Biomedical subjects

M M Mahfouz

Publications and source records attributed to M M Mahfouz.

At least 19 recordsLinked to original sources

PubMed2005

Atorvastatin reduces the plasma lipids and oxidative stress but did not reverse the inhibition of prostacyclin generation by aortas in streptozotocin diabetic rats.

The effect of atorvastatin (Lipitor) on diabetes-induced changes in plasma lipids, oxidative stress and the ability of aortic tissues to generate prostacyclin was studied in streptozotocin diabetic rats. In diabetic rats, plasma total cholesterol, triglycerides and serum glucose significantly increased compared to nondiabetic rats. Atorvastatin administration to diabetic rats did not affect hyperglycemia but significantly reduced plasma total cholesterol and triglycerides compared to diabetic rats. The oxidative stress markers urinary isoprostane, liver thiobarbituric acid reactive substances (TBARS) and plasma protein carbonyl content significantly increased in diabetic rats compared to nondiabetic rats. Atorvastatin admnistration to diabetic rats significantly reduced oxidative stress levels compared to diabetic rats, but urinary isoprostane and liver TBARS remained significantly higher than nondiabetic rats. Prostacyclin (PGI(2)) generation by aortic tissues significantly decreased in diabetic rats compared to nondiabetic rats. Atorvastatin administration to diabetic rats did not reverse that inhibition. These results were discussed in the light of the possible effects of hyperglycemia and statins on NAD(P)H-oxidase and cyclooxygenase-2 activities and the genetic difference between rats and other mammals regarding the level of vascular superoxide dismutase (SOD) activity.

Animals↗

PubMed2004

Vitamin C or Vitamin B6 supplementation prevent the oxidative stress and decrease of prostacyclin generation in homocysteinemic rats.

We hypothesize that homocysteinemia causes oxidative stress, decreases the aortic ability to generate prostacyclin and that antioxidants have a protective role. Four groups of eight rats each were fed for 8 weeks the control diet (group A), control diet with folic acid omitted and excess methionine (Me) added to drinking water (group B), diet B + 500 mg/kg of Vitamin C (group C) or diet B + 60 mg/kg Vitamin B6 (group D). The three groups of rats fed folic acid deficient (FD) diets (groups B, C and D) were homocysteinemic as indicated by the significant increase in their serum homocysteine (HC) concentration. Rats fed diet B had oxidative stress as indicated by an increase in serum thiobarbituric acid reactive substances (TBARS) and advanced oxidation protein products (AOPP) and urinary isoprostanes and had a decreased ability of their aortas to generate prostacyclin. Homocysteinemic rats fed a FD diet + Vitamin C (group C) or Vitamin B6 (group D) also had high levels of serum homocysteine but the oxidative stress markers and the ability of their aortas to generate prostacyclin returned to normal. This indicates that the homocysteinemic effect is through an oxidative mechanism and that Vitamin C as a free radical scavenger prevents these effects. Serum Vitamin C and liver glutathione concentrations significantly increased in rats fed excess Vitamin B6 compared to the control or FD rats. This may explain why Vitamin B6 has an antioxidative effect.

Animals↗

PubMed2000

Oxidized low-density lipoprotein (LDL) enhances thromboxane A(2) synthesis by platelets, but lysolecithin as a product of LDL oxidation has an inhibitory effect.

Oxidation of low-density lipoprotein (LDL) by copper sulfate led to a significant increase in lysophosphatidylcholine (lyso PC) at the expense of phosphatidylcholine. Incubation of different concentrations of oxidized LDL (oxLDL) (32-650 microg protein/ml) with platelets for 1 h at 37 degrees C increased lyso PC content. The increase was dependent on oxLDL concentration. Incubation of platelets with various concentrations of lyso PC in solution for 5 or 15 min showed that lyso PC percentage was increased in the platelet membrane and the increase was dose dependent. Platelets incubated with various concentrations of lyso PC (2-100 microM) for 5 or 15 min and then triggered with thrombin also showed a significant decrease of thromboxane A(2) (TXA(2)) release as lyso PC concentration reached 10 microM or 6 microM, respectively. The decrease of TXA(2) release was more significant as lyso PC concentration was increased. The present study showed that this inhibition of TXA(2) release by lyso PC was due to 1) inhibition of phospholipase A(2) and the decrease of free arachidonic acid liberation from platelet phospholipid and 2) inhibition of cyclooxygenase. These inhibitory effects of lyso PC were discussed in relation to its effect on membrane fluidity. Lyso PC at concentrations of 30, 50, and 100 microM caused a sudden drop in TXA(2) release and a sudden increase of lactic dehydrogenase loss from the platelets due to their lysis and inhibition of cyclooxygenase enzyme. The present study shows that oxLDL contains high levels of lyso PC that are transferable to the platelets and can weaken their responsiveness to thrombin and decrease TXA(2) release. In our previous study, we found that oxLDL also contained high levels of oxysterols and thiobarbituric acid reactive substances (TBARS), which enhanced platelet reactivity to thrombin and increased TXA(2) release. We conclude that the net effect of oxLDL on platelets will depend on its degree of oxidation and the ratio between oxysterols plus TBARS/lyso PC. Variations in this ratio may explain some of the contradictions cited in the literature concerning the effect of oxLDL on platelet activation.

