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The effects of chronic administration of ethanol on synaptosomal fatty acid composition: modulation by oil enriched with gamma-linolenic acid.

Chronic ethanol administration significantly decreased the percentage of arachidonate and significantly increased the linoleate: arachidonate ratio in the cortical synaptosomal phosphatidylinositol (PI) of rats. However, concomitant administration of evening primrose oil (rich in gamma-linolenic acid) reversed the effects seen with ethanol alone. These results suggest that the decrease of arachidonate, especially in PI, caused by chronic administration of ethanol may be overcome by systemic administration of gamma-linolenic acid.

Alcoholism↗

Trans-10,cis-12 conjugated linoleic acid suppresses the desaturation of linoleic and alpha-linolenic acids in HepG2 cells.

The objective of this study was to determine the effects of cis-9,trans-11 and trans-10,cis-12 CLA on the fatty acid desaturation in a human hepatoma cell line, HepG2. Therefore, experiments were conducted in which HepG2 cells were incubated with various concentrations of those fatty acids and the concentrations of fatty acids in various lipid fractions of HepG2 cells were determined. In the presence of linoleic acid as substrate, cells treated with 25 micromol/L of trans-10,cis-12 CLA had lower ratios of dihomo-gamma-linoleic acid to linoleic acid and of arachidonic acid to linoleic acid in phospholipids than control cells; with alpha-linolenic acid as substrate, they had a lower ratio of eicosapentaenoic acid to alpha-linolenic acid in phospholipids than control cells. Cells treated with cis-9,trans-11 CLA did not differ in these ratios from control cells. Cells treated with trans-10,cis-12 CLA had also a markedly lower ratio of monounsaturated fatty acids (MUFA) to saturated fatty acids (SFA) in lipids than control cells; cells treated with cis-9,trans-11 CLA had a slightly lower MUFA:SFA ratio than control cells. These findings suggest that trans-10,cis-12 CLA suppresses Delta9-, Delta6- and Delta5-desaturation in HepG2 cells; cis-9,trans-11 CLA slightly reduces Delta9-desaturation but does not inhibit Delta6- and Delta5-desaturation. Moreover, HepG2 cells treated with 100 micromol/L of trans-10,cis-12 CLA released larger amounts of 6-keto-prostaglandin F(1alpha) and prostaglandin F(2alpha) than control cells. Treatment of cells with cis-9,trans-11 CLA did not alter the release of these eicosanoids compared with control cells. In conclusion, this study suggests that trans-10,cis-12 CLA has significant effects on the metabolism of essential fatty acids in HepG2 cells, whereas cis-9, trans-11 CLA does not have any effect in this respect.

Eicosanoids↗

The effect of gamma-linolenic acid on plasma and membrane lipids and renal prostaglandin synthesis in older subjects.

UNLABELLED: Senescence is associated with a decreased activity of enzyme delta-6 desaturase, which converts linoleic acid to gamma-linolenic acid. This enzymatic defect may alter the composition of plasma and membrane lipids, and influences the biosynthesis of renal prostaglandins. Exogenous supplementation of GLA during 3 months increases the plasma level of dihomo-gamma-linolenic acid (p < 0.002), and to a smaller degree, the level in erythrocyte membrane lipids. This treatment was associated with a beneficial reduction of cardiovascular risk factors (arterial hypertension, total cholesterol, apolipoprotein B, HDL-cholesterol, apolipoprotein A-I) and the renal function has become stable reached. Epogam treatment also increased the biosynthesis of renal prostaglandins, especially that of prostaglandin E2, which has a vasodilatory effect on vessel walls and reduces the elevated blood pressure. CONCLUSION: Dietary supplementation of essential fatty acids such as gamma-linolenic acid to old subjects has beneficial effect on their health condition. (Tab. 6, Fig. 5, Ref. 37.)

Aged↗

Accretion of n-3 fatty acids in the brain and retina of chicks fed a low-linolenic acid diet supplemented with docosahexaenoic acid.

