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PubMed1983

Concerted stimulation and inhibition of desaturation, chain elongation, and esterification of essential fatty acids by cultured neuroblastoma cells.

Neuroblastoma (N1E-115) cells in culture rapidly incorporated exogenous fatty acyl chains suspended as albumin complexes in the medium. The essential fatty acids, linoleic (18:2(n - 6)) and linolenic (18:3(n - 3)) acids, were converted to polyunsaturated acids by delta 6 and delta 5 desaturation and chain elongation. The major end products (20:4 from 18:2(n - 6) and 20:5 and 22:5 from 18:3(n - 3)) were preferentially esterified to phospholipids, whereas intermediates were esterified primarily or equally to triacylglycerol. The effects of unlabeled exogenous fatty acids (eg. 40 microM 18:2(n - 6), 18:3(n - 6), 18:3(n - 3), 20:3(n - 6), 20:4(n - 6), trans-18:2(n - 6), 18:1(n - 9), trans-18:1(n - 9), or 16:0) on the conversion of 2 microM [1-(14)C]18:2(n - 6), 18:3(n - 3), 20:3(n - 6), 20:4(n - 6), or 16:0 and on accumulation of products and unaltered substrates in phospholipids and triacylglycerol were examined after incubations of 2-24 h. With [1-(14)C]18:2, formation and esterification of 20:4 to phospholipids was (i) stimulated 4-8-fold by 18:2(n - 6), 20:3(n - 6), or 20:4(n - 6), (ii) inhibited by 18:3(n - 3) or trans-18:2(n - 6), or (iii) unaffected by 18:3(n - 6), 18:1(n - 9), trans-18:1(n - 9), and 16:0. Specific but less marked effects were observed with the other 1-(14)C-substrate acids. Thus, various fatty acids influenced the metabolism of essential fatty acids both at the level of conversion by desaturation and elongation and at esterification to complex lipids by mechanisms specific to individual acids. Product inhibition was not a major feedback mechanism; however, the complement of available fatty acids evidently modulates the acyl chain composition of membrane phospholipids through processes in addition to acyltransferase selectivity. The data support a closely coordinated or concerted enzyme system for directed synthesis of esterified polyunsaturated acyl chains.

Animals↗
PubMed1985

Effects of essential fatty acid deficiency and indomethacin on histologic, ultrastructural, and phagocytic responses of hepatic macrophages to glucan.

Glucan administration in the rat induces a hyperplasia and hypertrophy of the reticuloendothelial system (RES) and a concomitant leukocytosis. Increased phagocytic function and lysozymal immunoreactivity of macrophages are also characteristic of the glucan effect. The potential role of arachidonic acid metabolites in mediating this hepatic inflammatory response induced by the RES stimulant glucan was assessed in the present study by two experimental approaches. In one study, rats were depleted of arachidonic acid by rendering them deficient in essential fatty acids (EFA). In another study, rats were pretreated with the fatty acid cyclooxygenase inhibitor indomethacin. Both treatment interventions markedly attenuated the hepatic Kupffer cell proliferative and granulomatous response to glucan and the associated leukocytosis. Lysozyme immunoreactivity of the Kupffer cells and rates of colloidal carbon clearance (T/2), however, were enhanced by the above treatments. Supplementation of EFA-deficient rats with ethyl arachidonate restored their glucan response to an extent that was not significantly different from nondeficient rats. Marked hepatic proliferative responses were apparent only in those treatment groups characterized by leukocytosis, which suggests that extrahepatic recruitment is an important component of the glucan response in normal, nutritionally adequate rats. Collectively these data suggest that arachidonic acid metabolites may play a role in modulating this extrahepatic recruitment and the associated cellular proliferative and granulomatous responses following glucan administration of the rat.

Animals↗
PubMed1987

Hepatic triacylglycerol accumulation induced by ethanol and carbon tetrachloride: interactions with essential fatty acids and prostaglandins.

