Influence of dietary lipids on the effect of chlorpromazine on membrane properties of rabbit red cells

The effect of diets containing different types of common natural oils on physical properties of red cells was investigated by using rabbits. The rabbits were fed for 18 months on a standard diet in which 8% of its energy content was provided by safflower oil and 32% energy by either more safflower oil or fish oil, linseed oil, olive oil or palm oil. Erythrocyte deformability was significantly decreased by the fish oil diet compared with each of the other diets. Osmotic fragility was significantly less (66 mM) for red cells from rabbits fed on the linseed oil diet, and significantly greater (71 mM) for red cells from rabbits on the fish oil diet, than for red cells from rabbits on the other three diets which did not differ significantly from each other (68 mM). With rabbits on the standard diet, the resistance of their erythrocytes to osmotic haemolysis was increased by chlorpromazine at concentrations below and decreased by concentrations above 30 microM. The dietary oils caused significant changes in the effects of chlorpromazine on osmotic fragility. The concentration at which the effect of chlorpromazine reversed from antihaemolytic to prohaemolytic was decreased by the safflower and linseed oil diets and increased by the fish oil diet, compared with the olive and palm oil diets. Analysis of the fatty acid compositions of the dietary oils on the one hand and of the red cell phospholipids on the other established, specifically, that in the presence of 30 microM chlorpromazine the percentage haemolysis was directly proportional to the linoleate content of the red cell phospholipids.     

Effects of Proteus mirabilis lipopolysaccharides with different O-polysaccharide structures on the plasma membrane of human erythrocytes

The effects of O33 and O49 P. mirabilis lipopolysaccharides (LPSs) on human erythrocyte membrane properties were examined. Physical parameters of the plasma membrane, such as membrane lipid fluidity, physical state of membrane proteins, and osmotic fragility, were determined. The fluidity of the lipids was estimated using three spin-labeled stearic acids of doxyl derivatives: 5-doxylstearic acid, 12-doxylstearic acid, and 16-doxylstearic acid. All the applied labels locate to different depths of the lipid layer and provide information on the ordering of phospholipid fatty acyl chain mobility. LPSs O49 increased the membrane lipid fluidity in the polar region of the lipid bilayer as indicated by spin-labeled 5-doxylstearic acid. An increase in fluidity was also observed in the deeper region using 12-doxylstearic acid only for O33 LPSs. The highest concentration of O33 LPSs (1 mg/ml) increased the motion of membrane proteins detected by the spin-label residue of iodoacetamide. These results showed different actions of O33 and O49 LPSs on the plasma membrane due to the different chemical structures of O-polysaccharides. P. mirabilis O33 and O49 LPSs did not induce changes in the membrane cytoskeleton, osmotic fragility and lipid peroxidation of erythrocytes. On the other hand a rise in the content of carbonyl compounds was observed for the highest concentrations of O33 LPS. This result indicated protein oxidation in the erythrocyte membrane. Lipid A, the hydrophobic part of LPS, did not change the membrane lipid fluidity and osmotic fragility of erythrocytes. Smooth and rough forms of P. mirabilis LPSs were tested for their abilities for complement-mediated immunohemolysis of erythrocytes. Only one out of seven LPSs used was a potent agent of complement-mediated hemolysis. It was rough, Ra-type of P. mirabilis R110 LPS. The O-polysaccharide-dependent scheme of reaction is presented.     

Physical and chemical changes in isolated chylomicrons: prevention by EDTA

When washed chylomicrons obtained from the lymph of rats, which had been fed corn oil, were maintained at 0-4 degrees C in 0.9% NaCl, the following physical and chemical changes were observed to occur: increased polarity of chylomicron lipids, increased ultraviolet absorption of chylomicron lipids at 232 nm, decreased linoleic acid content, and aggregation. These alterations occurred more rapidly at room temperature and were found to be associated with an increased lipid peroxide content. The behavior of isolated olive oil chylomicrons was qualitatively similar. All observed changes in the properties of washed chylomicrons were prevented by 0.25 mm EDTA; when tested, 25 micro m EDTA was equally effective. The changes were also prevented by 0.02% hydroquinone. The alterations in chylomicron lipids appear to result from the autoxidation of esterified linoleic acid. Studies with linoleic acid-U-(14)C-labeled chylomicrons indicated that cleavage of the linoleic acid carbon chain did not accompany the physicochemical changes. These results demonstrate the usefulness of EDTA in preventing these specific and progressive alterations in chylomicrons dispersed in aqueous systems.     

