No abstract available.
Animals ; Arachidonic Acid* ; Macrophages, Alveolar* ; Rats*

Three new fungal species of the genus Mortierella, Mortierella zychae, Mortierella ambigua, and Mortierella indohii, have been reported in Korea. The fungi were encountered during a study on the fungal community of soil samples collected from different locations in Korea. The species were identified based on molecular and morphological analyses. This study presents detailed descriptions of the morphological observations and molecular phylogenetic analysis of these three fungi. All three species were found to be sensitive to triphenyltetrazolium chloride staining. M. zychae demonstrated the highest intensity of mycelial staining, indicating that this species has the highest potential to produce arachidonic acid of the three species. The staining results indicated that the newly recorded species could potentially be useful for arachidonic acid production.
Arachidonic Acid ; Fungi ; Korea* ; Mortierella* ; Soil*

Arachidonic acids (AA) widely exist in multiple organs and can be metabolized into small lipid molecules with strong biological functions through several pathways. Among them, epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE), which are produced by cytochrome P450 enzymes, have attracted a lot of attentions, especially in vascular homeostasis. The regulation of vascular function is the foundation of vascular homeostasis, which is mainly achieved by manipulating the vascular structure and biological function. In the past 30 years, the roles of EETs and 20-HETE in the regulation of vascular function have been widely explored. In this review, we discussed the effects of EETs and 20-HETE on angiogenesis and vascular inflammation, respectively. Generally, EETs can dilate blood vessels and inhibit vascular inflammation, while 20-HETE can induce vasoconstriction and vascular inflammation. Interestingly, both EETs and 20-HETE can promote angiogenesis. In addition, the roles of EETs and 20-HETE in several vascular diseases, such as hypertension and cardiac ischemia, were discussed. Finally, the therapeutic perspectives of EETs and 20-HETE for vascular diseases were also summarized.
Arachidonic Acid ; Arachidonic Acids ; Cytochrome P-450 Enzyme System ; Humans ; Hydroxyeicosatetraenoic Acids ; Hypertension ; Vasoconstriction

This study investigated the effects of the methanol extracts of Morinda citrifolia containing numerous anthraquinone and iridoid on phospholipase A2 (PLA2) isozyme. PLA2 activity was measured using various PLA2 substrates, including 10-pyrene phosphatidylcholine, 1-palmitoyl-2-[14C]arachidonyl phosphatidylcholine ([14C]AA-PC), and [3H]arachidonic acid (AA). The methanol extracts suppressed melittin-induced [3H]AA release in a concentration-dependent manner in RAW 264.7 cells, and inhibited cPLA2/sPLA2-induced hydrolysis of [14C]AA-PC in a concentration- and time-dependent manner. A Dixon plot showed that the inhibition by methanol extracts on cPLA2 and sPLA2 appeared to be competitive with inhibition constants (Ki ) of 3.7microgram/ml and 12.6microgram/ml, respectively. These data suggest that methanol extracts of Morinda citrifolia inhibits both Ca2+-dependent PLA2 such as, cPLA2 and sPLA2. Therefore, Morinda citrifolia may possess anti-inflammatory activity secondary to Ca2+-dependent PLA2 inhibition.
Arachidonic Acid ; Cytosol ; Hydrolysis ; Methanol ; Morinda ; Phosphatidylcholines ; Phospholipases ; Phospholipases A2

No abstract available.
Arachidonic Acid* ; Ear, Middle* ; Humans* ; Otitis Media with Effusion*

BACKGROUND: To investigate the effect of manganese on lipid peroxidation and compositional changes of fatty acids in hippocampus of rat brain. METHODS: Seven rats in experimental group were given with MnCl2 intraperitoneally for 4 weeks (4 mg/kg once daily, 5 days per week). Twenty four hours after the last injection, rats were decapitated and, hippocampus were separated from the rat brain. RESULT: In Mn-treated group, manganese concentrations increased significantly in the hippocampus by 222% compared with control group (P<0.01). MDA concentrations increased significantly by 149% compared with control group (P<0.05). Among fatty acids, total n-6 polyunsaturated fatty acids (PUFAs) increased significantly by 237% compared with control group (P<0.05). Linoleic acid (LA) and arachidonic acids (AA) increased by 213%, 238% (P<0.05, P<0.01, respectively). Among n-3 PUFAs except linolenic acids, eicosapentanoic acid(EPA) and docosahexanoic acids (DHA) decreased significantly by 70%, 50% respectively compared with control group (both P<0.01). CONCLUSION: Our results suggest that manganese may cause compositional changes of fatty acids in hippocampus of rat brain. Characteristics of fatty acids compositional changes by manganese were the decrease of EPAs and DHAs (n-3 PUFAs), and increase of AA and LA (n-6 PUFAs). These changes with the increase of MDA, suggest that manganese neurotoxicity is caused by lipid peroxidation.
alpha-Linolenic Acid ; Animals ; Arachidonic Acid ; Arachidonic Acids ; Brain* ; Fatty Acids* ; Fatty Acids, Omega-3 ; Fatty Acids, Unsaturated ; Hippocampus* ; Linoleic Acid ; Linolenic Acids ; Lipid Peroxidation* ; Malondialdehyde ; Manganese* ; Rats*