Diets low in alpha-linolenic acid may not support normal brain accretion of n-3 fatty acids. An n-3 fatty acid-deficient diet was fed to laying hens and the resulting deficient chicks were fed a low-linolenic acid diet based on corn oil, or the same diet supplemented with docosahexaenoic acid. Control chicks from soybean oil-fed hens were fed a soybean oil-based diet. The fatty acid composition of the chick brains, retinas, livers, and serum was determined after 0-4 wk. The corn oil diet did not reverse the deficiency but the combination of corn oil and docosahexaenoic acid rapidly restored brain and retinal concentrations of docosahexaenoic acid. Supplemented chicks, however, showed a slight lowering of arachidonic acid in the brain and serum. This study demonstrates that a low-linolenic acid diet without docosahexaenoic acid fails to support accretion of n-3 fatty acids in the nervous tissue of chicks.

Animals↗

Effect of alpha-linolenic acid in the human diet on linoleic acid metabolism and prostaglandin biosynthesis.

The effect of dietary alpha-linolenic acid intake on linoleic acid metabolism and prostaglandin (PG) biosynthesis was investigated in two groups of six healthy females (25-32 yr). They were given isocaloric formula diets (FD) containing linoleic acid at a constant intake (4% of calories), with different amounts of alpha-linolenic acid: 0% (FD4/0), 4% (FD4/4), 8% (FD4/8) (group I) and 12% (FD4/12) or 16% (FD4/16) (group II); the diets were given for 2 weeks each. Comparing diet FD4/0 to FD4/16, enrichment of alpha-linolenic acid was greatest in cholesteryl esters (+6.8% in plasma, +7.1% in low density lipoproteins (LDL), +5.9% in high density lipoproteins (HDL)), less in phosphatidylcholine (+2.5% in plasma, +2.9% in LDL, +2.7% in HDL), and least in platelet lipids (+0.7%). The accumulation of alpha-linolenic acid was compensated by a decrease of oleic acid. Eicosapentaenoic acid (EPA), which was excluded from the diet, increased in all plasma lipids with augmented alpha-linolenic acid intake, indicating a chain elongation and desaturation of alpha-linolenic acid to EPA. However, even at the end of FD4/16, EPA was less than 2% of total fatty acids in all plasma lipids. Plasma linoleic acid levels were constant during all dietary regimes, according to the constant dietary intake of this fatty acid. No replacement of linoleic acid by alpha-linolenic acid could be observed. The percentage of arachidonic acid in all lipids was unaffected by alpha-linolenic acid intake. As arachidonic acid was not provided by the diet, it can be concluded that alpha-linolenic acid does not inhibit chain elongation and desaturation of linoleic acid to arachidonic acid in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Intake and sources of alpha-linolenic acid in Dutch elderly men.

OBJECTIVE: Intake of alpha-linolenic acid may have a beneficial effect on coronary heart disease, but little information is available on the intake and sources of alpha-linolenic acid (C18:3 n-3) in populations. We therefore assessed intake and sources of alpha-linolenic acid in Dutch elderly men. DESIGN AND SUBJECTS: Dietary histories were obtained from participants of the Zutphen Elderly Study, a Dutch cohort study. Food consumption data were available from 876 men in 1985 and from 541 of the same men in 1990. Daily intakes of alpha-linolenic acid were assessed using a food table developed for this purpose. Alpha-linolenic acid content of edible fats, seafood and some commonly eaten dishes were mainly derived from chemical analyses of Dutch foods, and other values were obtained from published food tables. RESULTS: Alpha-linolenic acid provided 0.5 +/- 0.1% of energy intake (mean +/- s.d.) or 1.30 +/- 0.46 g/day in 1985, and 1.21 +/- 0.52 g/day in 1990. The Pearson correlation coefficient for intake of alpha-linolenic acid in 1985 and 1990 was 0.34. Margarines were the main source (25.4%), followed by meat and the fats used in cooking meat (10.8%), bread (9.8%) and vegetables (7.8%). CONCLUSIONS: An increase in intake of alpha-linolenic acid, is most easily realized by the use of unhydrogenated oils rich in alpha-linolenic acid such as rapeseed and soybean oil, and of margarines and other fats containing such oils.

