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PubMed1981

Osmotic fragility and fluidity of erythrocyte membranes from rats raised on an essential fatty acid deficient diet.

Erythrocyte membranes from rats raised on a diet with low content of essential fatty acids were studied by osmotic sensitivity tests and spin labeling techniques. This diet induced significant modifications in acylglycerophosphocholine fatty acid composition with regard to 16 : 1, 18 : 1, 18 : 2 (n-6), 20 : 3 (n-9), and 20 : 4 (n-6). No changes in membrane fluidity as monitored by spin label motion were found but the diet caused an increased osmotic sensitivity in essential fatty acid deficient erythrocytes. 50% hemolysis was obtained at a 51.0% dilution of saline with H2O as compared to a 57.0% dilution for the control material. Membrane fluidity was unaffected by gamma-irradiation up to 80 krad.

Animals↗
PubMed1996

Dietary essential fatty acid deficiency differentially affects tissues of rats.

Quantitative variations of polyunsaturated fatty acids (PUFA) were studied in various tissues: red blood cells (RBC), hepatic microsomes, kidney, skeletal muscle and heart of young rats fed either a control diet (n = 7) or an essential fatty acid (EFA)-deficient diet (n = 7). After 4 wk, the EFA-[deficient rats had significantly lower proportions of (n-6) and (n-3) fatty acids in RBC, hepatic microsomes and kidney than the control group. Paradoxically, normal proportions of arachidonic acid [20:4(n-6)] and 5,8,11,14,17-eicosapentaenoic acid [20:5(n-3)] were retained in heart and skeletal muscle despite generally lower proportions of the precursors, 18:2(n-6) and 18:3(n-3). Moreover, absolute levels of 20:4(n-6) and 20:5(n-3) in skeletal muscle of the EFA deficient group were significantly higher than in controls and 22:5(n-3) and 22:6(n-3) levels were comparable. This suggests that fatty acid proportions alone, without any consideration of long-chain polyunsaturated fatty acid quantities, may not reflect the (n-6) and (n-3) PUFA status of individual tissues. This study indicates that diet-[induced changes in the PUFA composition of RBC, which are often used in clinical investigations, do not fully reflect the changes in the fatty acid composition of organs, and that individual tissues respond differently to EFA deficiency. The conservation of proportional and absolute levels of 20:5(n-3) and 20:4(n-6), and the decrease in the more unsaturated homologues in the heart, suggest that this organ may avidly retain 20:5(n-3) and 20:4(n-6) in order to maintain eicosanoid production.

Animals↗
PubMed1996

The effect of essential fatty acids on growth and urokinase-type plasminogen activator production in human prostate DU-145 cells.

Urokinase-type plasminogen activator (uPA) is an important protease enzyme in carcinogenesis, and is involved in both invasion and metastasis of cancer. Increased uPA activity and decreased essential fatty acid (EFA) levels have been reported in cancer. This phenomenon may be explained by the fact that certain EFAs, such as gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA), inhibit uPA activity. The effect of EFA on human prostate DU-145 cell growth and uPA production is still unknown and was investigated in this study. Data obtained from the different unsaturated fatty acids showed that oleic acid (OA) and EPA enhanced DU-145 cell proliferation at 0.004 and 0.04 mM for up to 4 days. However, alpha-linolenic acid (ALA), linoleic acid (LA), GLA and arachidonic acid (AA) suppressed cell proliferation under the same conditions, possibly as a result of inhibition of DNA and protein synthesis as measured using labelled thymidine and glycine incorporation. In contrast to the cell proliferation, uPA production was inhibited by all the unsaturated fatty acids under investigation. Therefore, the absence of EFAs, as reported, may affect invasion and metastasis of cancer.

Cell Adhesion↗
PubMed1996

Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation.

There is now convincing evidence that membrane phospholipid metabolism is abnormal in schizophrenic patients. Our own studies, consistent with those of other research groups, have shown marked depletion of essential fatty acids, particularly arachidonic acid and docosahexanoic acid, in red blood cell membranes from schizophrenic patients relative to healthy control subjects. We also present preliminary evidence that similar abnormalities are present in first degree relatives of schizophrenic patients. Furthermore, it appears that changes in diet, which modify membrane levels of fatty acids, can have significant effects upon symptoms of schizophrenia and tardive dyskinesia (TD). Thus, we have found that schizophrenic patients who eat more (n-3) fatty acids in their normal diet have less severe symptoms. In a pilot study of (n-3) fatty acid supplementation we observed significant improvement in both schizophrenic symptoms and tardive dyskinesia over a 6 week period.

Arachidonic Acids↗
PubMed2000

Keloids in rural black South Africans. Part 1: general overview and essential fatty acid hypotheses for keloid formation and prevention.

In the first part of this study a general overview on the hypertrophic scar and keloid phenomena regarding history, epidemiology, histopathology and aetiology, in general, together with an essential fatty acid approach as basis for hypotheses of keloid formation and prevention are given. Upon reviewing the literature in planning a strategy for prevention and treatment of keloids, one encounters an overwhelming amount of hypotheses on this topic. Based on a preliminary study on total fatty acid compositions in keloids, compared with normal skin of keloid prone and non-keloid prone patients, there can be argued as follows: an essential fatty acid deficiency of precursors and inflammatory competitors for arachidonic acid may be a factor in the multifactorial aetiology of keloid formations, and apart from a local essential fatty acid deficiency in the wound area, nutrition may also be a contributing factor in rural black South Africans. To confirm or refute the stated hypotheses of the role of essential fatty acids in keloid formation and prevention (outlined in this part of the study), dietary questionnaires and blood (plasma and red blood cell) phospholipid analyses for general information and true fatty acid intake and metabolism, respectively, in the diets of these patients (outlined in part II of this study), as well as a lipid model for keloid formations regarding phospholipids, triglycerides, cholesterol esters and free fatty acids (outlined in part III of this study), are given. The purpose of this comprehensive fatty acid study was an attempt to assess the enigma surrounding keloids and to end the nightmare of the plastic and reconstructive surgeon, since these dermal tumours are notoriously recurrent.

