bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of free α‐tocopherol and α‐tocopheryl acetate as sources of vitamin E in rats and humans
Authors: Burton Graham W. , Ingold Keith U. , Foster David O. , Cheng Shee C. , Webb Ann , Hughes Lise 
Published: November 2006

AbstractThe uptake of α‐tocopherol from 2R,4′R,8′R‐α‐tocopherol and 2R,4′R,8′R‐α‐tocopheryl acetate has been compared in rats and humans. The two forms of vitamin E were compared simultaneously in each subject (rat and human) by using a combination of deuterium‐substitution and gas chromatography‐mass spectrometry (GC‐MS) to distinguish and measure the competitive uptake of α‐tocopherol from an orally ingested mixture of the acetate and the free phenol forms. When rats were dosed in a manner analogous to that used in traditional bioassays, i.e., providing the two forms of vitamin E one daily in tocopherol‐stripped corn oil for four successive days immediately prior to sacrifice, the net uptake of α‐tocopherol from the free phenol form was only half that from the acetate. This result is consistent with the greater activity of the acetate that had been observed previously in bioassays. However, when the two forms of tocopherol were intubated into rats as a single dose mixed in with an aqueous bolus of standard laboratory diet, the amount of α‐tocopherol taken up from the free form after 24 hr was very similar to that derived from the acetate. In five adult humans, competitive uptake studies of the two forms after a single dose taken with a meal showed that the amount of α‐tocopherol from the free phenol form was equal to that from the acetate in plasma and red blood cells. These findings illustrate the value and potential of using deuterium‐substituted α‐tocopherol and GC‐MS in evaluating the effectiveness of different forms of vitamin E in human studies. The results also stress the need for caution in using data obtained from animal bioassays when considering comparative human nutritional standards.
Differential effects of dietary linoleic and α‐linolenic acid on lipid metabolism in rat tissues
Authors: Garg M. L. , Sebokova E. , Wierzbicki A. , Thomson A. B. R. , Clandinin M. T. 
Published: November 2006

AbstractComparative effects of feeding dietary linoleic (safflower oil) and α‐linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α‐linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.
Biosynthesis of membrane cholesterol during peripheral nerve development, degeneration and regeneration
Authors: Yao Jeffrey K. 
Published: November 2006

AbstractBiosynthesis of peripheral nerve cholesterol was investigated by the in vivo and in vitro incorporation of [1‐14C]‐acetate into sciatic endoneurium of normal rats during development, degeneration and regeneration. Labeled sterols were rapidly formed (<10 min) within the endoneurial portion of sciatic nerve after [1‐14C]acetate administration by intraneural injection. The majority of labeled sterols were initially found in lanosterol and desmosterol. After six hr, the14C‐labeling in both precursors was decreased to minimum, whereas cholesterol became the major labeled product of sterol. As myelination proceeded, the incorporation of [1‐14C]acetate into endoneurial cholesterol decreased rapidly and reached a minimum after six no. In mature adult nerve, an increased proportion of biosynthesis of lanosterol and desmosterol also was demonstrated. The in vitro incorporation of [1‐14C]acetate into cholesterol was inhibited during Wallerian degeneration. Instead, cholesteryl esters were labeled as the major sterol product. Such inhibition, however, was not observed in the adult Trembler nerve (Brain Res. 325, 21–27, 1985), which is presumed to be due to a primary metabolic disorder of Schwann cells. The cholesterol biosynthesis was gradually resumed in degenerated nerve by either regeneration of crush‐injured nerve or reattachment of the transected nerve. These results suggest that cholesterol biosynthesis in peripheral nerve relies on the axon to provide necessary substrates. De novo synthesis appears to be one of the major sources of endoneurial cholesterol that forms and maintains peripheral nerve myelin.
Fatty acid metabolism in renal ischemia
Authors: Ruidera E. , Irazu C. E. , Rajagopalan P. R. , Orak J. K. , Fitts C. T. , Singh I. 
Published: November 2006