Aged↗

High-performance liquid chromatography as a tool for identification of linolenic acid hydroperoxide prepared with soybean lipoxygenase.

Linolenic acid hydroperoxide, enzymatically produced by soybean lipoxygenase from linolenic acid, was purified by high-performance liquid chromatography (HPLC) using a Supelco LC-8 (5 microns), 22 cm X 4.6 mm I.D. column with a solvent system of acetonitrile-tetrahydrofuran-0.1% phosphoric acid (50.4:21.6:28, v/v/v). The hydroperoxide was converted to several derivatives, the hydroxy, methyl, and stearate which were analyzed by HPLC and identified by gas chromatography-mass spectrometry. The 13-hydroperoxy linolenic acid was the major hydroperoxide produced by soybean lipoxygenase.

Chromatography, High Pressure Liquid↗

Effects of eicosapentaenoic and gamma-linolenic acid on lung permeability and alveolar macrophage eicosanoid synthesis in endotoxic rats.

OBJECTIVES: Proinflammatory eicosanoids (cyclooxgenase and lipoxygenase metabolites of arachidonic acid) released by alveolar macrophages play an important role in endotoxin-induced acute lung injury. We investigated the effect of prefeeding rats for 21 days with enteral diets that provided the anti-inflammatory fatty acids, eicosapentaenoic acid and gamma-linolenic acid (derived from fish oil and borage oil, respectively), as compared with an n-6 fatty acid-enriched diet (corn oil) on the following: a) lung microvascular protein permeability, arterial blood pressure, and platelet and white blood cells in a model of endotoxin-induced acute lung injury; b) alveolar macrophage prostaglandin and leukotriene synthesis; and c) liver and alveolar macrophage phospholipid fatty acid composition. DESIGN: Prospective, randomized, controlled, double-blind study. SETTING: Research laboratory at a university medical center. SUBJECTS: Male Long-Evans rats, weighing 250 g. INTERVENTIONS: Rats were randomized into four dietary treatment groups and fed nutritionally complete diets (300 kcal/kg/day), containing 55.2% of the total calories from fat with either 97% corn oil, 20% fish oil, 20% fish and 5% borage oil, or 20% fish and 20% borage oil for 21 days. On day 22, lung microvascular protein permeability, mean arterial pressure, and platelet and white blood cell counts were determined for 2 hrs after an intravenous injection of Salmonella enteritidis endotoxin (10 mg/kg). In a second group of prefed rats, the phospholipid fatty acid composition was determined in liver and alveolar macrophages. Alveolar macrophages were harvested by bronchoalveolar lavage and stimulated in vitro with a calcium ionophore (A23187), and the concentrations of leukotrienes B4 and B5, thromboxane A2, prostaglandin E2, and 6-keto-prostaglandin F1 alpha were measured in a third group of prefed rats. MEASUREMENT AND MAIN RESULTS: Lung permeability was greatest with corn oil and was significantly attenuated with 20% fish oil and 20% fish and 5% borage oil, and this effect approached significance with 20% fish and 20% borage oil (p = .06). The early and late hypotensive effects of endotoxin were attenuated with 20% fish oil, 20% fish and 5% borage oil, and 20% fish and 20% borage oil, as compared with corn oil. Concentrations of leukotriene B4, prostaglandin E2, and thromboxane B2 released from A23187-stimulated alveolar macrophages were significantly lower with 20% fish oil and 20% fish and 20% borage oil, as compared with corn oil. The increase in lung microvascular protein permeability with 20% fish and 20% borage oil was not significantly different than the lung microvascular protein permeability that was found in animals receiving 20% fish oil (p = .20) and 20% fish and 5% borage oil (p = .31). Alveolar macrophage and liver phospholipid concentrations of arachidonic acid were lower, and the concentrations of eicosapentaenoic acid and docosahexaenic acid were higher, with 20% fish oil, and 5% borage oil, and 20% fish and 20% borage oil, as compared with corn oil. Dihomo-gamma-linolenic acid, the desaturated and elongated intermediate of gamma-linolenic acid, was increased with 20% fish and 20% borage oil, as compared with 20% fish oil and 20% fish and 5% borage oil. CONCLUSIONS: The severity of pulmonary microvascular protein permeability and the degree of hypotension were reduced with fish or fish and borage oil diets, as compared with corn oil, in endotoxic rats. The reduced synthesis of the proinflammatory arachidonic acid-derived mediators, leukotriene B4, thromboxane B2, and prostaglandin E2 from stimulated alveolar macrophages was indicative of a decrease in arachidonic acid and an increase in eicosapentaenoic acid and docosahexaenoic acid in cell membrane phospholipids.