Arachidonic Acid↗

PubMed2000

Cholesterol-rich diets have different effects on lipid peroxidation, cholesterol oxides, and antioxidant enzymes in rats and rabbits.

The objective of this study was to compare the effect of cholesterol feeding of rats and rabbits. The levels of lipid peroxidation products and oxysterols in the plasma of the two species plus the antioxidant enzyme activities in the liver and erythrocytes were measured to explain their different susceptibilities to atherosclerosis. Our study showed that rats are less susceptible than are rabbits to the atherogenic effect of a cholesterol-rich diet because of differences in lipid peroxidation products as well as antioxidant enzymes activities in their livers. In rabbits, cholesterol feeding produced severe hypercholesterolemia (43-fold increase) and increased plasma and liver lipid peroxidation. Total as well as the individual oxysterol contents of 7alpha-, 7beta-hydroxycholesterol, alpha-epoxy, beta-epoxycholesterol, cholestanetriol, 7-keto, and 27-hydroxycholesterol significantly increased in the plasma of hypercholesterolemic (HC) rabbits. Erythrocyte glutathione peroxidase (GSH-Px) activity significantly decreased whereas catalase activity significantly increased in HC rabbits. In rats cholesterol feeding increased the plasma cholesterol only twofold and had no effect on plasma or liver lipid peroxidation. Only 7alpha- and 7beta-hydroxycholesterol increased and no change was observed in any of the antioxidant enzymes activity in the erythrocytes. Although cholesterol feeding caused a 10-fold increase of liver cholesterol as ester in both rats and rabbits, the antioxidant enzyme GSH-Px and catalase activities in the liver significantly increased in rats but significantly decreased in rabbits. The increase of GSH-Px and catalase activities in the liver of cholesterol fed rats could have a protective role against oxidation, thus preventing the formation of lipid peroxidation and oxysterols.

Journal Article↗

PubMed1999

Effect of trans fatty acids on calcium influx into human arterial endothelial cells.

BACKGROUND: A recent task force of The American Society for Clinical Nutrition and American Society for Nutritional Sciences recommended in a position paper on trans fatty acids that models be developed to assess the effects of changes in fat intake on disease risk. OBJECTIVE: The objective was to investigate, using human arterial endothelial cells as a model, the influence of trans fatty acids and magnesium on cell membrane composition and on calcium influx into arterial cells, a hallmark of atherosclerosis. DESIGN: Endothelial cells were cultured for 3 d in media with high (adequate) or low (inadequate) amounts of magnesium plus various concentrations of trans,trans linoelaidic; cis,cis linoleic; trans elaidic; oleic; or stearic acids. The cells were then harvested and the fatty acid composition and the amount of (45)Ca(2+) incorporated into the cell was determined. RESULTS: The percentage of fatty acids incorporated into the endothelial cells was proportional to the amount added to the culture medium. Adequate magnesium was crucial in preventing calcium influx into endothelial cells. Without an adequate amount of magnesium in the culture medium, linoelaidic and elaidic acids, even at low concentrations, increased the incorporation of (45)Ca(2+) into the cells, whereas stearic acid and oleic acid did not (P < 0.05). CONCLUSION: Our model indicated that a diet inadequate in magnesium combined with trans fat may increase the risk of calcification of endothelial cells.

Calcium↗

PubMed1999

Hydrogenated fat high in trans monoenes with an adequate level of linoleic acid has no effect on prostaglandin synthesis in rats.

