durand G. 
Published: November 2006

AbstractThe combined effects of age and of diet deficient in n−3 fatty acids on Δ6 desaturation of linoleic acid and on lipid fatty acid composition were studied in the liver of the rat at 2, 6, 12, 18 and 24 mon of age. The profiles of Δ6 desaturase activity and fatty acid composition were studied in the deficient rats refed, at these different ages either with 18∶3n−3 (mixture of peanut and rapeseed oils) or with 20∶5n−3+22∶6n−3 (fish oil) diets for 2, 4, 8 or 12 wk. Results showed that the liver Δ6 desaturation activity in the control rats remained high at 2 and 6 mon, decreased by 30% from 6 to 12 mon, and then remained stable from 12 to 24 mon. In the deficient rats, this activity remained high during the entire period studied. Thus, the profile of liver Δ6 desaturase activity after puberty was not related to age only; it also depended on the polyunsaturated fatty acid (PUFA) n−6 and n−3 balance in the diet. In the controls, in parallel with the Δ6 desaturase activity, PUFA metabolism could be divided into three periods: a “young” period, and “old age” period, separated by a period of transition between 6 and 12 mon. Recovery from PUFA n−3 deficiency occurred at all ages but in a different manner depending on whether the rats were “young” or “old”. Recovery was faster if long‐chain n−3 PUFA rather than α‐linolenic acid were supplied in the diet.
Differential utilization of eicosapentaenoic acid and docosahexaenoic acid in human plasma
Authors: Hodge Jason , Sanders Kerrie , Sinclair Andrew J. 
Published: November 2006

AbstractIt has recently been shown that the ω3 fatty acid status in humans can be predicted by the concentration of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids in plasma phospholipids [Bjerve, K.S., Brubakk, A.M., Fougner, K.J., Johnsen, H., Midjthell, K., and Vik, T. (1993)Am. J. Clin. Nutr., in press]. In countries with low intake of ω3 fatty acids, the level of EPA in plasma phospholipids is often only about one‐fifth the concentration of DHA. The purpose of this study was to investigate whether this difference in the concentration of these two fatty acids was due to a selective loss of EPA relative to DHA or to a lower dietary intake of EPA. Seven female volunteers ingested four grams of MaxEPA daily for 2 wk and in the following 4 wk they ate a diet almost completely devoid of the long‐chain ω3 fatty acids. The concentrations of the ω3 fatty acids in the plasma cholesteryl esters, triglycerides and phospholipids and the high density lipoprotein phospholipids were examined at weekly intervals throughout the study. There was a more rapid rise in the concentration of EPA than in DHA levels in the supplementation period in all lipid fractions, but there was a disproportionate rise in DHA relative to EPA in the plasma lipids compared with the ratio in the supplement. In the depletion phase there was a rapid disappearance of EPA from all fractions, such that pre‐trial levels were reached by one week post‐supplementation. The disappearance of DHA was slower, particularly for the plasma phospholipids: at 4 wk post‐supplementation, the DHA concentration in this fraction was still 40% above the pre‐trial value. It is suggested that the low plasma EPA values relative to DHA are the result of increased β‐oxidation of EPA and/or low dietary intake, rather than a rapid conversion of EPA to DHA. One practical result of this experiment is that, compared with DHA, the maintenance of increased EPA levels in plasma (and therefore tissues) would require constant inputs of EPA due to its more rapid loss from the plasma.
Dietary α‐linolenic acid alters tissue fatty acid composition, but not blood lipids, lipoproteins or coagulation status in humans
Authors: Kelley Darshan S. , Nelson Gary J. , Love James E. , Branch Leslie B. , Taylor Peter C. , Schmidt Perla C. , Mackey Bruce E. , Iacono James M. 
Published: November 2006

AbstractWe examined the effect of dietary α‐linolenic acid (ALA) on the indices of lipid and coagulation status and on the fatty acid composition of serum and peripheral blood mononuclear cell (PBMNC) lipids in ten healthy men (age 21–37 yr) who consumed all their meals at the Western Human Nutrition Research Center for 126 d. There was a stabilization period of 14 d at the start when all 10 subjects consumed the basal diet (BD) containing 23.4 energy percent (en%) fat and two intervention periods of 56 d each. During the first intervention period, 5 subjects consumed the BD containing 23.4 en% fat, and 5 subjects consumed a diet providing 6.3% calories from α‐linolenic acid [flaxseed oil (FSO) diet containing 28.8 en% fat]. Diets were crossed over between the two groups during the second intervention period. Feeding the FSO diet did not nignificantly alter serum triglycerides, cholesterol, highdensity lipoproteins, low‐density lipoproteins, apoprotein A‐I and apoprotein B when compared to the corresponding values in the subjects fed the BD, nor was there any effect of the FSO diet on the bleeding time, prothrombin time and partial prothrombin time for these subjects. Feeding the ALA‐containing diet did cause a significant increase in ALA concentration in serum (P<0.001) and PBMNC lipids (P<0.05). It also caused a significant increase (P<0.05) in the eicosapentaenoic and docosapentaenoic acid contents of PBMNC lipids, and a decrease (P<0.01) in linoleic and eicosatrienoic acid contents of serum lipids. Thus, dietary ALA, fed for 56 d at 6.3% of calories, had no effect on plasma triglyceride or very low density lipoprotein levels or the common risk factors associated with atherosclerosis, although these parameters have been reported by others to be influenced by fatty acids, such as palmitic or linoleic acids, in the diet. Dietary ALA did significantly alter the fatty acid composition of plasma and PBMNC.