Animals↗

Effect of intravenous lipid emulsions enriched with gamma-linolenic acid on plasma n-6 fatty acids and prostaglandin biosynthesis after burn and endotoxin injury in rats.

OBJECTIVE: To study the effect of intravenous lipid emulsions enriched with gamma-linolenic acid on plasma fatty acids and series-2 prostaglandins to determine if the slow conversion of linoleic acid by delta-6-desaturase to gamma-linolenic acid could be bypassed to provide substrate for the formation of dihomo-gamma-linolenic acid, the immediate precursor for series-1 prostaglandins, in control and injured rats. Dihomo-gamma-linolenic acid can also compete with arachidonic acid for oxidative metabolism by cyclooxygenase to modulate series-2 prostaglandin biosynthesis. DESIGN: Prospective, randomized, controlled, double-blind study. SETTING: Research laboratory at a university medical center. SUBJECTS: Thirty-three control and thirty-one injured male Sprague-Dawley rats were randomized into one of four parenteral dietary treatment groups. INTERVENTIONS: Rats were injured by the combined actions of a 30% body surface area full-thickness skin burn and a nonlethal injection of endotoxin (1 mg/kg ip). The rats were parenterally fed 200 kcal/kg/day, 1.5 g nitrogen/kg/day, and 30% of nonprotein calories as lipid (20% soybean lipid emulsion enriched with 2.7%, 4.4%, or 6.1% gamma-linolenic acid derived from borage oil) for 3 days. Control rats were treated similarly but were not injured. A 20% soybean/safflower oil lipid emulsion was used as the control diet (0% gamma-linolenic acid). Plasma was analyzed on day 3 to determine the concentrations of total fatty acids, thromboxane B2, 6-keto-prostaglandin F1 alpha, and bicyclo-prostaglandin E. MEASUREMENTS AND MAIN RESULTS: Parenteral nutrition with 2.7%, 4.4%, and 6.1% gamma-linolenic acid increased the plasma percentages (mol%) of gamma-linolenic acid and dihomo-gamma-linolenic acid in a dose-dependent fashion in control and injured rats. Supplementation with gamma-linolenic acid did not increase the plasma percentage of arachidonic acid as compared with the 0% gamma-linolenic acid lipid emulsion in control and injured rats. The ratio of dihomo-gamma-linolenic acid to arachidonic acid was significantly increased in response to 4.4% and 6.1% gamma-linolenic acid in both the control and injured groups. The plasma ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha was substantially reduced with gamma-linolenic acid compared with 0% gamma-linolenic acid in injured rats. Bicyclo-prostaglandin E concentration was significantly higher with 2.7% gamma-linolenic acid in injured rats. Injured rats were protein catabolic, as evidenced by a net negative nitrogen balance and loss of body mass compared with controls, but neither group showed overt signs of intolerance to the diets. CONCLUSIONS: Supplementation of parenteral nutrition with gamma-linolenic acid had the following effects: a) increased plasma gamma-linolenic acid, dihomo-gamma-linolenic acid, and bicyclo-prostaglandin E; b) increased the plasma ratio of dihomo-gamma-linolenic acid to arachidonic acid; and c) favorably reduced the ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha in injured rats. These results reflect the potential capacity of gamma-linolenic acid-enriched lipid emulsions to have the following actions: a) to increase dihomo-gamma-linolenic acid, which is the fatty acid precursor of the antiaggregatory, anti-inflammatory eicosanoid, prostaglandin E1; and b) to modulate arachidonic acid-derived series-2 prostaglandins after injury.

