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Fish & Shellfish Immunology Jun 2022Improving the immune ability and guiding healthy culture for sea cucumber by purposefully screening the significant differential metabolites when Apostichopus japonicus...
Improving the immune ability and guiding healthy culture for sea cucumber by purposefully screening the significant differential metabolites when Apostichopus japonicus (A. japonicus) is infected by pathogens is important. In this study, 35 types of significant differential metabolites appeared when A. japonicus were infected by Vibrio splendens (VSI group) compared with the control A. japonicus group (CK group) by using liquid chromatography-mass spectrometry (LC-MS/MS)-based untargeted metabolomics. Based on that finding, the 10 types of key metabolic pathways were analyzed by MetPA. The "arachidonic acid (ARA) metabolism" pathway, which was screened by three elevated biomarkers: ARA, prostaglandin F2α and 2-arachidonoyl glycerol, had an important impact on immune stress in A. japonicus. Due to the similar changes in several metabolites in its metabolic pathway, the ARA metabolic pathway was selected for further study. The activities of ACP, AKP and lysozyme, which are important innate immune-related enzymes, the survival rates of A. japonicus infected with V. splendidus and the relative content of ARA in the body wall detected by GC-MS were all upregulated significantly by exogenous daily 0.60% and 1.09% ARA consumption over a short period of approximately 7 days. These results demonstrated that ARA and its metabolic pathway indeed played important roles in the immunity of A. japonicus infected by the pathogen. The findings also provide novel insights for the effects of metabolites in A. japonicum healthy culture.
Topics: Animals; Arachidonic Acid; Chromatography, Liquid; Immunity, Innate; Stichopus; Tandem Mass Spectrometry; Vibrio
PubMed: 35561951
DOI: 10.1016/j.fsi.2022.05.012 -
Journal of Pharmacological Sciences 2011Arachidonic acid (ARA) and docosahexaenoic acid (DHA) are major constituents of cell membranes and play important roles in preserving physiological and psychological... (Review)
Review
Arachidonic acid (ARA) and docosahexaenoic acid (DHA) are major constituents of cell membranes and play important roles in preserving physiological and psychological function. Recently, data from several studies have indicated that impairments in long-term potentiation (LTP), the process underlying plasticity in synaptic connections, are associated with a decrease in membrane ARA and DHA in aged rats; and treatment of aged rats with either of these polyunsaturated fatty acids (PUFAs) reverses age-related decrease in LTP and the decrease in membrane fatty acid concentration. This review focuses on our recent findings concerning the effects of ARA and DHA on the age-related decline in the function of the brain and cardiovascular system. ARA supplementation decreased P300 latency and increased P300 amplitude of event-related potentials in healthy elderly men. Cognitive impairments in patients with mild cognitive impairment (MCI) and patients with organic brain lesions were significantly improved with ARA and DHA supplementation. ARA and DHA supplementation also increased coronary flow velocity reserve in elderly individuals; this suggests beneficial effects of PUFAs on coronary microcirculation. In conclusion, ARA and DHA may be beneficial in preventing and/or improving age-related declines in brain and cardiovascular system function.
Topics: Aged; Aging; Animals; Arachidonic Acid; Brain; Cardiovascular System; Cognition Disorders; Dietary Supplements; Docosahexaenoic Acids; Event-Related Potentials, P300; Food, Organic; Humans; Neuronal Plasticity
PubMed: 21436600
DOI: 10.1254/jphs.10r39fm -
Bipolar Disorders Apr 2004The treatment of affective disorders continues to present significant clinical challenges, notwithstanding the existence of available mood stabilizers and... (Review)
Review
The treatment of affective disorders continues to present significant clinical challenges, notwithstanding the existence of available mood stabilizers and antidepressants. These difficulties include incomplete response, relapse, and intolerable medication side effects. Fundamental to the therapeutic impasse is incomplete knowledge concerning the neurobiology of mood disorders. Although some relevant biochemical pathways have been identified, including abnormalities of monoamine neurotransmission and of immunological functioning, a fuller understanding is likely to embrace other interrelated pathways. Arachidonic acid (AA) and prostaglandins (PGs) are important second messengers in the central nervous system that participate in signal transduction, inflammation and other vital processes. Their release, turnover, and metabolism represent the 'arachidonic acid cascade'. A significant body of diverse clinical and preclinical research suggests that the AA cascade may be important in affective states. This paper reviews the literature describing the association of affective illness with AA and its metabolites. Possible links between this and other prevailing hypotheses are considered, and implications for further research and for treatment are discussed.