Phospholipids of rat tissues after feeding pure phosphatidyl ethanolamine and lecithin

Pure phosphatidyl ethanolamine and lecithin from egg yolks were fed to rats in saline or in olive oil and the changes in individual phospholipids in the intestinal wall, liver, and plasma of the animals were studied. Ingestion of olive oil alone produced increased levels of all phospholipid fractions in each of the three tissues. Feeding phosphatidyl ethanolamine in saline resulted in slightly increased plasma phospholipids, but levels of liver total phospholipids were greatly reduced; when phosphatidyl ethanolamine was fed with olive oil, liver phospholipids were again reduced but this reduction was confined to the phosphatidyl ethanolamine and phosphatidic acid fractions. Feeding lecithin alone did not produce significant changes in levels of plasma or tissue phospholipids. The results suggest that liver phospholipid synthesis is depressed by feeding phosphatidyl ethanolamine; in the presence of olive oil, hepatic synthesis of phosphatidyl ethanolamine seems to be more selectively inhibited.     

Effects of a fish oil rich diet on hyperoxic lung damage in mice

Mice were fed a chow diet plus 10% cellulose, 10% fish oil or 10% sunflower oil for 3 weeks, then exposed to 100% oxygen for 75 h. Large changes in lung fatty acid composition occurred, but this did not affect hyperoxic lung damage nor levels of thiobarbituric acid reactive substances or myeloperoxidase in lungs of mice following exposure to hyperoxia. Thus there is no evidence that the ingestion of large quantities of fish oil increased the susceptibility to the oxidative stress induced by hyperoxia.     

A change in erythrocyte membrane permeability in rodents under the influence of fish oil, vitamin E and fatty acids]

In experiments on 370 gerbils (Meriones tamariscinus) and 56 albino rats, studies have been made on the effects of vitamin E, rancid cod-liver oil and unsaturated fatty acids (oleic, oxidated oleic and linoleic) upon the permeability of erythrocyte membrane. Osmotic fragility of erythrocytes to hypotonic NaCl solutions was measured. Seasonal changes in the permeability and sexual differences in these changes were observed. In M. tamariscinus the addition of vitamin E, cod-liver oil and unsaturated fatty acids to the food results in changes of erythrocyte permeability. The pattern of these changes depends on the season of year, differences in nutrition, as well as on fat and tocophenol stores in the organism, which are different in males and females. In albino rats, changes of erythrocyte permeability induced by vitamin E and cod-liver oil are rather insignificant.     

Physiological effects of γ-linolenic acid and sesamin on hepatic fatty acid synthesis and oxidation

Interrelated effects of γ-linolenic acid (GLA) and sesamin, a sesame lignan, on hepatic fatty acid synthesis and oxidation were examined. Rats were fed experimental diets supplemented with 0 or 2 g/kg sesamin (1:1 mixture of sesamin and episesamin) and containing 100 g/kg of palm oil (saturated fat), safflower oil rich in linoleic acid, or oil of evening primrose origin containing 43% GLA (GLA oil) for 18 days. In rats fed sesamin-free diets, GLA oil, compared with other oils, increased the activity and mRNA levels of various enzymes involved in fatty acid oxidation, except for some instances. Sesamin greatly increased these parameters, and the enhancing effects of sesamin on peroxisomal fatty acid oxidation rate and acyl-CoA oxidase, enoyl-CoA hydratase and acyl-CoA thioesterase activities were more exaggerated in rats fed GLA oil than in the animals fed other oils. The combination of sesamin and GLA oil also synergistically increased the mRNA levels of some peroxisomal fatty acid oxidation enzymes and of several enzymes involved in fatty acid metabolism located in other cell organelles. In the groups fed sesamin-free diets, GLA oil, compared with other oils, markedly reduced the activity and mRNA levels of various lipogenic enzymes. Sesamin reduced all these parameters, except for malic enzyme, in rats fed palm and safflower oils, but the effects were attenuated in the animals fed GLA oil. These changes by sesamin and fat type accompanied profound alterations in serum lipid levels. This may be ascribable to the changes in apolipoprotein-B-containing lipoproteins.     