Our study was designed to determine whether hydrogenated fat high in trans monoenes concentration affected prostaglandin synthesis. Corn oil (CO), butter (B), hydrogenated vegetable oil (HF) and coating fat (CF) were used in this study. These fats were fed to rats for 10 wk at 10 g/100 g diet. The phospholipid (PL) fatty acid content of platelets, aorta and heart was determined by gas liquid chromatography, and the in vitro aorta production of prostacyclin (PGI2) from exogenous or endogenous arachidonic acid (AA) was measured using the radioimmuno-assay (RIA) method. Serum thromboxane B2 (TXB2) released by platelets as thromboxane A2 (TXA2) during incubation of whole blood was also measured by this method. In the group fed CF, AA was significantly lower in the PL of aorta, platelet and heart, and the ratio 20:3(n-9)/20:4(n-6) was greater than in the groups fed CO, B or HF, indicating that the group fed CF was essential fatty acid (EFA) deficient. Although AA was significantly lower in the aorta and platelet PL of the group fed HF compared to the group fed CO, that difference did not affect the amounts of PGI2 or TXB2 produced in these groups. The group fed CF had significantly less PGI2 and TXB2 released by aorta and platelets than the other groups. This was the result of the reduced level of AA and the presence of higher amounts of 20:3(n-9) acid in the PL, which might act as a competitive inhibitor for cyclooxygenase. The aortic production of PGI2 from exogenous AA did not differ among the groups indicating that prostaglandin synthetase was not affected by the dietary fat. We conclude that the consumption of hydrogenated fats high in trans 18:1 acids with adequate amount of linoleic acid had no effect on the amount of thromboxane or prostacyclin produced by platelet or aorta in vitro.

Animals↗

PubMed1998

Oxysterols and TBARS are among the LDL oxidation products which enhance thromboxane A2 synthesis by platelets.

In this study, we compared the effects of normal LDL (nLDL) and oxidized LDL (oxLDL) on thromboxane (TXA2) release by platelets triggered by low concentration of thrombin, and we determined which component of oxLDL is responsible for that activation. After oxidation of LDL with copper sulfate, the small molecular weight fraction (< 10 kDa) which was high in TBARS was removed; using Amicon Centriprep-10 concentrator membrane. More than 67% of TBARS in the oxLDL preparation was found in solution while the remaining was covalently attached to the oxLDL particles. OxLDL contained significantly higher levels of oxysterols and TBARS than the nLDL. Platelets preincubated with low concentrations of oxLDL (33-132 micrograms protein/mL) produced significantly higher TXA2 than platelets preincubated with equivalent concentrations of nLDL when triggered with thrombin. Platelets treated with oxLDL also contained significantly higher levels of oxysterols than platelets treated with nLDL. Platelets preincubated with pure cholestanetriol (10 micrograms/mL) contained a high level of cholestanetriol in the membrane, and TXA2 release was significantly increased in these platelets compared to the control platelets. The TBARS in solution also was very potent in enhancing TXA2 release by thrombin-treated platelets. These results indicate that oxysterols and the free TBARS either in solution or covalently attached to the oxLDL particles are partly responsible for the stimulatory effect of oxLDL on TXA2 release by platelets. The present study also showed that this enhancement of TXA2 release was due to activation of phospholipase A2 and to the increase of arachidonic acid liberation from the platelet phospholipids.

Alkenes↗

PubMed1997

Effect of cholesterol-rich diets with and without added vitamins E and C on the severity of atherosclerosis in rabbits.

Oxysterols as oxidation products of cholesterol are considered an atherogenic factor in the development of atherosclerosis in the arteries of cholesterol-fed rabbits. We compared the atherogenic effects of diets enriched either with 0.5% oxidized cholesterol (OC; characterized by high amounts of oxysterols) or with pure cholesterol (PC). The effects of antioxidant vitamins E and C added to the PC diet were also evaluated in view of their antioxidative properties for lipoproteins and cholesterol and how this could affect the severity of atherosclerosis. Four groups of rabbits were fed the following for 11 wk: 1) a nonpurified stock diet, 2) this stock diet plus 0.5% OC, 3) the stock diet plus 0.5% PC, and 4) the stock diet plus 0.5% PC and 1000 mg vitamin E and 500 mg vitamin C/kg diet (PC + antioxidants). The OC and PC diets were equally hyperlipidemic and hypercholesterolemic. The severity of atherosclerotic lesions was highest with the OC diet and lowest with the PC + antioxidants diet. The plasma oxysterol concentration was proportional to the severity of atherosclerosis in all three groups of cholesterol-fed rabbits. beta-Very-low-density-lipoprotein modification was minimized by vitamins E and C as indicated by its polyacrylamide gel electrophoretic pattern and its increased binding to the rabbit liver membrane in vitro. This study indicated that OC and PC were equally atherogenic but that the addition of antioxidants to the PC diet significantly reduced its severity, even when hypercholesterolemia persisted. This indicated that atherogenesis can result from an excessive accumulation of oxidation products of cholesterol in the plasma.