Analysis of Variance↗

Safflower petals: a source of gamma linolenic acid.

Safflower petals have been shown to have a lot of medicinal and therapeutic values. Indian safflower petal samples were analyzed for the red pigment carthamin, protein and oil contents. The petal oil (4.0-5.8%) was further analyzed for its fatty acids followed by alpha linolenic acid (15-19%) and palmitic acids (14-16%). Gamma linolenic acid, which has a lot of therapeutic value was present to an extent of 2-3%; decanoic and dodecanoic acids (2-5%) were also present.

Fatty Acids↗

Modification of the dopaminergic neurotransmitters in striatum, frontal cortex and hippocampus of rats fed for 21 months with trans isomers of alpha-linolenic acid.

Deficiency in n-3 fatty acids is known to disturb the release of dopaminergic neurotransmitters in rat brain. Since isomerization reduces the bioavailability of dietary fatty acids, the effect of the conversion of alpha-linolenic acid into trans alpha-linolenic acid on the dopaminergic neurotransmission was studied. Rats were fed for 21 months with a control diet, a diet unbalanced in cis alpha-linolenic acid and containing trans alpha-linolenic acid or the same diet in which the imbalance was corrected by increasing the levels of cis alpha-linolenic acid. After 6 and 21 months of diet, the fatty acid composition and the amounts of endogenous dopaminergic neurotransmitters was assessed in the striatum, the frontal cortex and the hippocampus. The isomerization of a part of dietary alpha-linolenic acid induced some modifications of the levels of endogenous dopaminergic neurotransmitters in all brain areas but was related to a very low incorporation of trans polyunsaturated fatty acids. Increasing the dietary levels of cis alpha-linolenic acid succeeded in correcting the endogenous neurotransmitter concentrations only in the frontal cortex but not in the striatum and the hippocampus. Thus, the levels of dopamine were lowered by 95% in the hippocampus. These results suggest that in addition to the imbalance generated by their presence, trans fatty acids may directly act on the concentration of dopaminergic neurotransmitters.

3,4-Dihydroxyphenylacetic Acid↗

Alpha-linolenic acid deficiency in man: effect of ethyl linolenate on plasma and erythrocyte fatty acid composition and biosynthesis of prostanoids.

Treatment of human alpha-linolenic acid deficiency (ALAD) with ethyl linolenate is reported. The patient's scaly dermatitis nearly disappeared after 5-d supplementation with 0.1 mL ethyl linolenate. Pretreatment content of various n-3 fatty acids in RBC was 0-15% of healthy controls. After 14 d of supplementation, cholesterol and triglycerides were reduced by 70% of pretreatment values, 22:5n-3 and 22:6n-3 increased three- to fourfold while 18:3n-3 and 20:5n-3 remained low, indicating a rapid elongation and desaturation of 18:3n-3 in ALAD. Urinary excretion of PGI2-M was approximately 10 times higher than in healthy control subjects, while PGI3-M excretion was low. Linolenate supplementation increased PGI2-M excretion twofold, while PGI3-M remained near detection limit. Platelet capacity to synthesize TXA2, and urinary excretion of TXB2+3-M were nearly unaffected by supplementation. The results confirm that the minimal daily requirement of alpha-linolenic acid is 0.2-0.3% of total energy.

Aged↗

Rat vitamin E status and heart lipid peroxidation: effect of dietary alpha-linolenic acid and marine n-3 fatty acids.

