Brain Lipid Fractions Research Articles

Antiatherogenic effect of Tiger nut tubers (Cyperus esculentus L.) supplemented diet in apolipoprotein E knockout mice

The present study was carried out to evaluate the physiological effect of tiger nut tubers on lipid metabolism and peroxidation stress in apolipoprotein E knockout (apoE-/-) mice. Six male and five female mice, 6-7 wk old, was fed AIN 93G control diet supplemented with 25 % of whole powder of tiger nut tubers for 11 wk. Measurements were done for plasma, liver, aorta and brain lipid fractions. Peroxidation stress in mice serum and brain, i.e. vitamin E, nitric oxide and TBARS were evaluated and aortic valve lesions area was also determined. The obtained results showed that, type of diet and mice gender did not affect mice growth parameters. Serum and liver lipids were lowered in male mice fed tiger nut diet than that fed the control diet. However, the effect of tiger nut diet on the peroxidation parameters was not prominent. The mice fed on chufa-diet resulted in significant reduction in the aortic arch atherosclerotic lesions in both gender compared to that fed the basal diet. Our results show that tiger nut tubers have antiatherogenic effect and contain a gender dependent factor which regulates lipid metabolism in apoE-/- mice.

Multiple sclerosis: Presence of serum antibodies to lipids and predominance of cholesterol recognition.

A lot of available data on lipid immunology in multiple sclerosis (MS) have been derived from studies using synthetic lipids, therefore the role of lipids in the immunopathogenesis of MS remains poorly defined. The present study on the lipid response in MS was performed on native lipids from autopsied brain tissue. For this, lipid fractions (n = 9) were prepared from MS (n = 3) and control (n = 2) white matter according to the Folch procedure and were characterized depending on their solubility in chloroform/methanol. TLC showed that, in brain from MS cases, neutral lipids were rich in cholesterol and cholesterol esters while lipids from control brains displayed a predominance of phospholipids. MS serum IgG and IgM were found to bind to MS brain lipid fractions with a higher efficacy (p < 0.05) than the control serum. F(ab)2 fractionation revealed that MS serum IgG binding depended on a specific antibody-type of recognition. Pre-adsorption of serum with cholesterol, galactocerebrosides, sulfitides, and phosphatidylinositol prior to ELISA with MS brain lipids, showed that cholesterol diminished IgG and IgM binding up to 70%. Experiments with synthetic lipids confirmed the predominance of cholesterol binding by MS serum. Our results demonstrate that IgG and IgM fractions from MS serum specifically and predominantly recognize native cholesterol and cholesterol esters isolated from the brain tissue of patients with MS. © 2017 Wiley Periodicals, Inc.

Lipid microarrays identify key mediators of autoimmune brain inflammation

Recent studies suggest that increased T-cell and autoantibody reactivity to lipids may be present in the autoimmune demyelinating disease multiple sclerosis. To perform large-scale multiplex analysis of antibody responses to lipids in multiple sclerosis, we developed microarrays composed of lipids present in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain lipid fractions. Lipid-array analysis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebrospinal fluid (CSF) derived from individuals with multiple sclerosis. Sulfatide-specific antibodies were also detected in SJL/J mice with acute experimental autoimmune encephalomyelitis (EAE). Immunization of mice with sulfatide plus myelin peptide resulted in a more severe disease course of EAE, and administration of sulfatide-specific antibody exacerbated EAE. Thus, autoimmune responses to sulfatide and other lipids are present in individuals with multiple sclerosis and in EAE, and may contribute to the pathogenesis of autoimmune demyelination.

Activation and partial purification of the ATPase of clathrin-coated vesicles and reconstitution of the proton pump.

A N-ethylmaleimide-sensitive ATPase was extracted and partially purified from clathrin-coated vesicles of bovine brain. During purification the enzyme lost activity which was restored by a purified phospholipid fraction from brain. Phosphatidylserine, but no other commercial phospholipids tested, replaced the brain lipid fraction as activator. Particles depleted of the ATPase exhibited no H+ pump activity when reconstituted with brain phospholipids by the cholate dilution procedure. H+ pump activity was restored by incubating the reconstituted vesicles with the partially purified ATPase.

Lipogenesis in the brain of suckling rats. Studies on the mechansim of mitochondrial-cytosolic carbon transfer.