Animals↗

PubMed1996

Cholestane-3 beta, 5 alpha, 6 beta-triol stimulates phospholipid synthesis and CTP-phosphocholine cytidyltransferase in cultured LLC-PK cells.

The present study was conducted to examine the effect, if any, of triol on the rate of total or individual phospholipid synthesis by LLC-PK cells in culture. LLC-PK cells were incubated in medium with or without 10 micrograms/ml of 5 alpha-cholestane-3 beta, 5 alpha,6 beta-triol (triol) for 24 h. Triol-treated and control cells were then incubated with medium containing either [14C]glycerol or [32P]phosphate for 1, 6 or 12 hr. In triol-treated cells, the amount of labeled glycerol and [32P]phosphate incorporated into glycerophospholipids and phospholipids (PL), respectively, were higher in triol-treated cells than in control cells, indicating a higher rate of PL synthesis in triol-treated cells. The results also showed that the increase in PL synthesis was higher in magnitude for some PL than others, thus disturbing the ratios among the PL fractions in the cell membrane. CTP-phosphocholine cytidyltransferase activity was greatly enhanced in the cytosolic as well as the particulate fractions of the triol-treated cells, which explains the increase of PC synthesis under triol effect. The rate of [3H]acetate incorporation into the total and free fatty acid fractions was significantly increased in triol-treated cells. The activation of the cytidyl transferase enzyme was related to the enhanced de novo synthesis and cellular uptake of fatty acids in triol-treated cells, which make fatty acids more available in these cells and can upregulate the enzyme. The increased synthesis of phospholipids in the triol cells and the increased level of phospholipid in these cells (as micrograms lipid phosphorus/mg cell protein) observed in our previous study indicate changes in the phospholipid head group composition of the triol cells. These changes can affect several membrane properties and membrane bound enzymes.

Acetates↗

PubMed1995

Cigarette smoke increases cholesterol oxidation and lipid peroxidation of human low-density lipoprotein and decreases its binding to the hepatic receptor in vitro.

Low-density lipoprotein (LDL) was exposed to six puffs of cigarette smoke (CS) filtered through a glass wool filter and then incubated for 6 or 20 h at 37 degrees C. Control LDL was similarly treated but exposed to air. In cigarette smoke-treated LDL (CS-LDL), compositional changes of the lipid fraction were most detectable after 20 h incubation. These changes included a decrease of polyunsaturated fatty acids (PUFA), slight degradation of phosphatidylethanolamine (PE) and phosphatidylcholine (PC) to their lysophospholipid lysoPE and lyso-PC, elevation of oxidized cholesterol content as well as thiobarbituric acid reacting substance (TBARS), indicating an oxidative effect of CS on LDL. CS-LDL also showed higher anodic electrophoretic mobility and crosslinking of its apoprotein by nondisulfide bonds. The binding affinity of CS-LDL to liver membrane receptor was much lower than control LDL as measured by the calcium-dependent binding of LDL-gold conjugate to the solubilized membrane protein dot blotted onto nitrocellulose strips. Our results indicate that CS induces changes in LDL, making it more atherogenic and cytotoxic.

Apolipoproteins B↗

PubMed1994

Cholesterol oxides in plasma and lipoproteins of magnesium-deficient rabbits and effects of their lipoproteins on endothelial barrier function.