Three groups of sixteen male rats each were fed semi-purified diets containing 15% by weight of lipid for a period of 4 wk. The diets contained the same amount of polyunsaturated fatty acids (PUFA) (20% of total fatty acids) and saturated fatty acids (19% of total fatty acids). Dietary PUFA were represented exclusively by linoleic acid (18:2 diet), or 10% linoleic acid and 10% linolenic acid (18:3 diet), or 10% linoleic acid and 10% long-chain n-3 fatty acids (LCn-3 diet). The overall amount of vitamin E was similar in the three diets, i.e., 140, 133 and 129 mg/kg diet, respectively. Following appropriate extraction, tocopherol levels in heart, liver, brain, adipose tissue (AT) and plasma were measured by high-performance liquid chromatography. The level of vitamin E in the heart decreased with n-3 PUFA diets, most markedly with LCn-3 PUFA. Liver and AT vitamin E contents also decreased with n-3 PUFA diets when expressed as micrograms/mg total lipids and micrograms/mg phospholipids, respectively. Total plasma vitamin E was lower in rats fed the LCn-3 diet, but there was no significant difference when expressed as microgram/mg total lipids. Brain vitamin E was not affected by the various diets. In vitro cardiac lipid peroxidation was quantified by the thiobarbituric acid reactive substances (TBARS) test. Heart homogenates were incubated at 37 degrees C for 15 and 30 min in both the absence (uninduced) or presence (induced) of a free radical generating system (1 mM xanthine, 0.1 IU per mL xanthine oxidase, 0.2 mM/0.4 mM Fe/ethylenediaminetetraacetic acid). TBARS release was time-independent but significantly higher when LCn-3 fatty acids were fed to rats in either the uninduced or induced system. The study demonstrated that n-3 PUFA diets can influence vitamin E status of rats even in short-term experiments and can change the susceptibility of the heart to in vitro lipid peroxidation.

Adipose Tissue↗

[Antitumor effects of alpha-linolenic acid on the human tumor transplanted in nude mice and on the metastasis of Vx-7 tumor in rabbit].

Many epidemiological studies and laboratory experimentations have shown that dietary omega-6 fatty acids stimulate and omega-3 fatty acids suppress tumorigenesis. On the other hand, some reports presented that parenteral administrations of unsaturated free fatty acids such as oleic, linoleic and linolenic acids inhibited the growth of a transplantable syngeneic tumor in mice. In this report, I examined the effect of alpha-linolenic acid on the growth of 17 lines of human tumor transplanted in nude mice and on the metastasis of Vx-7 tumor transplanted in rabbits. When alpha-linolenic acid was emulsified with HCO-60 and subcutaneously injected in the peripheral region of the transplanted tumor, complete cure rates for MKN-1, MKN-28, NOC-S and PL-14 human tumors were 100, 57, 25 and 75% respectively at a dose of 250 mg/kg/day for four days once a day, although it was not effective on GCH-nu and SKG-III. Using other tumor lines, T/C ratios of the transplanted tumor weight on day 31 were 4% for Taneda, 34% for Lx-1, 47% for Li-7, 31% for Sk-14, 49% for Kuronuma and 16% for Sawayama. When alpha-linolenic acid was intermittently injected in the same manner on day 3, 13, 17 and 24, T/C ratios of tumor weight were 24% for ALL, 34% for Taneda, 23% for Lx-1, 50% for Li-7, 47% for Sk-14 and 54% for Kuronuma. Mammary tumor line (Mx-1) did not respond to administrations of alpha-linolenic acid. Rabbit Vx-7 tumor cells transplanted via lympho-duct were trapped in lymphonodi to metastasize to other organs. When alpha-linolenic acid mixed with Lipiodol was injected once via lympho-duct on day 8 after tumor transplantation at a dose of 250 mg/kg, the tumor growth was reduced in lymphonodi poplitei to 14%, and thus highly inhibited the metastasis of tumor cells to lung.

Animals↗