Triacylglycerol accumulation in the liver (fatty liver) caused by ethanol or carbon tetrachloride involves interactions with essential fatty acids and prostaglandins. The degree to which the fatty liver develops is dependent on total dietary fat intake. Both ethanol and carbon tetrachloride impair desaturation of linoleic acid and dihomo-gamma-linolenic acid and this appears to be relevant to the pathogenesis of fatty liver from two points of view. First, low arachidonic acid in liver phospholipids is associated with increased liver triacylglycerol content whether caused by ethanol, carbon tetrachloride, or essential fatty acid deficiency. Second, essential fatty acids including gamma-linolenic acid and arachidonic acid, as well as the prostaglandins, prevent ethanol- and carbon tetrachloride-induced fatty liver. Arachidonic acid and possibly the prostaglandins are therefore likely to be directly involved in lipoprotein and triacylglycerol secretion by the liver.

8,11,14-Eicosatrienoic Acid↗
PubMed1977

Recovery of brain from deficiency of essential fatty acids in rats.

Rats were made visibly deficient in essential fatty acids by feeding a deficient diet and were then fed a diet containing 5.0 per cent by weight corn oil as a source of essential fatty acids. After 11-13 weeks on deficient diet the weights of the brain were 25% less than those of rats on control diets. After 5 weeks on the control diet, deficient animals had regained normal brain weight and composition and had lost the deficiency symptoms. Lipids were extracted from the brains and analysed qualitatively and quantitatively, the overall effect of essential fatty acid deficiency being a reduction in the proportion of cerebrosides and sphingomyelin, the appearance of a high proportion of eicosatrienoic acid (20:3) and the reduction of arachidonic acid (20: 4) and the other essential fatty acids. It is considered that essential fatty acid deficiency retards maturing of brains and the present data show that this effect is reversible.

Animals↗
PubMed1984

Intravenous lipid emulsions in the treatment of essential fatty acid deficiency: studies in young pigs.

Essential fatty acid deficiency (EFAD) occurs in infants fed fat-free mixtures of glucose and amino acids. Although infusion of lipid emulsion rapidly reverses clinical symptoms, little is known about effects on tissue fatty acids. To study this question, five groups (n = 4/group) of neonatal pigs were studied. Three groups (I, II, and V) were made EFAD by feeding diets without essential fatty acids (EFA) for days 5 to 33 of life. Groups III and IV were fed a control diet. By 33 days, animals fed the deficient diet showed clinical symptoms and biochemical signs of EFAD. On days 33 to 54 of life, group I animals were fed the EFA-deficient diet and infused with lipid emulsion, providing 3.6% of energy as linoleic acid; group II animals were fed the deficient diet and infused with linoleic acid at 7.2% of energy; group V animals were fed the deficient diet with no lipid emulsion; group III and IV animals were fed the EFA-deficient diet and provided EFA intravenously. Infusion of lipid emulsion rapidly reversed clinical symptoms of EFAD and returned plasma phospholipid omega 6 fatty acids levels to normal. However, erythrocyte and liver phospholipid omega 6 fatty acid content and adipose tissue reserves of omega 6 fatty acids normalized more slowly. Three weeks of infusion of linoleic acid at 3.6% of energy and 2 weeks of infusion at 7.2% of energy were required to return erythrocyte phospholipid fatty acids to normal. Liver phospholipid fatty acid composition still showed biochemical evidence of EFAD in animals treated with linoleic acid at 3.6% of energy for 3 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Modulation of cytokine production in vivo by dietary essential fatty acids in patients with colorectal cancer.

1. The effects of essential fatty acids (gamma-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid), at a dose of 4.8 g/day, given in combination as dietary supplements, on cytokine production were investigated in patients with colorectal cancer. 2. Total serum cytokines--interleukin (interleukin-1 beta, 2, 4 and 6), tumour necrosis factor-alpha and interferon-gamma--were analysed using the enzyme-linked immunosorbent assay technique at different time intervals during the course of essential fatty acid supplementation. 3. Fatty acid uptake and patient compliance were confirmed by a significant increase in serum levels of gamma-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid in all three fractions: tricylglycerol, cholesterol and phospholipid. 4. There was no significant alteration in total serum cytokine concentration/levels in the first 2 months of essential fatty acid ingestion, but the levels of serum cytokines steadily declined thereafter, reaching minimum levels after 6 months of essential fatty acid supplementation. 5. Essential fatty acids, at the dose and duration (6 months) used in this study, reduced total serum interleukin-1 beta levels by 61% (P = 0.044), interleukin-2 by 63% (P = 0.05), interleukin-4 by 69% (P = 0.025), interleukin-6 by 83% (P = 0.030), tumour necrosis factor-alpha by 73% (P = 0.040) and interferon-gamma by 67% (P = 0.050). 6. Three months after cessation of essential fatty acid intake, however, these cytokine levels returned to presupplementation values. 7. This present study has shown that long-term n-3 and n-6 EFA ingestion results in a significant reduction in circulating key cytokines. The precise mechanism of this reduction is unclear.