FABP3 and FABP10 in Atlantic salmon (Salmo salar L.)--general effects of dietary fatty acid composition and life cycle variations

The increased use of dietary plant oil supplementation combined with high dietary lipid loads challenges the lipid transport systems of cultivated fish species. Fatty acid binding proteins (FABPs) have been thoroughly studied as intracellular fatty acid transporters in vertebrates, but no data have been reported in Atlantic salmon. In the present study, comparative characterizations were performed, and dietary influence of plant oil supplementation on FABP3 and FABP10 expression was studied for several tissues in two separate dietary trials. In trial I, groups (6 fish each) were fed diets for 42 weeks (body mass 142+/-1 to 1463+/-83 g) (mean+/-S.D.), containing graded levels of rapeseed oil substituting for fish oil using a linear regression design. In trial II, groups (3 fish each) were fed 100% fish oil or 100% plant oil for 22 months (0.160+/-0.052 to 2523+/-590 g) (mean+/-S.D.) and sampled at regular intervals. Liver and muscle tissues appeared to express several FABPs possibly linked to different metabolic functions. FABPs mRNA expression did not change with dietary inclusion of 75% rapeseed oil, whereas FABP3 protein expression seemed to be affected by dietary rapeseed oil inclusion. Significant changes in red muscle FABP3 mRNA expression correlate to significant changes in total beta-oxidation capacity during the energy consuming process of smoltification.     

Effect of dietary alpha-linolenic acid on the activity and gene expression of hepatic fatty acid oxidation enzymes

The activities of hepatic fatty acid oxidation enzymes in rats fed linseed and perilla oils rich in alpha-linolenic acid (alpha-18:3) were compared with those in the animals fed safflower oil rich in linoleic acid (18:2) and saturated fats (coconut or palm oil). Mitochondrial and peroxisomal palmitoyl-CoA (16:0-CoA) oxidation rates in the liver homogenates were significantly higher in rats fed linseed and perilla oils than in those fed saturated fats and safflower oil. The fatty oxidation rates increased as dietary levels of alpha-18:3 increased. Dietary alpha-18:3 also increased the activity of fatty acid oxidation enzymes except for 3-hydroxyacyl-CoA dehydrogenase. Unexpectedly, dietary alpha-18:3 caused great reduction in the activity of 3-hydroxyacyl-CoA dehydrogenase measured with short- and medium-chain substrates but not with long-chain substrate. Dietary alpha-18:3 significantly increased the mRNA levels of hepatic fatty acid oxidation enzymes including carnitine palmitoyltransferase I and II, mitochondrial trifunctional protein, acyl-CoA oxidase, peroxisomal bifunctional protein, mitochondrial and peroxisomal 3-ketoacyl-CoA thiolases, 2, 4-dienoyl-CoA reductase and delta3, delta2-enoyl-CoA isomerase. Fish oil rich in very long-chain n-3 fatty acids caused similar changes in hepatic fatty acid oxidation. Regarding the substrate specificity of beta-oxidation pathway, mitochondrial and peroxisomal beta-oxidation rate of alpha-18:3-CoA, relative to 16:0- and 18:2-CoAs, was higher irrespective of the substrate/albumin ratios in the assay mixture or dietary fat sources. The substrate specificity of carnitine palmitoyltransferase I appeared to be responsible for the differential mitochondrial oxidation rates of these acyl-CoA substrates. Dietary fats rich in alpha-18:3-CoA relative to safflower oil did not affect the hepatic activity of fatty acid synthase and glucose 6-phosphate dehydrogenase. It was suggested that both substrate specificities and alterations in the activities of the enzymes in beta-oxidation pathway play a significant role in the regulation of the serum lipid concentrations in rats fed alpha-18:3.     