AbstractThe increase in free fatty acids in the ischemic tissue is a consistent observation and these free fatty acids are considered, to play a role in the cellular toxicity. To elucidate the cause of higher levels of free fatty acids in ischemic tissue, we examined the catabolism of fatty acids. The β‐oxidation of lignoceric (24∶0), palmitic (16∶0) and octanoic (8∶0) acids and the peroxidation of fatty acids were measured at different times of renal ischemia in whole kidney homogenate. The enzymatic activities for the oxidation of fatty acids decreased with the increase in ischemia time. However, the lipid peroxide levels increased 2.5‐fold of control with ischemic injury. Sixty min of ischemia reduced the rate of oxidation of octanoic, palmitic and lignoceric acids by 57, 59 and 69%, respectively. Almost similar loss of fatty acid oxidation activity was observed in the peroxisomes and mitochondria. These data suggest that loss of mitochondrial and peroxisomal fatty acid β‐oxidation enzyme activities from ischemic injury may be one of the factors responsible for the higher levels of free fatty acids.
Effects of 2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) on de novo fatty acid and cholesterol synthesis in the rat
Authors: Lakshman M. R. , Campbell Barbara S. , Chirtel Stuart J. , Ekarohita Nisa 
Published: November 2006

AbstractThe effects of 1, 5, 10 and 20 μg/kg dosages of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) upon de novo fatty acid and cholesterol synthesis in liver and adipose tissue were determined in pair‐fed rats. The incorporation of tritium from3H2O into tissue lipids was measured. Hepatic and adipose fatty acid synthetic rates (μmoles acetyl units g−1 hr−1 in the control groups were 19.6±4 and 75.7±18.5, respectively, and the liver cholesterol synthetic rate was 2.9±0.5 TCDD (1 μg/kg) inhibited fatty acid synthesis in the liver and adipose tissue, by 44% and 41% respectively, and the liver cholesterol synthesis was inhibited by 37%. The extent of these inhibitions increased with increasing dosages of TCDD. The effect of TCDD on sterol synthesis in adipose tissue could not be determined, because the tritium incorporation into the sterol fraction in this tissue was not detectable.
Dietary manipulation of macrophage phospholipid classes: Selective increase of dihomogammalinolenic acid
Authors: Chapkin Robert S. , Somers Scott D. , Erickson Kent L. 
Published: November 2006

AbstractBecause alterations in the dietary content of fatty acids are an important method for modulating macrophage eicosanoid production, we have quantitated the levels of n−6 and n−3 polyunsaturated fatty acids in peritoneal macrophage individual phospholipids from mice fed diets (3 wk) with either safflower oil (SAF), predominantly containing 18∶2n−6, borage (BOR) containing 18∶2n−6 and 18∶3n−6, fish (MFO) containing 20∶5n−3 and 22∶6n−3, and borage/fish mixture (MIX) containing 18∶2n−6, 18∶3n−6, 20∶5n−3 and 22∶6n−3. Dietary n−3 fattya cids were readily incorporated into macrophage phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS) and phosphatidylinositol (PI). The increase in n−3 fatty acid levels was accompanied by a decrease in the absolute levels of 18∶2n−6, 20∶4n−6 and 22∶4n−6 in PC, PE and PS. Interestingly, PI 20∶4n−6 levels were not significantly lowered (P>0.05) in MIX and MFO macrophages relative to SAF and BOR. These data demonstrate the unique ability of this phospholipid to selectively maintain its 20∶4n−6 levels. In BOR and MIX animals, 20∶3n−6 levels were significantly increased (P<0.05) in all phospholipids relative to SAF and MFO. The combination of borage and fish oils (MIX diet) produced the highest 20∶3n−6/20∶4n−6 ratio in all phospholipids. These data show that the macrophage eicosanoid precursor levels of 20∶3n−6, 20∶4n−6 and n−3 acids can be selectively manipulated through the use of specific dietary regimens. This is noteworthy because an increase in phospholipid levels of 20∶3n−6 and 20∶5n−3, while concomitantly reducing 20∶4n−6, may have therapeutic potential in treating inflammatory disorders.
Lipid abnormalities in pancreatic tissue of streptozotocin‐induced diabetic rats
Authors: Levy Emile , Roy Claude C. , Lepage Guy , Bendayan Moise 
Published: November 2006

AbstractPancreatic lipid and fatty acid composition was determined in streptozotocin‐induced diabetic rats and compared to control and insulin‐treated diabetic rats. A pronounced decrease of total fatty acids was recorded and mainly accounted for by a drop of fatty acids in glycerides. Cholesterol, on the other hand, was significantly increased two‐ to three‐fold, leading to an elevated cholesterol/phospholipid ratio. Morpho‐cytochemical studies confirmed these findings because the multiple lipid droplets present in acinar cells of diabetic animals were found to be of cholesterol nature. The major alterations in phospholipid‐fatty acid composition were characterized by an increase of linoleate coupled to a decrease of monounsaturates and arachidonate, suggesting defective metabolism of saturates and of linoleate. This was further supported by fatty acid ratios that suggested low Δ5 and Δ9 desaturation. Daily administration of insulin for 10 days restored and overcorrected the various lipid alterations. This study suggests that there are alterations in lipid composition and metabolism in the exocrine pancreas of chronic streptozotocin‐induced diabetic rats. Their possible role in the mechanism regulating pancreatic function and secretion remains to be elucidated.
Formation of trimers of α‐tocopherol and its model compound, 2,2,5,7,8‐pentamethylchroman‐6‐ol, in autoxidizing methyl linoleate
Authors: Yamauchi Ryo , Kato Koji , Ueno Yoshimitsu 
Published: November 2006