Aged↗
PubMed1993

Evidence that liver microsomes of human neonates desaturate essential fatty acids.

delta 6- and delta 5-Desaturation of essential fatty acids of n-6 and n-3 series are required for the biosynthesis of polyunsaturated fatty acids (PUFAs), which are precursors of eicosanoids and constituents of membrane phospholipids. This pathway could be of special importance during the perinatal period, when PUFAs accretion in the central nervous system is very active. However, experimental evidence of delta 6- and delta 5-desaturase activities in man is very scarce, and no data are available for newborns. We report the delta 6- and delta 5-desaturase activities detected in human liver microsomes from three neonates who died from associated malformations. Radiochemical assays of delta 6- and delta 5-desaturase activities performed with reverse phase HPLC analysis of the products in the n-6 series ranged from 4.8-13.6 to 3.2-16.4 pmol substrate converted.min-1.mg-1 microsomal proteins, respectively. In the n-3 series delta 6-desaturase activity ranged from 5.3 to 12.8 pmol.min-1.mg-1. The relationships between enzyme activities and substrate concentrations suggest excess substrate inhibition for n-6 and not for n-3 fatty acids. These results demonstrate significant delta 6- and delta 5-desaturase activities in human liver of neonates, but this activity was lower than previously reported in adult humans and in mammals, especially rodents.

Delta-5 Fatty Acid Desaturase↗
PubMed1992

Essential fatty acid deficiency in cultured SK-N-SH human neuroblastoma cells.

SK-N-SH neuroblastoma cells grown under standard culture conditions contain significant amounts of Mead acid (20:3 omega 9) in phospholipids, indicating essential fatty acid (EFA) deficiency. The amount of esterified 20:3 omega 9 was augmented by growth in a chemically defined EFA-free medium, whereas its presence could be virtually eliminated by supplementation of the culture medium with either arachidonic (20:4 omega 6; AA), eicosapentaenoic (20:5 omega 3; EPA), or linolenic (18:3 omega 3) acids. Substitution of Mead acid for omega 6 fatty acids, particularly evident in phosphatidylinositol (PI), indicates a compensatory replacement of omega 9 for omega 6 fatty acids during EFA deficiency. Studies evaluating [3H]scopolamine binding to the M3 muscarinic acetylcholine receptors (mAChRs) present in these neurotumor cells as well as effects of carbachol on phosphoinositide turnover and intracellular Ca2+ mobilization, indicate that the biosubstitution of 20:4 omega 6 with 20:3 omega 9 does not detectably impair these measures of signal transduction. Stimulation of mAChRs with carbachol increased the cellular mass of diacylglycerol (DAG) approximately 60%. On the basis of distinctive fatty acid "signatures" of each of the phospholipid classes, it is concluded that the DAG initially released following muscarinic stimulation is derived from phosphoinositide breakdown. After several minutes, however, a significant amount of DAG comes from phosphatidylcholine (PC) as well. In contrast to DAG, the composition of phosphatidate (PA) following receptor stimulation closely resembles that of the phosphoinositides, even at the later time points examined. These results support a selective phosphorylation of DAG arising from the stimulated breakdown of phosphoinositides, favoring the conservation of the 1-stearoyl, 2-arachidonoyl (or 20:3 omega 9) moiety.

8,11,14-Eicosatrienoic Acid↗
PubMed1985

Incorporation into the tissues and turnover of arachidonic acid after administration to normal and essential fatty acid deficient rats.