Topics: Arachidonic Acid; Cell Membrane; Fatty Acids, Essential; Humans; Mood Disorders; Nutritional Physiological Phenomena; Prostaglandins; Signal Transduction
PubMed: 15005747
DOI: 10.1046/j.1399-5618.2003.00094.x -
Neuroscience Dec 1994Arachidonic acid (20:4) is a component of membrane lipids that has been implicated as a messenger both in physiological and pathophysiological processes, including...
Arachidonic acid (20:4) is a component of membrane lipids that has been implicated as a messenger both in physiological and pathophysiological processes, including ischemic injury and synaptic plasticity. In order to clarify direct trophic or toxic effects of arachidonic acid on central neurons, primary cultures of rat hippocampal neurons were exposed to arachidonic acid under chemically-defined conditions. Arachidonic acid present in the culture medium at concentrations over 5 x 10(-6) M showed profound toxicity, whereas at lower concentrations (10(-6) M) it significantly supported the survival of hippocampal neurons. These effects were not mimicked by oleic acid (18:1) or palmitic acid (16:0). The toxic action of 10(-5) M arachidonic acid was markedly and significantly prevented by a lipoxygenase inhibitor nordihydroguaiaretic acid (10(-6) M). AA861 and baicalein (each at 10(-6) M), a selective inhibitor for 5- and 12-lipoxygenase, respectively, also showed a significant protective effect, whereas cyclooxygenase inhibitor indomethacin (10(-5) M) had no effect. The toxic action was also prevented by an antioxidant alpha-tocopherol (10(-6) M), but not by superoxide dismutase (100 U/ml) or catalase (200 U/ml). The trophic effect of 10(-6) M arachidonic acid was not suppressed by the treatments listed above. At lower concentrations (10(-7)-10(-6) M), arachidonic acid promoted neurite elongation, which was not inhibited by nordihydroguaiaretic acid or indomethacin. Overall, arachidonic acid has both trophic and toxic actions on cultured hippocampal neurons, part of which involves its metabolism by lipoxygenases. The mechanisms and the physiological significance of these effects are discussed.
Topics: Animals; Antioxidants; Arachidonic Acid; Cell Survival; Cells, Cultured; Culture Media; Cyclooxygenase Inhibitors; Fatty Acids; Free Radicals; Hippocampus; Lipoxygenase Inhibitors; Neurites; Neurons; Rats
PubMed: 7898670
DOI: 10.1016/0306-4522(94)90515-0 -
Biochimica Et Biophysica Acta.... Aug 2021The biogenesis of peroxisomes in relation to the trafficking of proteins to peroxisomes has been extensively examined. However, the supply of phospholipids, which is...
Clofibric acid increases molecular species of phosphatidylethanolamine containing arachidonic acid for biogenesis of peroxisomal membranes in peroxisome proliferation in the liver.