AbstractThe reaction products of α‐tocopherol and its model compound, 2,2,5,7,8‐pentamethylchroman‐6‐ol, during the autoxidation of methyl linoleate at 37 C were investigated. Two isomeric trimers were obtained as the major reaction products of α‐tocopherol, and a trimer was obtained as that of its model chroman. The structure of each trimer has been characterized by IR, UV,1H and13C NMR, and mass spectroscopy. The13C NMR spectra showed the presence of a quaternary carbon atom and a carbon atom bearing two oxy substituents in the molecule. On methanolysis of each trimer, equimolar amounts of the 5‐methoxymethyl compound and the dihydroxy dimer were formed, indicating the presence of a ketal group in the molecule. From these results, new trimeric structures are proposed. The reaction products of α‐tocopherol could be well‐separated by reverse‐phase high performance liquid chromatography. When methyl linoleate was autoxidized in the presence of 1 mol% α‐tocopherol, spirodiene dimer was the initial reaction product of α‐tocopherol, and trimers were formed with the decrease of α‐tocopherol.
Phospholipid analysis of human eosinophils: High levels of alkylacylglycerophosphocholine (PAF precursor)
Authors: Ojima‐Uchiyama Ayako , Masuzawa Yasuo , Sugiura Takayuki , Waku Keizo , Saito Hiroshi , Yui Yasuo , Tomioka Hisao 
Published: November 2006

AbstractThe phospholipid composition and fatty acid profiles of human eosinophils were studied. Extremely high levels of ether phospholipids were found in this type of cell, such as alkylacylglycerophosphocholine (GPC) and alkenyl‐acylglycerophosphoethanolamine (GPE); these two ether phospholipids accounted for about three‐fourths of the choline and ethanolamine glycerophospholipids (CGP and EGP), respectively. Fatty acid analyses revealed that very large portions of arachidonic acid (20∶4) were esterified to alkylacyl‐GPC (92.0% in CGP) and alkenylacyl‐GPE (86.6% in EGP), respectively. While high amounts of alkylacyl‐GPC and the abundance of 20∶4 in this ether phospholipid have been observed in other types of blood cells of various animals, these percentages for human eosinophils are the highest among such cells. These results suggest that alkyl and alkenyl ether phospholipids play essential roles in human eosinophils in various physiological and pathological conditions.
Divinyl ethers and hydroxy fatty acids from three species ofLaminaria (brown algae)
Authors: Proteau Philip J. , Gerwick William H. 
Published: November 2006

AbstractThree species of brown algae,Laminaria sinclairii, L. saccharina andL. setchellii, have been investigated for the presence of oxylipins. From one,L. sinclairii, three new divinyl ether fatty acids have been characterized as methyl ester derivatives (methyl 12‐[1′ (Z),3′(Z)‐hexadienyloxy]‐6(Z), 9(Z), 11(E)‐dodecatrienoate, methyl 12‐[1′ (Z), 3′ (Z)‐hexadienyloxy]‐9(Z), 11(E)‐dodecatrienoate, and methyl 14‐[1′ (Z),3′ (Z)‐hexadienyloxy]‐9(Z),11(E)‐dodecadienoate, and methyl 14‐[1′ (Z),3′(Z)‐hexadienyloxy]‐5(Z),8(Z),11(Z),13(E)‐tetradecatetraenoate) by a variety of spectroscopic methods. In addition, one new [13(S)‐hydroxy‐6(Z),9(Z),11(E),15(Z)‐octadecatetraenoic acid] and four known monohydroxy polyunsaturated fatty acids have been isolated from all three species as their methyl ester derivatives. The occurrence of these compounds in brown algae strongly suggests that these organisms possess an active lipoxygenase(s) with ω6 specificity.
Separation of bile acid methyl esters by high‐performance liquid chromatography
Authors: Kuhajda K. , Kandrac J. , Dobanović‐Slavica S. , Hranisavljević J. , Miljković D. 
Published: November 2006