A comparison was made of the incorporation into the tissues and metabolism of [1-14C] arachidonic acid (AA) after i.v. administration to normal and EFA-deficient rats. At different times, ultra-thin whole body sections were prepared and the distribution of the radioactivity determined by autoradiograms. After 5 min, a considerable incorporation occurs in the following organs: subcutaneous and perispinal fat, liver, heart muscle, kidney and adrenal. The EFA deficient rats show a similar distribution but the radioactivity is longer retained. The total amount of radioactivity in the heart, liver, kidney and adrenal was measured at different times. A decline occurs in the heart, and an increase in the adrenal. In the urine, the highest amount of radioactivity is excreted on the first day. The excretion is lower in the EFA-deficient rats. Small amounts of radioactive metabolites with the chromatographic characteristics of PGE2 and 13,14 dihydro-15ketoPGE2 were isolated from urine. The amounts of 14CO2 produced were determined after the administration of [1-14C] AA. Half times were: 39 +/- 2.9 min in the EFA-deficient and 28 +/- 2.8 min in the normal rats. In the heart, AA is incorporated into phospholipids and neutral lipids. The following percentages were determined: phosphatidylinositol: 6.9 +/- 0.6%, phosphatidylcholine: 44 +/- 4.1%, phosphatidylethanolamine: 10.0 +/- 1.0%, neutral lipids: 9.3 +/- 1.6%. Several explanations can be given for the higher requirements of some tissues for AA. It could be, that this substance is used in the formation of particular membranes with a high AA content. Differences in the amounts of metabolites produced may also play a role.

Animals↗
PubMed1987

Low prevalences of coronary heart disease (CHD), psoriasis, asthma and rheumatoid arthritis in Eskimos: are they caused by high dietary intake of eicosapentaenoic acid (EPA), a genetic variation of essential fatty acid (EFA) metabolism or a combination of both?

The low prevalences of CHD, psoriasis, asthma and rheumatoid arthritis in Eskimos have been attribute to the high dietary intake of EPA from fish and marine mammals. However, even on a Western diet, Eskimos have plasma arachidonic acid (AA) levels far below those seen in Europeans while dihomogammalinolenic acid (DGLA) levels are higher in Eskimos. These low AA and high DGLA levels seem to be due to a genetic abnormality in EFA desaturation since they are found even when EPA intakes are low. Since AA is known to be important in the pathogenesis of CHD, asthma, psoriasis and arthritis, while DGLA has properties which make it of likely therapeutic value in these conditions, the genetically high DGLA and low AA are likely to be as important as dietary EPA in determining Eskimo disease patterns.

Arthritis, Rheumatoid↗
PubMed1994

Amelioration of both early and late radiation-induced damage to pig skin by essential fatty acids.

PURPOSE: To evaluate the possible role of essential fatty acids, specifically gamma-linolenic and eicosapentaenoic acid, in the amelioration of early and late radiation damage to the skin. METHODS AND MATERIALS: Skin sites on the flank of 22-25 kg female large white pigs were irradiated with either single or fractionated doses (20 F/28 days) of beta-rays from 22.5 mm diameter 90Sr/90Y plaques at a dose rate of approximately 3 Gy/min. Essential fatty acids were administered orally in the form of two 'active' oils, So-1100 and So-5407, which contained gamma-linolenic acid and a mixture of that oil with eicosapentaenoic acid, respectively. Oils (1.5-6.0 ml) were given daily for 4 weeks prior, both 4 weeks prior and 10-16 weeks after, or in the case of one single dose study, just for 10 weeks after irradiation. Control animals received a 'placebo' oil, So-1129, containing no gamma linolenic acid or eicosapentaenoic acid over similar time scales before and after irradiation. Acute and late skin reactions were assessed visually and the dose-related incidence of a specific reaction used to compare the effects of different treatment schedules. RESULTS: A reduction in the severity of both the early and late radiation reactions in the skin was only observed when 'active' oils were given over the time course of the expression of radiation damage. Prior treatment with oils did not modify the radiation reaction. A 3.0 ml daily dose of either So-1100 or So-5407 given prior to, but also after irradiation with single and fractionated doses of beta-rays produced the most significant modification to the radiation reactions, effects consistent with dose modification factors between 1.06-1.24 for the acute reactions of bright red erythema and/or moist desquamation, and of 1.14-1.35 for the late reactions of dusky/mauve erythema and dermal necrosis. There was the strong suggestion of an effect produced by the 'placebo' oil, So-1129, after higher daily doses of oil. CONCLUSIONS: Essential fatty acids can modulate normal tissue reactions when given over the time when radiation damage is normally expressed. Dose modification factors suggest that a > or = 10% higher dose is required to produce the same level of normal tissue injury. Clinical application of selected essential fatty acids at appropriate doses may lead to a significant increase in the therapeutic gain in patients treated for cancer by radiotherapy.