PURPOSE: We aimed to investigate the impact of nonsurgical periodontal treatment combined with one-year dietary supplementation with omega (omega)-3 on the serum levels of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and arachidonic acid (AA). METHODS: Fifteen patients with chronic generalized periodontitis were treated with scaling and root planing. The test group consisted of seven patients (43.1+/-6.0 years) supplemented with omega-3, consisting of EPA plus DHA, three capsules, each of 300 mg of omega-3 (180-mg EPA/120-mg DHA), for 12 months. The control group was composed of eight patients (46.1+/-11.6 years) that took a placebo capsule for 12 months. The periodontal examination and the serum levels of DPA, EPA, DHA, and AA were performed at baseline (T0), and 4 (T1), and 12 (T2) months after therapy. RESULTS: In the test group, AA and DPA levels had been reduced significantly at T1 (P<0.05). AA and EPA levels had been increased significantly at T2 (P<0.05). The DeltaEPA was significantly higher in the test compared to the placebo group at T2-T0 (P=0.02). The AA/EPA had decreased significantly at T1 and T2 relative to baseline (P<0.05). CONCLUSIONS: Nonsurgical periodontal treatment combined with omega-3 supplementation significantly increased the EPA levels and decreased the AA/EPA ratio in serum after one year follow-up. However, no effect on the clinical outcome of periodontal therapy was observed.
Arachidonic Acid ; Capsules ; Dietary Supplements ; Eicosapentaenoic Acid ; Fatty Acids* ; Follow-Up Studies ; Humans ; Periodontitis ; Root Planing

Many reports represent that angiotensin II (ANG II) caused a dose dependent biphasic effects on fluid transport in the proximal tubule. However, respective roles of different signaling pathways in mediating these effects remain unsettled. The aim of the present study was to examine signaling pathways at high doses of ANG II on the Na+ uptake of primary cultured rabbit renal proximal tubule cells(PTCs) in hormonally defined serum-free medium. High concentrations of ANG II (> 10(-9) M) inhibited Na+ uptake and increased (Ca2+)i level in the PTCs. However, low concentrations of (< 10(-11) ANG II) stimulated Na+ uptake and did not affect (Ca2+)i level. 8-(N, N-diethylamino)-octyl-3,3,5- trimethoxybenzoate (TMB-8), ethylene glycol-bis(beta-amino ethyl ether)-N,N,N', N'-tetra acetic acid (EGTA), and nifedifine partially blocked the inhibitory effects of ANG II on Na+ uptake. When ANG II and bradykinin (BK) were treated together, Na+ uptake was further reduced (88.47 +/- 1.98% of that of ANG II, 81.85 +/- 1.84% of that of BK). In addition, W-7 and KN-62 blocked the ANG II-induced inhibition of Na+ uptake. Arachidonic acid reduced Na+ uptake in a dose-dependent manner. When ANG II and arachidonic acid were treated together, inhibitory effects on Na+ uptake significantly exhibited greater reduction than that of each group, respectively. When PTCs were treated by mepacrine (10(-6) M) and AACOCF, (10-5 M) for 1 hr before the addition of 10(-9) M ANG II, the inhibitory effect of ANG II was reversed. In addition, econazole (10(-6) M) blocked ANG II-induced inhibition of Na+ uptake. In conclusion, the (Ca2+)i (calcium-calmodulin-dependent kinase) and phospholipase A2 (PLA2) metabolites are involved in the inhibitory effects of ANG II on Na+ uptake in the PTCs.
Acetic Acid ; Angiotensin II* ; Angiotensins* ; Arachidonic Acid ; Bradykinin ; Econazole ; Ion Transport* ; Kidney ; Negotiating ; Phospholipases A2 ; Quinacrine

TREK (TWIK-RElated K+ channels) and TRAAK (TWIK-Related Arachidonic acid Activated K+ channels) were expressed in COS-7 cells, and the channel activities were recorded from inside-out membrane patches using holding potential of -40 mV in symmetrical 150 mM K+ solution. Intracellular application of an oxidizing agent, 5,5'-dithio-bis (2-nitrobenzoic acid) (DTNB), markedly decreased the activity of the TREK2, and the activity was partially reversed by the reducing agent, dithiothreitol (DTT). In order to examine the possibility that the target sites for the oxidizing agents might be located in the C-terminus of TREK2, two chimeras were constructed: TREK2 (1-383)/TASK3C and TREK2 (1-353)/TASK3C. The channel activity in the TREK2 (1-383)/TASK3C chimera was still inhibited by DTNB, but not in the TREK2 (1-353)/TASK3C chimera. These results indicate that TREK2 is inhibited by oxidation, and that the target site for oxidation is located between the amino acid residues 353 and 383 in the C-terminus of the TREK2 protein.
Animals ; Arachidonic Acid ; Chimera ; COS Cells ; Dithionitrobenzoic Acid ; Dithiothreitol ; Membranes ; Oxidants

12-HETE is a metabolite of arachidonic acid (AA). AA is normally present in membrane phospholipids. The exposure to different stimuli can trigger the release of AA through the activity of phospholipase A₂ (PLA₂) by cells. An important metabolic pathway which utilizes AA as its substrate is 12-Lipoxygenase (12-LOX), resulting in the formation of 12-HETE. 12-HETE plays an important role in many diseases such as cancer, diabetes, hypertension, and participates in the pathogenesis of inflammation and oxidative stress and other pathological processes.Current research shows that it participates in metamorphism and exudation in the process of inflammation. This review is aimed at summarizing its role in inflammation and oxidative stress, with improved understanding of 12-HETE.
12-Hydroxy-5,8,10,14-eicosatetraenoic Acid ; Arachidonic Acid ; Humans ; Inflammation ; Oxidative Stress