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Arachidonic Acid Food Sources and Recommendation for the Vegetarian
Abstract
Arachidonic acid (AA) is an omega-6 polyunsaturated fatty acid found in the phospholipids of the membranes of the human bodys cells, and is abundant in the brain, muscles, and liver. This fatty acid is particularly obtained from meat products including chicken, beef, pork, and fishes. An interesting source of AA is through its accumulation in a green microalga, Myrmecia incisa, enhanced by nitrogen starvation. The general functions of AA and its metabolites including its association with coronary heart disease, oxidative stress and cancer, metabolic syndrome, insulin resistance, and its endocrine response to stress are also discussed.
... 38 Another interesting food-related chemical identified by our method is Arachidonic acid(ARA), an omega-6 polyunsaturated fatty acid found in the phospholipids of the cell membranes and is abundant in the brain, muscles, and liver. 42 Arachidonic acid occurs in the animal source diet such as eggs, poultry, and meat. 43 This could explain and suggest a possible contributing factor to the increased incidence of asthma in western societies due to their consumption of such a pro-inflammatory diet and thus promoting the release of pro-inflammatory arachidonic acid metabolites (leukotrienes and prostanoids). ...
Background
: With the increasing incidence of asthma, more attention is focused on the diverse and complex nutritional and environmental triggers of asthma exacerbations. Currently, there are no established risk assessment tools to evaluate asthma triggering potentials of most of the nutritional and environmental triggers encountered by asthmatic patients.
Purpose
The objective of this study is to devise a reliable workflow, capable of estimating the toxicogenomic effect of such factors on key player genes in asthma pathogenesis.
Methods
Gene expression extracted from publicly available datasets of asthmatic bronchial epithelium were subjected to a comprehensive analysis of differential gene expression to identify significant genes involved in asthma development and progression. The identified genes were subjected to Gene Set Enrichment Analysis using a total of 31,826 gene sets related to chemical, toxins, and drugs to identify common agents that share similar asthma-related targets genes and signaling pathways.
Results
Our analysis identified 225 differentially expressed genes between severe asthmatic and healthy bronchial epithelium. Gene Set Enrichment Analysis of the identified genes showed that they are involved in response to toxic substances and organic cyclic compounds and are targeted by 41 specific diets, plants products, and plants related toxins (eg adenine, arachidonic acid, baicalein, caffeic acid, corilagin, curcumin, ellagic acid, luteolin, microcystin-RR, phytoestrogens, protoporphyrin IX, purpurogallin, rottlerin, and salazinic acid). Moreover, the identified chemicals share interesting inflammation-related pathways like NF-κB.
Conclusion
Our analysis was able to explain and predict the toxicity in terms of stimulating the differentially expressed genes between severe asthmatic and healthy epithelium. Such an approach can pave the way to generate a cost-effective and reliable source for asthma-specific toxigenic reports thus allowing the asthmatic patients, physicians, and medical researchers to be aware of the potential triggering factors with fatal consequences.
Eicosapentaenoic acid (EPA) and arachidonic acid (ARA) are long-chain polyun-saturated fatty acids (PUFAs) that play a significant role in human growth and development, which deficiency can trigger several metabolic-related diseases. Since the availability of PUFA sources is limited, there arises a need to explore alternative sources. Therefore, the present study aimed to investigate whether an Escherichia coli which are engineered with Δ5Des-Iso gene isolated from Isochrysis sp. could be utilized to synthesize PUFAs. Full-length gene Δ5Des-Iso (1149 bp) was isolated from Isochrysis sp. that encodes 382 amino acids and identified as Δ5-desatruase gene using different bioinformatic analysis. Heterolo-gous gene expression was carried out in E. coli having Δ5Des-Iso with precursor fatty acids. The Δ5Des-Iso produced novel fatty acids of EPA (ω-3) and ARA (ω-6) as respective products were identified by GC-MS. Gene expression and PUFA synthesis in E. coli were optimized by temperature, time, and concentrations of precursor fatty acid substrates. Δ5Des-Iso RNA transcript level was inversely proportional to the time and fatty acid synthesis. And, the significant production of EPA (4.1 mg/g) and ARA (8.3 mg/g) in total fatty acids was observed in E. coli grown at 37°C for 24 h with 25 μM of external fatty acid substrate as an optimum growth conditions. E. coli could be used as alternative organism to synthesis PUFAs and widely applicable in many nutraceuticals and pharmaceuticals industry for human use.