Arachidonic Acid↗
PubMed1992

Effect of an essential fatty acid deficient diet on experimental infection with Trypanosoma cruzi in germfree and conventional mice.

1. To investigate the possible role of essential fatty acid deficiency in host cell/parasite interaction, weanling germfree (GF) and conventional (CV) CFW mice maintained on an essential fatty acid-deficient (-) or a control (+) diet for 110 days were infected with Trypanosoma cruzi. 2. Blood parasitemia indicated that the disease was milder in the animals maintained on the essential fatty acid-deficient diet than in the GF and CV controls (maximum parasitemia: GF+ 33,300, GF-26,200, CV+ 17,100 and CV- 6,400 trypomastigotes/ml blood). 3. Survival 30 days after infection was 12% for GF+, 28% for GF-, 37% for CV+ and 65% for CV- mice. 4. Linoleic and arachidonic acid levels were significantly lower in animals kept on the essential fatty acid-deficient diet (GF-: 28.0 +/- 9.3, 23.4 +/- 8.6; CV-: 37.6 +/- 5.8, 19.9 +/- 3.6) than in controls (GF+: 164.4 +/- 48.8, 162.6 +/- 45.8; CV+: 147.1 +/- 26.5, 107.5 +/- 23.6) confirming the deficiency. 5. Before the infection, succinic dehydrogenase levels were higher in liver of all CV mice (4.52 micrograms phosphate/mg fresh tissue) than in GF mice (0.84 micrograms phosphate/mg fresh tissue), whereas the opposite was true for 5'-nucleotidase levels in brain and liver, respectively (GF: 2.84 and 3.18 micrograms phosphate/mg fresh tissue; CV: 1.25 and 1.54 micrograms phosphate/mg fresh tissue). 6. The disease was milder in deficient than in control animals in both the GF and CV groups on the basis of parasitemia and survival, indicating that fatty acid-deficient mice are partially protected against Chagas' disease. The mechanism underlying this phenomenon requires further investigation.

5'-Nucleotidase↗
PubMed1999

Essential fatty acids and related molecular and cellular mechanisms in multiple sclerosis: new looks at old concepts.

Essential polyunsaturated fatty acids, their metabolism and their effects represent a ubiquitous system important for cellular membrane stability, for immunological and inflammatory regulations, for inter- and intracellular signalling. There are complex links to other regulatory and effector mechanisms - to the reactive oxygen species, nitric oxide and peroxynitrite anion, to eicosanoids and related compounds. The relation of polyunsaturated acids to multiple sclerosis was extensively discussed some time ago. Recently, a number of data placing these concepts in a new light have emerged, which are reviewed in the present article. The recent knowledge indicates that this topic deserves further attention in both the basic and the clinical research of multiple sclerosis.

Animals↗
PubMed1990

Effect of high doses of essential fatty acids on the postviral fatigue syndrome.

Sixty-three adults with the diagnosis of the postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study of essential fatty acid therapy. The patients had been ill for from one to three years after an apparently viral infection, suffering from severe fatigue, myalgia and a variety of psychiatric symptoms. The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids and either it, or the placebo, was given as 8 x 500 mg capsules per day over a 3-month period. The trial was parallel in design and patients were evaluated at entry, one month and three months. In consultation with the patient the doctors assessed overall condition, fatigue, myalgia, dizziness, poor concentration and depression on a 3-point scale. The essential fatty acid composition of their red cell membrane phospholipids was analysed at the first and last visits. At 1 month, 74% of patients on active treatment and 23% of those on placebo assessed themselves as improved over the baseline, with the improvement being much greater in the former. At 3 months the corresponding figures were 85% and 17% (p less than 0.0001) since the placebo group had reverted towards the baseline state while those in the active group showed continued improvement. The essential fatty acid levels were abnormal at the baseline and corrected by active treatment. There were no adverse events. We conclude that essential fatty acids provide a rational, safe and effective treatment for patients with the post-viral fatigue syndrome.

Adult↗
PubMed1980

Reduction of essential fatty acid deficiency in rat fed a low iron fat free diet.

Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron (FF+Fe). The relative levels of 16:1 and 18:1 to 18:0 in the total fatty acids of liver and other tissues (plasma, erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet, the levels of essential fatty acids (18:2 omega 6 + 20:4 omega 6) in tissues were 2- to 3-fold greater than in the corresponding tissues of rats fed the FF+Fe diet. Eicosatrienoic acid (20:3 omega 9) levels in tissue lipids from rats fed the FF+Fe diet were high (8-16%), whereas they were low (2-5%) in the case of animals fed the FF-Fe diet. The proportion of 20:4 in total fatty acids of tissues was 2- to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels of 20:3 omega 9/20:4 omega 6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2-0.3 in animals fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16:1, 18:1, 20:3 and 20:4 and the metabolism of 20:4.

Animals↗