Lipid composition of liver microsomes in rats fed a high monounsaturated fatty acid diet

The fatty acid and cholesterol contents of tissue membranes are the determinants of membrane stability and functionality. This study was designed to evaluate the influence of a high monounsaturated fatty acid diet on the fatty acid composition of rat liver microsomes and on their cholesterol and lipid phosphorus content. Weanling animals were fed for 5 weeks with high fat diets containing olive oil or corn oil. Saturated fatty acids were increased and oleic acid decreased in microsomal total phospholipids and in the three major phosphoglycerides, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylinositol (PI), of rats fed corn oil as compared to the olive oil group. The percentage of linoleic acid was higher in the corn oil group, but only for total phospholipids and PC. Linoleic and alpha-linolenic metabolites were significantly increased in total phospholipids of olive oil-fed animals with respect to those fed corn oil. These changes were responsible for the low unsaturation index found in microsomal phospholipids of the corn oil group. The diet did not affect the microsome cholesterol or the lipid phosphorus content. These results show that, in olive oil-fed rats, the cholesterol content and the degree of unsaturation of liver microsomes was similar to that observed in weanling animals; this probably suggests an adequate maintenance of functionality of membranes in olive oil-fed animals.     

Long-chain fatty acid perturbations in Mycoplasma pneumoniae

The fatty acid content of Mycoplasma pneumoniae increased 2.5- to 9.6-fold when the growth medium was supplemented with a saturated, unsaturated, or beta-hydroxy fatty acid, the greatest increase occurring with palmitic acid. The amount of each supplemented fatty acid found within this organism was 2.8 to 5.5% of the total fatty acid content; the exception was palmitic acid. Up to 57% of the palmitic acid was utilized from the supplemented medium, whereas only 0.2 to 10% of the other fatty acids was utilized. Chromatographic and isotopic analyses revealed that 22% of the labeled palmitic acid incorporated from the palmitic acid-supplemented medium remained free in this organism. Also, even though complex lipid synthesis increased a minimum of 3.8-fold under these conditions, this mycoplasma continued to incorporate intact complex lipids from the growth medium. Bacteriostatic and bactericidal studies which used high concentrations of various long-chain fatty acids showed that only palmitic, myristic, and beta-hydroxydecanoic acids were not bactericidal. The addition of palmitic acid to the growth medium resulted in the formation of exceedingly long, filamentous cells in approximately 25% of the population. Osmotic fragility and electron spin resonance spectroscopy studies showed a correlation among this increased fatty acid content, decreased membrane fluidity, and the increased osmotic fragility of palmitic acid-grown cells. In addition, these cells had a lowered cholesterol content. The effect of such compositional changes on osmotic fragility is discussed in this paper. Finally, the profound increase in the total fatty acid content of palmitic acid-grown cells altered neither sensitivity to tetracycline or erythromycin nor the amount of hydrogen peroxide secreted.     

Fatty acid oxidation by liver and muscle preparations of exhaustively exercised rats.

The influence of exhaustive exercise on the capacity of liver and muscle of rats to oxidize fatty acids was investigated in vitro. The rate of oxidation of fatty acids by liver preparations was significantly elevated as a result of exhaustion. Concurrently, the concentrations of beta-hydroxybutyrate were elevated in the plasma of the exhausted rats, suggesting that oxidation of fatty acids was also elevated in vivo. These findings are analogous to the findings of increased oxidation of fatty acids that results from training. In muscle, oxidation of palmitate, palmitoylcarnitine and beta-hydroxybutyrate by homogenates and isolated mitochondria was depressed with exercise. Despite the decrease in the oxidative capacity of the muscle preparations, the activities of several enzymes of beta-oxidation were either increased or unchanged as a result of exercise, suggesting that the depression in fatty acid oxidation may not be related to alterations in the process of beta-oxidation. Further studies showed that oxidation of [2-(14)C]pyruvate by muscle was depressed, whereas oxidation of [1-(14)C]pyruvate was not changed as a result of exercise. These results suggest that the decrease in fatty acid oxidation may be related to aberrations in the oxidation of acetyl-CoA. The changes in fatty acid oxidation that were observed, which are at variance with what is reported to occur with training, may have resulted from increased fragility of muscle mitochondria as a result of exercise. This increased fragility may render the mitochondria more susceptible to experimental manipulations in vitro and a subsequent loss of normal function.     