This study examined the effects of dietary saturated and polyunsaturated fat on the chemical composition and metabolism of low density lipoproteins (LDL) in eight normal male subjects. The influence of these diets on fecal sterol excretion was also measured in four of the subjects. When compared with the saturated fat diet, the polyunsaturated diet lowered both plasma cholesterol polyunsaturated diet lowered both plasma cholesterol (23%, P less than 0.001) and triglyceride (14%, P less than 0.001) levels. Sixty-seven percent of the reduction in the former lipid resulted from a fall in LDL cholesterol (23%, P less than 0.001), although very low density (VLDL) and high density lipoprotein (HDL) cholesterol levels also fell (by 27% and 20% of their respective control value). These changes were accompanied by significant alterations in LDL composition. Specifically, during polyunsaturated fat feeding, the relative percentage cholesterol in the LDL fraction fell while that of phospholipid rose. There was no change in the percentage protein or triglyceride. The fatty acid components of LDL triglyceride, cholesteryl esters, and phospholipid were also affected by dietary fat saturation level. Overall, polyunsaturated fat feeding produced an enrichment in linoleate with reciprocal changes in palmitate, stearate, and oleate which affected triglycerides more than cholesteryl esters and phospholipids. The above changes in LDL composition were associated with alterations in the metabolism of LDL apoprotein (apoLDL). The polyunsaturated deit lowered plasma apoLDL by 13% (P less than 0.05). This resulted from an increase in the fractional catabolic rate of LDL (whether determined by plasma decay curve analysis (P less than 0.05) or urine/plasma radioactivity ratios (P less than 0.001) without significant alteration of its corporeal distribution or synthetic rate. The polyunsaturated fat diet did not cause a consistent change in fecal neutral or acidic steroid excretion. We conclude that the hypocholesterolemic action of polyunsaturated fat diets is effected by multiple mechanisms whose expression may vary from patient to patient.
This study was conducted to determine the effects of arachidonic acid (AA) supplementation on human immune response (IR) and on the secretion of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4). Ten healthy men (20-38 yr) participated in the study and lived at the Metabolic Suite of the Western Human Nutrition Research Center. They were fed a basal diet (57, 27, and 16 energy percentage from carbohydrate, fat, and protein, respectively, and AA 200 mg/d) for the first 15 d of the study. Additional AA (1.5 g/d) was added to the diet of six men from day 16 to 65, while the remaining four subjects remained on the basal diet. The diets of the two groups were crossed-over from day 66 to 115. In vitro indices of IR were examined using blood drawn on days 15, 58, 65, 108, and 115. Influenza antibody titers were determined in the sera prepared from blood drawn on days 92 and 115 (23 d postimmunization). AA supplementation caused significant increases in the in vitro secretion of LTB4, and PGE2, but it did not alter the in vitro secretion of tumor necrosis factor alpha; interleukins 1 beta, 2, 6; and the receptor for interleukin 2. Nor did it change the number of circulating lymphocytes bearing markers for specific subsets (B, T, helper, suppressor, natural killer) and the serum antibody titers against influenza vaccine. The opposing effects of PGE2 and LTB4 may have led to the lack of change in immune functions tested.
ALTHOUGH the existence of essential fatty acids (EFA) has been known for 30 years, clinical interest in these dietary substances has been slight until recently. The possible relationship of EFA to the prevention or therapy of degenerative diseases such as atherosclerosis has projected these nutrients into the first rank of medical problems and interest. Unfortunately, there are many misconceptions regarding EFA. The lag between laboratory investigation and clinical application is great. It is the aim of this article to define a few terms, correct a few false impressions and provide some background on the subject, to indicate the current status and trend of research in EFA, and to attempt the difficult extrapolation from theory to practice.
The term "essential fatty acids" has been used in several different meanings since it was first used by Burr and Burr in 1929.1 They described a deficiency syndrome, caused by the rigid exclusion
Two normolipemic subjects, one mildly hyperlipemic subject, and two severely hyperlipemic subjects were fed diets of ordinary foods containing either 4 or 18% of calories as linoleic acid. During ingestion of the diet containing 4% of calories from linoleate, the content of palmitic acid was high and the content of oleic and linoleic acids lower in the plasma triglycerides of the hyperlipemic subjects as compared to the normolipemic individuals.
The ingestion of a diet containing 18% of calories from linoleate resulted in a fall in the concentration of all lipid classes in both normal and hyperlipemic subjects. An increase was noted in the percent of linoleic acid in all lipid fractions and a decrease was observed in the percent of arachidonic acid in the cholesterol ester and phospholipid fractions in both normal and hyperlipemic persons. The percentage of arachidonic acid was lower in the plasma cholesterol esters and phospholipids of the hyperlipemic individuals while consuming both diets.
In both the hyperlipemic and normolipemic individuals there were significant differences between the fasting and non-fasting nonchylomicron triglyceride fatty acid composition, the changes reflecting a shift toward the composition of the fat ingested. There were no significant differences, however, in the fatty acid composition of the cholesterol ester and phospholipid in fasted and nonfasted subjects. These results suggest that data reflecting the fasting fatty acid composition of the plasma cholesterol ester and phospholipid fractions can be obtained from nonfasting blood samples if chylomicrons are removed.