The biogenesis of peroxisomes in relation to the trafficking of proteins to peroxisomes has been extensively examined. However, the supply of phospholipids, which is needed to generate peroxisomal membranes in mammals, remains unclear. Therefore, we herein investigated metabolic alterations induced by clofibric acid, a peroxisome proliferator, in the synthesis of phospholipids, particularly phosphatidylethanolamine (PE) molecular species, and their relationship with the biogenesis of peroxisomal membranes. The subcutaneous administration of clofibric acid to rats at a relatively low dose (130 mg/kg) once a day time-dependently and gradually increased the integrated perimeter of peroxisomes per 100 μm hepatocyte cytoplasm (PA). A strong correlation was observed between the content (μmol/mg DNA) of PE containing arachidonic acid (20:4) and PA (r = 0.9168). Moreover, the content of PE containing octadecenoic acid (18:1) positively correlated with PA (r = 0.8094). The treatment with clofibric acid markedly accelerated the formation of 16:0-20:4 PE by increasing the production of 20:4 and the activity of acyl chain remodeling of pre-existing PE molecular species. Increases in the acyl chain remodeling of PE by clofibric acid were mainly linked to the up-regulated expression of the Lpcat3 gene. On the other hand, clofibric acid markedly increased the formation of palmitic acid (16:0)-18:1 PE through de novo synthesis. These results suggest that the enhanced formation of particular PE molecular species is related to increases in the mass of peroxisomal membranes in peroxisome proliferation in the liver.
Topics: Animals; Arachidonic Acid; Clofibric Acid; Intracellular Membranes; Liver; Male; Peroxisomes; Phosphatidylethanolamines; Rats; Rats, Wistar
PubMed: 33945875
DOI: 10.1016/j.bbalip.2021.158963 -
Biochemical Society Transactions Oct 2008Both stimulatory and detrimental effects of NEFAs (non-esterified fatty acids) on pancreatic beta-cells have been recognized. Acute exposure of the pancreatic beta-cell... (Review)
Review
Both stimulatory and detrimental effects of NEFAs (non-esterified fatty acids) on pancreatic beta-cells have been recognized. Acute exposure of the pancreatic beta-cell to high glucose concentrations and/or saturated NEFAs results in a substantial increase in insulin release, whereas chronic exposure results in desensitization and suppression of secretion followed by induction of apoptosis. Some unsaturated NEFAs also promote insulin release acutely, but they are less toxic to beta-cells during chronic exposure and can even exert positive protective effects. In the present review, we focus on exogenous and endogenous effects of NEFAs, including the polyunsaturated fatty acid, arachidonic acid (or its metabolites generated from cyclo-oxygenase activity), on beta-cell metabolism, and have explored the outcomes with respect to beta-cell insulin secretion.
Topics: Animals; Arachidonic Acid; Cell Line; Fatty Acids, Nonesterified; Glucose; Insulin; Insulin-Secreting Cells
PubMed: 18793168
DOI: 10.1042/BST0360955 -
Advances in Experimental Medicine and... 1996Epidemiologic evidence in humans and controlled trials in animal models indicate that total dietary fat increases the risk of cancer. The animal evidence indicates that... (Review)
Review
Epidemiologic evidence in humans and controlled trials in animal models indicate that total dietary fat increases the risk of cancer. The animal evidence indicates that the greatest efficacy in promoting carcinogenesis is achieved with omega-6 fatty acids with little or no effect from either the omega-3 or monounsaturated fatty acid families. Epidemiologic studies in humans indicate a positive association between meat intake and colon cancer, but a negative association with chicken and fish. There is also a negative association between non-steroidal anti-inflammatory drug (NSAID) intake and colon cancer. Red meat is a potentially significant source of dietary arachidonic acid, which is the primary substrate for the eicosanoids whose production is blocked by NSAIDs. Thus there is a positive association between carcinogenesis and dietary intake of both the omega-6 fatty acid precursor linoleic acid and its product arachidonic acid, and a negative association with use of a drug blocking its metabolism to eicosanoids. Another potentially important factor in arachidonate metabolism is variation in its endogenous distribution. We have recently reported abnormal distribution of arachidonic acid between lipid fractions in human obesity, and parallel abnormalities in animal models of genetic obesity. This implies a potential role for variation in the endogenous distribution of arachidonic acid in the etiology of cancers which have increased incidence in human obesity. This paper addresses the role of arachidonate intake, its endogenous production, and its distribution within lipid fractions in carcinogenesis.