AbstractConjugated bile acids, namely glyco‐ and tauro‐3α,6α‐dihydroxy‐5β‐cholanoic acid (hyodeoxycholic acid), 3α,7α‐dihydroxy‐5β‐cholanoic acid (chenodeoxycholic acid), 3α,6α,7α‐trihydroxy‐5β‐cholanoic acid (hyocholic acid) and 3α‐hydroxy‐6‐oxo‐5β‐cholanoic acid (6‐keto‐litocholic acid) were isolated from pig bile, and subsequently transformed into the corresponding methyl esters. Separation of the methyl esters of the isolated bile acids by high‐performance liquid chromatography (HPLC) was accomplished on a ZORBAX‐CN column (Dupont, Boston, MA) withn‐hexane/2‐propanol/methylene chloride (89∶6∶5, by vol) as the mobile phase containing traces (≈1%) of amyl alcohol and water as moderators. HPLC analysis of the methyl esters also showed the presence of methyl 3α‐hydroxy‐6‐oxo‐5α‐cholanoate, which was probably produced in the course of alkaline hydrolysis of the conjugated bile acids.
In vitro oxidation of vitamins C and E, cholesterol, and thiols in rat brain synaptosomes
Authors: Vatassery G. T. 
Published: November 2006

AbstractFree radical‐induced oxidation of vitamins C, E, sulfhydryl compounds, and cholesterol in brain synaptosomes from Fisher 344 rats was studied. The synaptosomes were incubated at 37°C with 2,2′‐abobis‐(2‐amidinopropane) dihydrochloride (AAPH), which undergoes thermal decomposition to yield free radicals. After incubation, the synaptosomes were sedimented, saponified, and extracted with hexane to isolate tocopherol and cholesterol. Ascorbate and tocopherol were assayed by liquid chromatography, cholesterol by gas chromatography, and total sulfhydryls by spectrophotometry. Under thein vitro conditions used in this study, the approximate order for the ease of oxidation of the various compounds was: ascorbate ≫tocopherol>sulfhydryl compounds⋙cholesterol. However, tocopherol and sulfhydryl oxidation occurred even before all of the ascorbate had been consumed. Therefore, the fate of a specific antioxidant at a particular cellular location cannot be predicted with complete accuracy using thein vitro order for ease of oxidation shown here. Ascorbate may play a major role in protecting brain against oxidative damage because: (i) ascorbate concentration is high in brain, (ii) it can regenerate vitamin E from its radical oxidation product, and (iii) it is one of the first antioxidants to be consumed during oxidative reactions.
Sesame seed and its lignans produce marked enhancement of vitamin E activity in rats fed a low α‐tocopherol diet
Authors: Yamashita Kanae , Iizuka Yoshie , Imai Tomoko , Namiki Mitsuo 
Published: November 2006

AbstractThree series of experiments demonstrated that sesame seed and its lignans cause significant elevation of α‐tocopherol content in rats. In Experiment 1, 20% sesame seed (with a negligible amount of α‐tocopherol) supplementing 10 (low), 50 (normal), or 250 (high) mg/kg α‐tocopherol diets (protein and fat concentrations in diets were adjusted to 200 and 110 g/kg, respectively) all caused a significant increase of α‐tocopherol in the blood and tissue of rats. In Experiment 2, groups of rats were fed five different diets: a vitamin E‐free control diet, a low α‐tocopherol diet, and three low α‐tocopherol diets supplemented with 5, 10, and 15% sesame seed. Changes in lipid peroxides in liver, red blood cell hemolysis, and pyruvate kinase activity, as indices of vitamin E deficiency, were examined. These indices were high in the low α‐tocopherol diet, whereas supplementation with even 5% sesame seed suppressed these indices completely and caused a significant increase of α‐tocopherol content in the plasma and liver. In Experiment 3 two diets containing sesame lignan (sesaminol or sesamin) and low α‐tocopherol were tested. Results in both of the sesame lignan‐fed groups were comparable to those observed in the sesame seed‐fed groups as shown in Experiment 2. These experiments indicate that sesame seed lignans enhance vitamin E activity in rats fed a low α‐tocopherol diet and cause a marked increase in α‐tocopherol concentration in the blood and tissue of rats fed an α‐tocopherol‐containing diet with sesame seed or its lignans.
Suppression by carotenoids of microtenoids of microcystin‐induced morphological changes in mouse hepatocytes
Authors: Matsushima‐Nishiwaki Rie , Shidoji Yoshihiro , Nishiwaki Shinji , Yamada Tetsuya , Moriwaki Hisataka , Muto Yasutoshi 
Published: November 2006