Evidence linking the beneficial effect of dietary polyunsaturated fat on systolic and distolic blood pressure is reported. Under controlled dietary conditions, i.e., when the polyunsaturated fat to saturate fat ratio (P/S) is maintained at about 1.0, with fat providing 25% of total energy intake, blood pressure is significantly lowered in healthy males and females in the 40- to 60-year age group. The subjects selected for these studies were either normotensive or mildly hypertensive. When the subjects resumed their usual diets, their blood pressures reverted to baseline values. Body weights of the subjects remained relatively constant in these studies, and sodium chloride intakes averaged 8 to 12 g per day. It is suggested that the lowering of blood pressure by dietary linoleic acid is mediated through prostaglandins.
Arachidonic acid (AA) is a precursor of eicosanoids, which influence human health and the in vitro activity of immune cells. We therefore examined the effects of dietary AA on the immune response (IR) of 10 healthy men living at our metabolic suite for 130 d. All subjects were fed a basal diet containing 27 energy percentage (en%) fat, 57 en% carbohydrate, and 16 en% protein (AA, 200 mg/d) for the first and last 15 d of the study. Additional AA (1.5 g/d) was incorporated into the diet of six men from day 16 to 65 while the remaining four subjects continued to eat the basal diet. The diets of the two groups were crossed-over from day 66 to 115. In vitro indexes of IR were examined using the blood samples drawn on days 15, 58, 65, 108, 115, and 127. The subjects were immunized with the measles/mumps/rubella vaccine on day 35 and with the influenza vaccine on day 92. Dietary AA did not influence many indexes of IR (peripheral blood mononuclear cell proliferation in response to phytohemagglutinin, Concanavalin A, pokeweed, measles/mumps/rubella, and influenza vaccines prior to immunization, and natural killer cell activity). The post-immunization proliferation in response to influenza vaccine was about fourfold higher in the group receiving high-AA diet compared to the group receiving low-AA diet (P = 0.02). Analysis of variance of the data pooled from both groups showed that the number of circulating granulocytes was significantly (P = 0.03) more when the subjects were fed the high-AA diet than when they were fed the low-AA diet. The small increases in granulocyte count and the in vitro proliferation in response to influenza vaccine caused by dietary AA may not be of clinical significance. However, the lack of any adverse effects on IR indicates that supplementation with AA may be done safely when needed for other health reasons.
Normal healthy male volunteers (n = 10) were fed diets (high-AA) containing 1.7 g/d of arachidonic acid (AA) for 50 d. The control (low-AA) diet contained 210 mg/d of AA. Dietary AA had no statistically significant effect on the blood cholesterol levels, lipoprotein distribution, or apoprotein levels. Adipose tissue fatty acid composition was not influenced by AA feeding. The plasma total fatty acid composition was markedly enriched in AA after 50 d (P < 0.005). The fatty acid composition of plasma lipid fractions, cholesterol esters, triglycerides, free fatty acids, and phospholipid (PL) showed marked differences in the degree of enrichment in AA. The PL plasma fraction from the subjects consuming the low-AA diet contained 10.3% AA while the subjects who consumed the high-AA diet had plasma PL fractions containing 19.0% AA. The level of 22:4n-6 also was different (0.67 to 1.06%) in the plasma PL fraction after 50 d of AA feeding. After consuming the high-AA diet, the total red blood cell fatty acid composition was significantly enriched in AA which mainly replaced linoleic acid. These results indicate that dietary AA is incorporated into tissue lipids, but selectively into different tissues and lipid classes. Perhaps more importantly, the results demonstrate that dietary AA does not alter blood lipids or lipoprotein levels or have obvious adverse health effects at this level and duration of feeding.
Animal studies showed that dietary flaxseed oil [rich in the n-3 polyunsaturated fatty acid alpha-linolenic acid (ALA)], evening primrose oil [rich in the n-6 polyunsaturated fatty acid gamma-linolenic acid (GLA)], and fish oil [rich in the long-chain n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] can decrease natural killer (NK) cell activity. There have been no studies of the effect on NK cell activity of adding these oils to the diet of humans.
Our objective was to determine the effect of dietary supplementation with oil blends rich in ALA, GLA, arachidonic acid (AA), DHA, or EPA plus DHA (fish oil) on the NK cell activity of human peripheral blood mononuclear cells.
A randomized, placebo-controlled, double-blind, parallel study was conducted. Healthy subjects aged 55-75 y consumed 9 capsules/d for 12 wk; the capsules contained placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA plus DHA. Subjects in these groups consumed 2 g ALA, 770 mg GLA, 680 mg AA, 720 mg DHA, or 1 g EPA plus DHA (720 mg EPA + 280 mg DHA) daily, respectively. Total fat intake from the capsules was 4 g/d.
The fatty acid composition of plasma phospholipids changed significantly in the GLA, AA, DHA, and fish oil groups. NK cell activity was not significantly affected by the placebo, ALA, GLA, AA, or DHA treatment. Fish oil caused a significant reduction (mean decline: 48%) in NK cell activity that was fully reversed by 4 wk after supplementation had ceased.
A moderate amount of EPA but not of other n-6 or n-3 polyunsaturated fatty acids can decrease NK cell activity in healthy subjects.