The cholesterol oxide (ChO) levels in the plasma and low density lipoproteins (LDL and VLDL) in four groups of rabbits fed for seven weeks either normal (NC) or high cholesterol (HC) with low or normal magnesium (Mg) diets were determined and compared with the NC group fed a standard rabbit diet. The plasma from the NC group contained low levels of different cholesterol oxides. These cholesterol oxides were significantly elevated in the plasma of rabbits fed a HC-normal magnesium or a HC-low magnesium diet. In the NC-low Mg group, 7 alpha-hydroxycholesterol, 7 beta-hydroxycholesterol and 7-ketocholesterol were elevated while the other cholesterol oxides remained within the normal range of the NC group. When the cholesterol oxides were assayed in the LDL and VLDL fractions as micrograms/mg protein, the fractions obtained from the groups fed NC-low Mg, HC-normal Mg or HC-low Mg diets showed higher levels of cholesterol oxides than the fractions obtained from the NC group. When LDL and VLDL fractions from the different groups were incubated at equal protein concentration with confluent endothelial cell monolayers, transendothelial albumin transfer was significantly increased by the lipoproteins from the experimental groups as compared to the control group. These results suggest that elevation of cholesterol oxides in magnesium deficiency or hypercholesterolaemia may be related to their atherogenic effects through decreasing the endothelial barrier function which could enhance the deposition of cholesterol rich lipoproteins into the arterial wall.

Animal Feed↗

PubMed1994

Effect of dietary magnesium deficiency with/without cholesterol supplementation on phospholipid content in liver, plasma and erythrocytes of rabbits.

The effect of magnesium deficiency with/without supplementary cholesterol on phospholipid content in liver, plasma and erythrocytes was investigated in New Zealand White male rabbits. After the rabbits had been fed a low magnesium and/or high cholesterol diet for seven weeks, the phospholipid content in liver, plasma and erythrocytes was measured. Dietary magnesium deficiency produced a marked elevation of total phospholipid and certain individual phospholipids in the rabbit liver. The elevation was accentuated by cholesterol supplementation. In the plasma, a low magnesium intake enhanced plasma phosphatidylcholine, phosphatidic acid, phosphatidylinositol, and sphingomyelin, but an activated conversion from phosphatidylethanolamine to phosphatidylcholine made the increase in phospholipid insignificant. On the other hand, a low magnesium intake restricted the increase in magnitude of phospholipid caused by cholesterol supplementation. In the erythrocytes, total phospholipid, phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine were decreased by a low magnesium and/or a high cholesterol intake. We suggest that the increased contents of total phospholipid and/or certain individual phospholipids in the livers and plasma resulted from the enhanced synthesis of phospholipid in the liver by low magnesium intake. A decreased utilization of food by low magnesium diet limited the magnitude of plasma phospholipid increase produced by cholesterol supplementation.

Animals↗

PubMed1992

Decreased uptake of low density lipoprotein by LLC-PK cells cultured at low magnesium concentration.

LLC-PK cells grown in tissue culture on medium containing normal or deficient amounts of magnesium were presented with 125I-low density lipoprotein (LDL) and the uptake determined. Total LDL uptake by Mg-deficient cells decreased as the magnesium concentration decreased. The receptor binding of LDL and the internalization of LDL by the Mg-deficient cells were reduced. Degradation of LDL by Mg-deficient cells, when corrected for the reduced uptake, was less affected.

Animals↗

PubMed1991

Dietary fat and plasma lipid physical properties in swine.

Changes in the lipid composition of swine lipoprotein were induced by feeding highly saturated or highly unsaturated diets. The diet higher in oleic acid, even when this was a highly unsaturated diet, resulted in a lower order parameter (more fluid) than in the other diets, as has been observed by others. This difference could be detected in whole unfractionated lipoprotein and in isolated high-density lipoprotein. Changes in order parameter with changes in cholesterol/triglyceride, reported by others, were not observed, possibly because of the weighted average effect of measuring whole plasma lipoprotein.

Animals↗

PubMed1989

Changes of linoleic acid metabolism and cellular phospholipid fatty acid composition in LLC-PK cells cultured at low magnesium concentrations.

LLC-PK cells grown on media containing normal (480 microM) or reduced magnesium levels (25, 6.3 or 2.5 microM) were used to study the effect of magnesium deficiency on linoleic acid metabolism and cellular membrane fatty acids. The fatty acid composition of the cellular phospholipids showed a significant decrease in 20:4(n-6) and 22:4(n-6) acids and a significant increase in 18:2(n-6), 18:3(n-6) and 20:3(n-6) fatty acids in magnesium-deficient cells compared to magnesium-sufficient cells. When [1-14C]linoleic acid was incubated with control (480 microM Mg2+) or magnesium deficient cells (2.6 microM Mg2+) the rate of tetraenoic acid synthesis (20:4(n-6) + 22:4(n-6) was significantly reduced in magnesium-deficient cells, indicating that the metabolic conversion of 18:2(n-6) to 20:4(n-6) is impaired in magnesium deficiency. This reduction in conversion may be due to the impairment of either the delta(5)- or the delta(6)-desaturase, or both. This study shows that magnesium deficiency perturbs essential fatty acid (EFA) metabolism and decreases the cellular membrane polyunsaturated fatty acid (PUFA) content. These alterations are likely to have adverse effects on cellular membrane properties and functions.