The saturation and isomerization of dietary fatty acids and the respiratory properties of rat heart mitochondria

Weanling rats were fed semi-purified diets containing 15% by weight of either corn oil, a high oleic acid safflower oil, lard or hydrogenated soybean oil. Significant changes in the fatty acid composition of heart mitochondrial preparations were induced by these dietary fats. Despite these changes in membrane composition, no effects on the respiratory properties of the mitochondria were observed. These results suggest that mitochondrial membranes adapt to changes in dietary fatty acids in a way which prevents changes in their functional properties.     

The effect of fish oil on physical aggression in schoolchildren--a randomized, double-blind, placebo-controlled trial

OBJECTIVES: The aim of the study was to investigate whether fish oil supplementation affected Japanese schoolchildren's behavior, with changes in aggression over time as the primary endpoint. DESIGN AND SUBJECTS: A placebo-controlled double-blind study with 166 schoolchildren 9-12 years of age was performed. The subjects of the fish oil group (n=83) took fish oil-fortified foods (bread, sausage and spaghetti). These foods were provided in amounts such that each subject in the fish oil group had an intake of 3600 mg of docosahexaenoic acid+840 mg of eicosapentaenoic acid (EPA)/week for 3 months. The rest (the controls, n=83) took control supplements. At the start and end of the study, psychological tests were performed to assess their aggression. RESULTS: Physical aggression assessed by Hostility-Aggression Questionnaire for Children in girls increased significantly (median: 13 to 15, n=42) in the control group and did not change (13 to 13, n=43) in the fish oil group with a significant intergroup difference (P=.008) with baseline as covariate. The changes in physical aggression scores over time and those of the ratio of EPA/arachidonic acid in RBC (DeltaEPA/AA) were significantly correlated in girls who agreed to blood collection (r=-.53, P=.01, n=23). On the contrary, there were no significant changes in physical aggression in boys. Aggression against others (extraggression) assessed by Picture Frustration Study did not change in the control group (median: 5 to 5) but increased significantly in the fish oil group (4 to 5) with a significant intergroup difference (P=.02) with baseline as covariate. These changes in extraggression might be explained partly by significantly lower baseline values of extraggression in the fish oil group (P=.02) than in the control group. There were no significant correlations between Deltaextraggression and DeltaEPA/AA in blood-sampled children (n=49). Impulsivity of girls assessed by parents/guardians using the diagnostic criteria for attention deficit/hyperactivity disorder of DSM-IV was reduced in the fish oil group (1 to 0) with a significant (P=.008) intergroup difference from the control group (1 to 1). There were no significant correlations between Deltaimpulsivity and DeltaEPA/AA in blood-sampled girls. In males, impulsivity reduced in both groups without any intergroup differences. CONCLUSION: There is a possibility that changes in fatty acid nutrition might affect physical aggression especially in girls.     

On lysosomal fragility and induction of liver hexose-monophosphate dehydrogenases in the fasted-refed rat.