1. Studies on the incorporation of [3-(14)C]pyruvate and d-3-hydroxy[3-(14)C]butyrate into the brain lipid fraction by brain homogenates of the suckling (7-day-old) rat have been carried out. 2. Whereas approximately twice as much CO(2) was evolved from pyruvate compared with 3-hydroxybutyrate metabolism, similar amounts of the radioactivity of these two precursors were incorporated into the lipid fraction. Furthermore, in both cases the incorporation into lipid was almost tripled when glucose (10mm) or NADPH (2.5mm) was added to the incubation media. 3. If 5mm-(-)-hydroxycitrate, an ATP-citrate lyase inhibitor, was added to the incubation the incorporation of carbon from pyruvate was inhibited to 39% of the control and from 3-hydroxybutyrate to 73% of the control, whereas CO(2) production from both precursors was not affected. 4. The incorporation from pyruvate or 3-hydroxybutyrate into lipids was not affected by the presence of 10mm-glutamate in the medium (to encourage N-acetylaspartate production). However, incorporation from pyruvate was inhibited by 21% in the presence of 5mm-amino-oxyacetate (a transaminase inhibitor) and by 83% in the presence of both hydroxycitrate (5mm) and amino-oxyacetate. 5. Incorporation from 3-hydroxybutyrate into brain lipids was inhibited by 20% by amino-oxyacetate alone, but by 55% in the presence of both hydroxycitrate and amino-oxyacetate. 6. It is concluded that the mechanism of carbon transfer from pyruvate into lipids across the mitochondrial membrane in the suckling rat brain is mainly via citrate and N-acetylaspartate. 3-Hydroxybutyrate, in addition to using these routes, may also be incorporated via acetoacetate formation and transport to the cytosol.

21 - Incorporation of 14c-hydralazine into rat brain lipid fraction in vitro.

21 - Incorporation of 14c-hydralazine into rat brain lipid fraction in vitro.

THE INCORPORATION OF [1‐14C]LINOLENATE INTO LIPIDS OF DEVELOPING RAT BRAIN DURING ESSENTIAL FATTY ACID DEPRIVATION

Abstract— Twenty‐one‐day old essential fatty acid (EFA) deprived rats incorporated about twice the radioactivity from [1‐14C]linolenate into brain lipid fractions as did controls. At 5 min after injection, 2/3 of the radioactivity was associated with the less polar lipid fraction of both control and EFA deprived animals. By 30 min after injection, 70% of the radioactivity was in the phospholipid fraction. This value increased to 90% at later time points.The specific activity of brain phospholipids from EFA deprived rats was always greater than that of controls. This held true for the individual phosphatide fractions also. In general, phosphatidylcholine (PC) was labeled most rapidly. With increasing time intervals, radioactivity was transferred to phospha‐tidylethanolamine (PE) and phosphatidylserine + phosphatidylinositol (PS + PI).The transfer of fatty acid radioactivity into phospholipid and the distribution of radioactivity among individual phosphatides did not appear to be affected by the dietary state. However, the total amount of radioactivity incorporated was related to the amount initially retained by brain after injection. Our data suggest that one or more components of the less polar lipid fraction may act as a ‘trap’ or reservoir for fatty acids which are required for phospholipid synthesis.

Effects of acute δ1-tetrahydrocannabinol treatment, of hypothermia and of ambient temperature on choline incorporation into mouse brain

[Me- 14C]-choline was injected intravenously in mice after acute i.p. treatment with Δ 1-THC and the uptake of radioactive label by brain was measured in its aqueous and lipid extracts. The endo-genous plasma choline level of 4.96 μg/ml was not affected by Δ 1-THC treatment. At an ambient temperature of 22° only the higher dose of Δ 1-THC (15 mg/kg) influenced the appearance of label in the brain: incorporation into the lipid fraction fell by 52 per cent, and into the brain as a whole by 23 per cent. Phenobarbitone (300 mg/kg) showed similar effects. Both drugs, when administered to mice housed at 22°, caused a marked lowering of rectal temperature for the duration of the radioactive studies. At an ambient temperature of 33.5°, most or all of the hypothermie effects of Δ 1-THC (15 mg/kg) and phenobarbitone were abolished. At this temperature, Δ 1-THC (15 mg/kg) inhibited radioactive incorporation into the brain lipid fraction by 19 per cent. Phenobarbitone also had a smaller effect but also inhibited incorporation into the whole brain in both its aqueous and lipid fractions (by 19% and 23% respectively). At 33.5° the lower dose of Δ-THC (3.75 mg/kg) caused an increase in incorporation into the brain aqueous (26%) and lipid (25%) fractions. These different responses are discussed in relation to the effects of (a) hypothermia, which caused decreased radioactive incorporation into brain, (b) ambient temperature, which increased incorporation when high, and (c) the spontaneous motor activity of the mice.

Action of Depressor-I, a hypotensive phospholipid from bovine brain, on systemic and arterial blood pressures of various species.

Effects of "Depressor-I" (D-I), a new hypotensive phospholipid obtained from bovine brain lipid fraction, on systemic arterial blood pressure were investigated. The hypotensive activity of D-I in urethane anaesthetized rats was dose dependent and tachyphylaxis and/or sensitization were not observed. Increments of the respiration and the heart rate were observed with sharp falls in blood pressures following intravenous administration of D-I, in simultaneous recordings in anaesthetized rats. D-I elicited hypotension in all species of animals examined, and the sensitivities to D-I were much the same, however, there were two types in patterns of duration on responses and the durations were also dose dependent. D-I exhibited depressor-responses even in conscious rats, though responses were much smaller compared with those seen in anaesthetized rats. In a comparison of anaesthetic agents in rats, the highest hypotensive activity of D-I was observed with pentobarbital anaesthesia, a moderate response was seen with alpha-chloralose and the least response was seen with urethane. In spinal rats or those pretreated with reserpine or antagonists, such as atropine, diphenhydramine, propranolol and hexamethonium, D-I also elicited hypotension. These results suggest that "Depressor-I" does not elicit the depressor action via the stimulation of the central and the autonomic nervous systems but rather by a direct action on peripheral blood vessels.