Animals↗

PubMed1989

Changes in phospholipid composition and calcium flux in LLC-PK cells cultured at low magnesium concentrations.

Monolayers of porcine kidney cells (LLC-PK) were grown in a series of Nu-Serum-supplemented media containing different Mg(2+) concentrations (480, 250, 25, 6.3 or 2.6 microM) to study the effect of Mg(2+) depletion on cellular phospholipid changes and the consequent effect on the membrane permeability to Ca(2+). Cells grown on 6.3 or 2.6 microM Mg(2+) showed a decrease in PE, PS, Sph, PI and an increase of PC. These changes were attributed mainly to the decreased rate of Sph synthesis through the transfer of phosphocholine from PC to ceramide, or due to the increase of PE N-methylation as found in Mg(2+)-deficient cells. The (45)Ca uptake was increased in cells grown on 25.0 microM Mg(2+), while it was decreased in cells grown on 6.3 or 2.6 microM Mg(2+). These changes in Ca(2+) uptake were related to changes of cellular phospholipids and fatty acids which affect adenylate cyclase activity in the membrane, as well as the membrane fluidity.

Animals↗

PubMed1989

Effect of magnesium deficiency on delta 6 desaturase activity and fatty acid composition of rat liver microsomes.

Experimental Mg2+ deficiency was induced in a group of rats by feeding them a Mg2+-deficient diet for 23 days. They were pair-fed to compare with a control group of rats fed a Mg2+-sufficient diet. In the Mg2+-deficient group the plasma total cholesterol and triglyceride levels were increased while HDL-cholesterol was decreased. In the Mg2+-deficient group the plasma level of thiobarbituric acid reacting substances (TBARS) used as a measure for lipid peroxidation was increased. The increase was attributed to the increased cytosolic Ca2+ in Mg2+-deficiency which can cause: 1) increase of hydro and endoperoxide levels as a consequence of the increase of arachidonic acid release and eicosanoid synthesis in Mg2+-deficiency, and 2) inhibition of the mitochondrial respiratory activity and activation of Ca2+-dependent proteases which may activate the conversion of xanthine dehydrogenase to xanthine oxidase which generates active O2 species. In the Mg2+-deficient group, the fatty acid composition of the liver microsomes indicated a slower rate of conversion of linoleic acid to arachidonic acid which was consistent with the decrease of delta 6 desaturase activity in liver microsomes of Mg2+-deficient rats as measured in vitro. The decrease of delta 6 desaturase activity was attributed to the lower concentration of actual enzyme molecules as a result of the decreased rate of protein synthesis in Mg2+-deficiency. The possible effects of the increased catecholamine release in Mg2+-deficiency are discussed.

Adenosine Triphosphate↗

PubMed1984

Effect of dietary fats on desaturase activities and the biosynthesis of fatty acids in rat-liver microsomes.

Four groups of rats were fed diets containing 15% (w/w) high-oleic safflower oil (SFO, rich in cis-18:1 acids), a mixture of 80% partially hydrogenated soybean oil plus 20% corn oil (H + CO, rich in trans-18:1 acids), lard (L, rich in saturated fatty acids) and corn oil (Co, rich in 18:2 omega 6). Fatty acid composition of liver microsomes and activities of the delta 5, delta 6 and delta 9 desaturases were determined. Microsomal delta 6 desaturase activity and arachidonic acid were lower in the H + CO group compared with SFO of L. No difference was found in the delta 5 or delta 6 desaturase activity of CO and SFO groups. Thus, the oleic-acid level of the SFO diet had no effect on the metabolism of 18:2 omega 6. Fluorescent polarization studies, using trans-parinaric acid as a probe, showed no differences between the physical states of phospholipid vesicles made from lipids isolated from each group. We concluded that the trans-18:1 acids in partially hydrogenated soybean oil have a more inhibitory effect than saturated acids on EFA metabolism, even in the presence of adequate amounts of essential fatty acid.

Animals↗