Young adult male rats were fasted for 3 days, then fed a glucose-rich diet, ad libitum. At the end of the fasting period, the specific activity of liver glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase was decreased to 60% of control (nonfasted) levels. After 24 to 72 h of refeeding, the specific activity of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase increased seven- and twofold, respectively. During the fasting period, the liver lysosome fragility increased, as judged by increased release of bound acid phosphatase and β-N-acetylglucosammidase activity during standard homogenization. Three hours after feeding a carbohydrate-rich diet, a further increase in liver lysosomal fragility was observed that returned to control values prior to the induction of the dehydrogenases. Similarly, the susceptibility of liver lysosomes from fasted rats to increased fragility by the intraperitoneal injection of glucose or galactose was also observed. Prior starvation was not a requisite for labilization of lysosomal membranes by injected glucose, but induction of the pentose phosphate shunt dehydrogenase was not observed.In a group of 6-week old male rats fed a commercial pellet diet throughout, the injection of insulin caused no change in liver lysosomal fragility, though hypoglycemia resulted. Similar animals made diabetic by treatment with Streptozotocin and diabetic rats given insulin, showed no change in liver lysosmal fragility based on the percentage of free to total activities of β-N-acetylglucosaminidase, β-glucuronidase, β-galactosidase, and Cathespin D. However, when adult female rats were fasted for 24 h, then injected with sufficient insulin to produce hypoglycemia, liver lysosomal fragility, based on the release of β-N-acetylglucosaminidase during homogenization, increased nearly threefold. These studies demonstrate that stimulated lysosomal fragility can be initiated by refeeding fasted animals a carbohydrate-rich diet, by intraperitoneal injections of fasted rats with glucose or galactose, or by administering insulin alone to fasted rats. However, hyperglycemia induced by diabetogenic doses of Streptozotocin, or hypoglycemia induced in well-fed animals by insulin injection failed to elicit an enhanced liver lysosomal fragility. Whether induction of the enzymes of lipogenesis by rat liver is dependent upon a prior lysosomal membrane labilization remains to be determined.     

Influence of mitochondrial membrane fatty acid composition on proton leak and H2O2 production in liver

Mitochondrial membrane fatty acid composition has been proposed to play a role in determining mitochondrial proton leak rate. The purpose of this study was to determine if feeding rats diets with different fatty acid sources produces changes in liver proton leak and H(2)O(2) production. Six-month-old male FBNF(1) rats were fed diets with a primary fat source of either corn or fish oil for a 6-month period. As expected, diet manipulations produced substantial differences in mitochondrial fatty acid composition. These changes were most striking for 20:4n6 and 22:6n3. However, proton leak and phosphorylation kinetics as well as lipid and protein oxidative damage were not different (P > 0.10) between fish and corn oil groups. Metabolic control analysis, however, did show that control of both substrate oxidation and phosphorylation was shifted away from substrate oxidation reactions to increased control by phosphorylation reactions in fish versus corn oil groups. Increased mitochondrial H(2)O(2) production was observed in corn versus fish oil-fed rats when mitochondria were respiring on succinate alone or on either succinate or pyruvate/malate in the presence of antimycin A. These results show that mitochondrial H(2)O(2) production and the regulation of oxidative phosphorylation are altered in liver mitochondria from rats consuming diets with either fish or corn oil as the primary lipid source.     

Boron deprivation decreases liver S-adenosylmethionine and spermidine and increases plasma homocysteine and cysteine in rats

Two experiments were conducted with weanling Sprague–Dawley rats to determine whether changes in S-adenosylmethionine utilization or metabolism contribute to the diverse responses to boron deprivation. In both experiments, four treatment groups of 15 male rats were fed ground corn-casein based diets that contained an average of 0.05 mg (experiment 1) or 0.15 mg (experiment 2) boron/kg. In experiment 2, some ground corn was replaced by sucrose and fructose to increase oxidative stress. The dietary variables were supplemental 0 (boron-deprived) or 3 (boron-adequate) mg boron/kg and different fat sources (can affect the response to boron) of 75 g corn oil/kg or 65 g fish (menhaden) oil/kg plus 10 linoleic acid/kg. When euthanized at age 20 (experiment 1) and 18 (experiment 2) weeks, rats fed the low-boron diet were considered boron-deprived because they had decreased boron concentrations in femur and kidney. Boron deprivation regardless of dietary oil increased plasma cysteine and homocysteine and decreased liver S-adenosylmethionine, S-adenosylhomocysteine, and spermidine. Plasma concentration of 8-iso-prostaglandin F_2α (indicator of oxidative stress) was not affected by boron, but was decreased by feeding fish oil instead of corn oil. Fish oil instead of corn oil decreased S-adenosylmethionine, increased spermidine, and did not affect S-adenosylhomocysteine concentrations in liver. Additionally, fish oil versus corn oil did not affect plasma homocysteine in experiment 1, and slightly increased it in experiment 2. The findings suggest that boron is bioactive through affecting the formation or utilization of S-adenosylmethionine. Dietary fatty acid composition also affects S-adenosylmethionine formation or utilization, but apparently through a mechanism different from that of boron.     