Action of Depressor-I, A Hypotensive Phospholipid from Bovine Brain, on Systemic and Arterial Blood Pressures of Various Species

Effects of “Depressor-I” (D-I), a new hypotensive phospholipid obtained from bovine brain lipid fraction, on systemic arterial blood pressure were investigated. The hypotensive activity of D-I in urethane anaesthetized rats was dose dependent and tachyphylaxis and/or sensitization were not observed. Increments of the respiration and the heart rate were observed with sharp falls in blood pressures following intravenous administration of D-I, in simultaneous recordings in anaesthetized rats. D-I elicited hypotension in all species of animals examined, and the sensitivities to D-I were much the same, however, there were two types in patterns of duration on responses and the durations were also dose dependent. D-I exhibited depressor-responses even in conscious rats, though responses were much smaller compared with those seen in anaesthetized rats. In a comparison of anaesthetic agents in rats, the highest hypotensive activity of D-l was observed with pentobarbital anaesthesia, a moderate response was seen with α-chloralose and the least response was seen with urethane. In spinal rats or those pretreated with reserpine or antagonists, such as atropine, diphenhydramine, propranolol and hexamethonium, D-I also elicited hypotension. These results suggest that “Depressor-I” does not elicit the depressor action via the stimulation of the central and the autonomic nervous systems but rather by a direct action on peripheral blood vessels.

The incorporation of orally administered radiolabeled dihomo gamma-linolenic acid (20 : 3 omega 6) into rat tissue lipids and its conversion of arachidonic acid.

Radioactivity from orally administered radiolabeled dihomo-gamma-linolenic acid (20 : 3 omega 6) was recovered from the liver, plasma and brain lipid fractions. After administration the fatty acid was metabolized to arachidonic acid, the 22 carbon chain length fatty acid, and was also beta-oxidized. However, 22 hr after administration of [1-14C] 20 : 3 between one-third and one-half of the recovered radioactivity was still associated with dihomo-gamma-linolenic acid in the liver and plasma lipid fractions. Orally administered dihomo-gamma-linolenic acid is incorporated into lipid fractions and is, therefore, available in the metabolic pool for PGE1 synthesis.

Isolation of an acute hypotensive substance from bovine brain lipid fraction.

A depressor substance was found in acetone extract of bovine brain, greatly purified with the use of various chromatographic techniques, and tentatively named as D-I. It caused a sharp fall in arterial blood pressure of anesthetized cats with intravenous injections of 10 μg level of purified sample per kg animal body weight on a weight basis. Its hypotensive activity was not affected by previous treatment of cats with atropine, diphenhydramine, or hexamethonium. In the enzymic assay with the use of prostaglandin dehydrogenase (PGDH), neither prostaglandin E (PGE) nor prostaglandin F (PGF) compound was found. In the test of an incubation with a proteinase (nagase), the depressor activity was recovered almost completely. This depressor substance is definitely distinguishable from other depressor compounds and relatively resemble to lysolecithin, in the comparison of its attitude on TLC or in the course of purification process.

Inhibition of influenza virus haemagglutination by a brain lipid fraction.

THERE exists a rather ill-defined group of complex lipids that could be subsumed under the name of ‘mucolipids’. These substances, while possessing constituents commonly considered characteristic of the cerebrosides, share some properties with the mucoproteins. Thus, they are soluble in water and include amino-sugars and a nitrogen-containing acid which gives rise to a violet colour with Bial's reagent and to a colour reaction with p-dimethylamino-benzaldehyde without previous treatment with alkali. We shall here refer to the substance yielding a direct Ehrlich reaction as ‘direct chromogen’, since we are not in a position to decide whether we are dealing with sialic acid1, which was first isolated from submaxillary gland mucin2, or with neuraminic acid3 found in a group of lipids later designated as ganglio-sides4; nor indeed whether these two compounds differ.

Experimental allergic encephalomyelitis following administration of homologous brain lipid fractions.

Experimental allergic encephalomyelitis following administration of homologous brain lipid fractions.

Action of thromboplastinase on human brain lipid fractions.

SummaryThe action of the bacterial enzyme thromboplastinase on thromboplastically active lipid material has been presented. In all cases, loss in clotting potency was accompanied by a liberation of acid soluble organic phosphorus. A still unidentified phosphorus containing compound has been isolated from the reaction mixture after TPase action. The results are discussed and several possible implications presented.