Animals↗
PubMed1986

Influence of different dietary fatty acid sources on erythrocyte lipids and plasma and liver essential fatty acids in hamsters fed ethanol.

Hamsters fed ethanol were given three different dietary sources of essential fatty acids; safflower oil, evening primrose oil (both mainly n-6 fatty acids) or linseed oil (mainly n-3 fatty acids). After 7 weeks, plasma, erythrocyte and liver lipids and fatty acids were analyzed. Plasma and liver lipids were not significantly different in the ethanol-fed hamsters compared to the controls. Erythrocyte total phospholipid was increased only in the ethanol-fed groups given n-6 but not n-3 fatty acids. Some fatty acid changes induced by ethanol were predictable, e.g. lower 20:4 n-6 in hamsters fed n-6 fatty acids, but others were not predictable, e.g. higher 22:6 n-3 in all the ethanol-fed groups. The effect of ethanol on hamster lipids and fatty acid composition appears dependent on the predominant class of dietary fatty acids.

Alcohol Drinking↗
PubMed1998

Effects of alpha-lipoic acid on neurovascular function in diabetic rats: interaction with essential fatty acids.

Elevated oxidative stress and impaired n-6 essential fatty acid metabolism contribute to defective nerve conduction velocity (NCV) and perfusion in diabetic rats, which may be corrected by free radical scavenger and gamma-linolenic acid (GLA) treatments. Alpha-lipoic acid (LPA) has antioxidant actions and both LPA racemate (racLPA) and GLA treatments produced benefits in clinical neuropathy trials. The aims were to study LPA action on neurovascular function in diabetic rats and to investigate potential interactions for co-treatment with GLA and other essential fatty acids. After 6 weeks of diabetes, 2 weeks of racLPA treatment corrected 20% sciatic motor and 14% saphenous sensory NCV deficits. The ED50 for motor NCV restoration was approximately 38 mg kg(-1) day(-1). racLPA also corrected a 49% diabetic deficit in sciatic endoneurial blood flow. R and S-LPA enantiomers were equipotent in correcting NCV and blood flow deficits. Treatment of diabetic rats with low doses (20 mg kg(-1) day(-1)) of racLPA and GLA, while having modest effects on their own, showed evidence of marked synergistic action in joint treatment, completely correcting motor NCV and blood flow deficits. This was also noted for the novel compound, SOC0150, which contains equimolar proportions of LPA and GLA (ED50 9.3 mg kg(-1) day(-1), containing 3.5 mg LPA). NCV effects also showed marked synergism when racLPA:GLA ratios were varied over a 1:3-3:1 range. In contrast, a compound containing LPA and the n-3 component, docosahexaenoic acid, showed similar activity to LPA alone. Thus, LPA-GLA interactions yield drug combinations and compounds with an order of magnitude increase in efficacy against experimental diabetic neuropathy and are worthy of consideration for clinical trials.

Animals↗
PubMed1989

The essential fatty acid requirement for azoxymethane-induced intestinal carcinogenesis in rats.