Effects of selenium deficiency on fatty acid metabolism in rats fed fish oil-enriched diets.

The hepatic fatty acid metabolism was investigated in rats stressed by selenium deficiency and enhanced fish oil intake. Changes in the composition of lipids, peroxides, and fatty acids were studied in the liver of rats fed either a Sedeficient (8 microg Se/kg) or a Se-adequate (300 microg Se/kg) diet, both rich in n-3 fatty acid-containing fish oil (100 g/kg diet) and vitamin E (146 mg alpha-tocopherol/kg diet). The two diets were identical except for their Se content. Se deficiency led to a decrease in hair coat density and quality as well as to changes in liver lipids, individual lipid fractions and phospholipid fatty acid composition of the liver. The low Se status did reduce total and reduced glutathione in the liver but did not affect the hepatic malondialdehyde level. In liver phospholipids (PL), Se deficiency significantly reduced levels of palmitic acid [16:0], fatty acids of the n-3 series such as DHA [22:6 n-3], and other long-chain polyunsaturates C-20-C-22, but increased n-6 fatty acids such as linoleic acid (LA) [18:2 n-6]. Thus, the conversion of LA to arachidonic acid was reduced and the ratio of n-6/n-3 fatty acids was increased. As in liver PL, an increase in the n-6/n-3 ratio was also observed in the mucosal total fatty acids of the small intestine. These results suggest that in rats with adequate vitamin E and enhanced fish oil intake, Se deficiency affects the lipid concentration and fatty acid composition in the liver. The changes may be related to the decreased levels of selenoenzymes with antioxidative functions. Possible effects of Se on absorption, storage and desaturation of fatty acids were also discussed.     

Relations between the changes of the phagocytic activity of the reticuloendothelial system and the alterations in protein and nucleic acids contents of the rat liver (author's transl)]

The phagocytic activity of the reticuloendothelial system (RES) was evaluated after a single oral administration of soya-bean oil to male rats (15 g/kg). 1. An emulsion of soya-bean oil administered to the rat by gastric intubation activated the phagocytosis of colloidal carbon; the stimulation appeared on the 2nd day after treatment and persisted up to the 3rd day. There was also a relation between the stimulation of RES activity, under our experimental conditions, and the increased level observed in the protein and nucleic acid contents of the liver. 2. In contrast, without emulsion, soya-bean oil depressed the phagocytic activity on the 2nd and 3rd days after administration of the oil. These changes were associated with a diminution in ribonucleic acid and protein contents of the liver. Although the mechanisms of soya-bean oil-induced alterations of phagocytic activity were not clarified, there was a relationship between the RES stimulation or inhibition and the modifications in nucleic acid and protein contents of rat liver.     

Influence of essential oil of Hyssopus officinalis on the chemical composition of the walls of Aspergillus fumigatus (Fresenius)

The cell walls of the growing hyphae of Aspergillus fumigatus (Fresenius) cultured in the presence or absence of the essential oil of Hyssopus officinalis were isolated and their chemical composition analysed. The presence of the essential oil led to a reduction in levels of neutral sugars, uronic acid and proteins, whereas amino sugars, lipids and phosphorus levels were increased. HPLC analysis of the neutral sugars showed that they consisted mainly of glucose, mannose and galactose, while the amino sugars consisted of glucosamine and galactosamine. The presence of the essential oil in the culture medium induced marked changes in the content of galactose and galactosamine. Cell walls were fractionated by treatment with alkali and acid. The essential oil induced similar alterations in the various fractions with a more marked effect on the major constituents. The alterations were related to changes in the structure of the cells. This revised version was published online in August 2006 with corrections to the Cover Date.