AbstractMicrocystin‐LR is a liver tumor promoter in the okadaic acid class, a group of potent inhibitors of protein phosphatases 1 and 2A. Because of inhibition of protein phosphatases, microcystin‐LR induces hyperphosphorylation of cellular proteins, including cytoskeletal proteins—cytokeratins 8 and 18—and causes morphological changes in mouse hepatocytes in primary culture. We studied the effects of carotenoids to antagonize microcystin‐LR‐induced morphological changes in hepatocytes. β‐Carotene (100 nM to 100 μM), suppressed the morphological changes induced by 100 nM microcystin‐LR in a dose‐dependent manner. Other carotenoids tested exerted similar suppressive effects, although retinoids, such as all‐trans retinol, all‐trans retinoic acid, and 9‐cis retinoic acid, were only weakly suppressive. The relative potency of the suppression correlated significantly with the number of conjugated double bonds in thetrans configuration. β‐Carotene strongly suppressed the hyperphosphorylation of cellular proteins induced by microcystin‐LR without significant changes in the basal phosphorylation level. Other antioxidants, such as α‐tocopherol, did not protect the cells against microcystin‐LR. Taken together, the antagonistic effects of carotenoids against microcystin‐LR are difficult to explain by their antioxidant or provitamin A activities. Suppression of the hyperphosphorylation of cellular proteins may be a novel mechanism by which carotenoids inhibit tumor promotion.
Urinary Malondialdehyde‐Equivalents during ingestion of meat cooked at high or low temperatures
Authors: Brown Ellen D. , Morris Virginia C. , Rhodes Donna G. , Sinha Rashmi , Levander Orville A. 
Published: November 2006

AbstractExcretion of malondialdehyde (MDA)‐generating substances in the urine has been suggested as an indicator ofin vivo lipid peroxidation. However, MDA in the urine also reflects the amount of lipid peroxidation products consumed in the diet. We determined MDA as the thiobarbituric acid (TBA)‐MDA complex in urine of 19 healthy adults (10 male and 9 female) fed large quantities (3.6–4.1 g/kg body weight) of ground beef cooked at a low or a high temperature. Subjects are a controlled diet with no alcohol or nutritional supplements. For 7 d they consumed ground beef cooked at 100°C for 20 min (low‐temperature meat) followed by 7 d with meat fried at 250°C for 22 min (high‐temperature meat). Prior to the study, subjects consumed their normal free choice diet with moderate amounts of meat. The concentration of MDA in urine at baseline was 2.1±0.3 μmol TBA‐MDA equivalents/day (mean±SEM). After 7 d of low‐temperature meat, urinary TBA‐MDA equivalents increased to 23.1±1.4 μmol/d. Urinary TBA‐MDA equivalents were consistently lower (6.9–8.0 μmol/d) 1, 2, 3, and 7 d after subjects changed to high‐temperature meat. After 7 d of treatment, 97% of the MDA‐equivalents in the meat was recovered in 24‐h urine samples. The low temperature meat had 3–4 times more MDA than did the high‐temperature meat. These data indicate that the amount of meat eaten and the cooking procedures used can dramatically alter urinary MDA. Dietary sources of MDA must be controlled if urinary MDA is to be used as an indicator of oxidative stress.
Diabetes and proteolysis: Effects on carnitine palmitoyltransferase‐I and malonyl‐CoA binding
Authors: Kashfi Khosrow , Cagen Lauren , Cook George A. 
Published: November 2006

AbstractMalonyl‐CoA binding and malonyl‐CoA inhibition of carnitine palmitoyltransferase‐1 (CPT‐I) were measured in hepatic mitochondria from normal and diabetic rats and in protease‐treated mitochondria from fed rats to test the hypothesis that proteolysis represents a mechanism by which diabetes produces changes in the sensitivity of CPT‐I to inhibition by malonyl‐CoA. As in diabetes, protease treatment increased the apparent Ki values for malonyl‐CoA. Palmitoyl‐CoA greatly diminished malonyl‐CoA specific binding in the mitochondrial system being studied, suggesting strong competition at the malonyl‐CoA binding site. Proteolysis decreased capacity for specific binding of malonyl‐CoA by 60–80%, but it had no effect on binding affinity. In contrast, the decreased specific binding of malonyl‐CoA seen in the diabetic state is accompanied by increased binding affinity. Furthermore, observed Kd values differed from Ki values by a factor of 10 or more, suggesting that measured Kd and Ki may represent different ligand‐protein complexes. These data suggest that alterations in inhibition of CPT‐I by malonyl‐CoA occurring in the diabetic state may involve mechanisms other than simple proteolytic removal of malonyl‐CoA binding sites.