Topics: Animals; Arachidonic Acid; Fatty Acids; Humans; Neoplasms; Obesity; Terminology as Topic
PubMed: 8937550
DOI: 10.1007/978-1-4613-1151-5_7 -
Journal of Obstetric, Gynecologic, and... 1992
Topics: Arachidonic Acid; Humans; Prostaglandins
PubMed: 1564589
DOI: No ID Found -
European Review For Medical and... Feb 2020The aim of this study is to understand whether the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to stress increases excessively with aging in...
OBJECTIVE
The aim of this study is to understand whether the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to stress increases excessively with aging in senescence-accelerated mice-prone 10 (SAMP10) and to investigate the role of arachidonic acid (ARA) in this process.
MATERIALS AND METHODS
The area under the curve of CORT concentration (CORT-AUC), an index of the HPA axis responsiveness to stress, was assessed in SAMP10 subjected to a 30-minute restraint stress up to 120 minutes after the restraint stress onset. Furthermore, the HPA axis responsiveness was evaluated in aged SAMP10 fed 0.4% ARA-containing diet (ARA group) or control diet (CON group) for 4 weeks. Three weeks later, these mice were divided into a group with a 30-minute restraint stress (CON-S or ARA-S group) and a group without restraint stress (CON-NS or ARA-NS group). Hippocampi were collected after stress release and fatty acid and glucocorticoid receptor (GR) protein levels were evaluated in the nucleus and cytosol.
RESULTS
The CORT-AUC of aged SAMP10 was 21% significantly higher than that of young SAMP10. In the ARA group, hippocampal ARA was 0.5% significantly higher than that in the CON group. CORT-AUC in the ARA group was 24% significantly lower than that in the CON group. The ratio of GR protein levels in the nucleus and cytosol in the ARA-S group was 1.72 times significantly higher than that in the ARA-NS group but no difference was observed between the CON-S and CON-NS groups.
CONCLUSIONS
Dietary ARA seems to suppress age-related excessive enhancement of the HPA axis responsiveness via attenuation of age-related decline in hippocampal GR translocation into the nucleus after stress loading, which may contribute to an improvement of mental health.
Topics: Aging; Animals; Arachidonic Acid; Dietary Supplements; Hypothalamo-Hypophyseal System; Mice; Pituitary-Adrenal System; Stress, Physiological
PubMed: 32141581
DOI: 10.26355/eurrev_202002_20391 -
Platelets 2019The use of arachidonic acid (AA) to stimulate platelets is considered as a specific approach to study aspirin treatment efficacy. However, very high concentrations of AA...
The use of arachidonic acid (AA) to stimulate platelets is considered as a specific approach to study aspirin treatment efficacy. However, very high concentrations of AA are used, and it has been previously reported that AA can induce cell lysis in other settings. Several clinical studies have reported decreased responses to AA in whole blood tests in the presence of clopidogrel. Our aim was to investigate whether unspecific effects contribute to AA-induced aggregation and platelet activation in light transmission aggregometry (LTA) in platelet-rich plasma (PRP), and in assays using whole blood, multiple electrode aggregometry (MEA, Multiplate®), and flow cytometry. We report that cell lysis, especially of red blood cells, does occur at concentrations of AA used in the clinical tests and that ADP is very important for the AA-induced platelet activation responses. In flow cytometry, very limited platelet activation was detected before reaching AA concentrations in the millimolar range, where cell lysis also occurred, making it problematic to develop a reliable flow cytometry assay using AA as reagent. We conclude that cell lysis and ADP release contribute to AA-induced platelet responses, most markedly in whole blood assays. This finding could potentially explain some differences between studies comparing methods using whole blood and PRP and also how clopidogrel treatment could influence AA-induced aggregation results in previously published studies. Our findings highlight some issues with AA as reagent for platelet activation, which also have an impact on how platelet activation assays using AA should be interpreted.
Topics: Arachidonic Acid; Blood Cells; Female; Humans; Male; Platelet Activation; Platelet Function Tests
PubMed: 30580677
DOI: 10.1080/09537104.2018.1557614