The essential fatty acid requirement for the development of intestinal carcinogenesis was determined and compared to the overall essential fatty acid status of the animals as measured by the triene/tetraene ratio in the plasma, liver and colon. To induce tumors, male Sprague-Dawley rats were given two weekly injections (20 mg/kg body wt) of azoxymethane. Two weeks after the last injection, the rats were divided into groups of 25 and given one of six diets containing various levels of essential fatty acids (as linoleate). The diets contained 5% total fat and were prepared by mixing safflower oil (high essential fatty acids, beef fat (low essential fatty acids), and medium chain triglyceride oil (no essential fatty acids). One group of rats was fed a 20% beef fat diet. The range of essential fatty acids was from less than 0.03% to 1.28% (w/w). Twenty-six weeks after the first azoxymethane injection, the animals were killed and intestinal tumor incidence and multiplicity were determined. Samples of plasma, liver and colon were also taken for measurement of the triene/tetraene ratio by gas chromatography. Large bowel tumor incidence showed a dependence on the essential fatty acid content of the diet. The results were as follows: (percent essential fatty acids: percent tumor incidence) Group A (1.28: 72.4), Group B (0.60: 73.3), Group C (0.11: 55.2), Group D (0.08: 39.3), Group E (less than 0.03: 37.9) and Group F, which was fed 20% beef fat, (0.34: 88.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Possible compensation of structural and viscotropic properties in hepatic microsomes and erythrocyte membranes of rats with essential fatty acid deficiency.

The effect of essential fatty acid deficiency on the structural and dynamic properties of the lipid matrix of rat liver microsomes and erythrocyte membranes was studied. The rate and range of the rotational mobility of 1,6-diphenyl-1,3,5-hexatriene and 2-, 7-, and 12-(9-anthroyloxy)stearate probes in the native membranes and in lipid vesicles prepared with the total lipid extracts of these membranes were evaluated by using differential polarized phase fluorometry. For the anthroyloxystearate probes, two modes of rotation (in and out of the plane of the aromatic anthracene ring) were partially resolved by measuring at different excitation wavelengths. The fat-free diet produces important changes in the fatty acid composition of the different glycerophospholipid classes without affecting the total double-bond number, the relative contents of cholesterol, phospholipid, and protein, and the glycerophospholipid class distribution. The principal changes, more pronounced in liver microsomes than in erythrocytes, are: an increase in nonessential monoene and triene (18:1n-9 and 20:3n-9) and a decrease in essential diene (18:2n-6) and tetraene (20:4n-6). These changes modify the double-bond distribution as a function of the distance from the interphase toward the bilayer interior, with a significant deficit (15% in erythrocytes and 30% in liver microsomes) in the double-bond density in the intermediate region of the membrane leaflet, corresponding to the carbon number 11-12 of an extended saturated acyl chain, and where the 12-anthroyloxystearate probe is located. In spite of the changes in fatty acid composition and double-bond distribution, with the only exception of a slight increase (about 15%) in the "out of the plane" rotation rate of the 7-(9-anthroyloxy)stearate probe in the erythrocyte lipid vesicles, no other significant change is observed. Thus, the changes in fatty acid composition would take place in such a way that at least the average structural and viscotropic properties of the lipid phase of the membrane, sensed by these probes, would be almost exactly compensated.

Animals↗
PubMedDate not supplied

Essential fatty acid status in patients on long-term home parenteral nutrition.

BACKGROUND: Patients on total parenteral nutrition are known to be at risk of the development of essential fatty acid deficiency, presenting as a syndrome with scaly skin lesions and characterized by low plasma and erythrocyte linoleic acid concentrations. The essential fatty acid status of patients on long-term home parenteral nutrition who do have access to oral feeds has not been studied. METHODS: With the use of an isocratic high-performance liquid chromatography method, fatty acids were measured in the erythrocytes and plasma of 25 nonfasting patients on long-term home parenteral nutrition and the findings compared with those of 46 hospital outpatients not on nutrition support and five laboratory staff. RESULTS: Statistically significant differences in the two groups were limited to the erythrocytes. Linoleic acid was significantly lower (25.2 vs 40.7 mumol/10(6) red blood cells, p < .0001) and showed a significant correlation with triceps skinfold thickness (r = .52, p = .013). Palmitoleic and oleic acids were higher in patients than controls (10.8 vs 8.4 mumol/10(6) red blood cells, p = .009; 61.2 vs 51.7 mumol/10(6) red blood cells, p = .003). CONCLUSIONS: Despite IV linoleic acid administration, patients on long-term home parenteral nutrition have low erythrocyte stores of this essential fatty acid. This appears to be related to their low body fat stores. We suggest that they may be using much of the infused linoleic acid as an energy source and therefore are at risk of subclinical essential fatty acid deficiency.

Adolescent↗