Exact Mass: 625.3032852
Exact Mass Matches: 625.3032852
Found 19 metabolites which its exact mass value is equals to given mass value 625.3032852,
within given mass tolerance error 0.0002 dalton. Try search metabolite list with more accurate mass tolerance error
4.0E-5 dalton.
Leukotriene C4
Leukotriene C4 (LTC4) is a cysteinyl leukotriene (CysLT), a family of potent inflammatory mediators. Eosinophils, one of the principal cell types recruited to and activated at sites of allergic inflammation, is capable of elaborating lipid mediators, including leukotrienes derived from the oxidative metabolism of arachidonic acid (AA). Potentially activated eosinophils may elaborate greater quantities of LTC4, than normal eosinophils. These activated eosinophils thus are primed for enhanced LTC4 generation in response to subsequent stimuli. Some recognized priming stimuli are chemoattractants (e.g. eotaxin, PAF) that may participate in the recruitment of eosinophils to sites of allergic inflammation. The mechanisms by which chemoattractants and other activating cytokines (e.g. interleukin (IL)-5) or extracellular matrix components (e.g. fibronectin) enhance eosinophil eicosanoid formation are pertinent to the functions of these eicosanoids as paracrine mediators of allergic inflammation. Some eosinophil-derived eicosanoids may be active in down-regulating inflammation. It is increasingly likely that eicosanoids synthesized within cells, including eosinophils, may have intracellular (e.g. intracrine) roles in regulating cell functions, in addition to the more recognized activities of eicosanoids as paracrine mediators of inflammation. Acting extracellularly, the cysteinyl leukotrienes (CysLTs) LTC4 and its extracellular derivatives, LTD4 and LTE4 are key paracrine mediators pertinent to asthma and allergic diseases. Based on their receptor-mediated capabilities, they can elicit bronchoconstriction, mucus hypersecretion, bronchial hyperresponsiveness, increased microvascular permeability, and additional eosinophil infiltration. Eosinophils are a major source of CysLTs and have been identified as the principal LTC4 synthase expressing cells in bronchial mucosal biopsies of asthmatic subjects (PMID: 12895596). Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. Leukotriene c4, also known as ltc4 or 5s,6r-ltc(sub 4), is a member of the class of compounds known as oligopeptides. Oligopeptides are organic compounds containing a sequence of between three and ten alpha-amino acids joined by peptide bonds. Thus, leukotriene c4 is considered to be an eicosanoid lipid molecule. Leukotriene c4 is practically insoluble (in water) and a moderately acidic compound (based on its pKa). Leukotriene c4 can be synthesized from icosa-7,9,11,14-tetraenoic acid. Leukotriene c4 is also a parent compound for other transformation products, including but not limited to, leukotriene C4 methyl ester, 11,12-dihydro-(12R)-hydroxyleukotriene C4, and 11,12-dihydro-12-oxoleukotriene C4. Leukotriene c4 can be found in a number of food items such as gram bean, maitake, caraway, and burbot, which makes leukotriene c4 a potential biomarker for the consumption of these food products. Leukotriene c4 can be found primarily in blood and cerebrospinal fluid (CSF), as well as throughout most human tissues. In humans, leukotriene c4 is involved in several metabolic pathways, some of which include trisalicylate-choline action pathway, antipyrine action pathway, nepafenac action pathway, and fenoprofen action pathway. Leukotriene c4 is also involved in a couple of metabolic disorders, which include leukotriene C4 synthesis deficiency and tiaprofenic acid action pathway. Moreover, leukotriene c4 is found to be associated with eczema. Leukotriene C4 (LTC4) is a leukotriene. LTC4 has been extensively studied in the context of allergy and asthma. In cells of myeloid origin such as mast cells, its biosynthesis is orchestrated by translocation to the nuclear envelope along with co-localization of cytosolic phospholipase A2 (cPLA2), Arachidonate 5-lipoxygenase (5-LO), 5-lipoxygenase-activating protein (FLAP) and LTC4 synthase (LTC4S), which couples glutathione to an LTA4 intermediate.The MRP1 transporter then secretes cytosolic LTC4 and cell surface proteases further metabolize it by sequential cleavage of the γ-glutamyl and glycine residues off its glutathione segment, generating the more stable products LTD4 and LTE4. All three leukotrienes then bind at different affinities to two G-protein coupled receptors: CYSLTR1 and CYSLTR2, triggering pulmonary vasoconstriction and bronchoconstriction .
11-trans-Leukotriene C4
11-trans-Leukotriene C4 (11-trans-LTC4) is a leukotriene derivative formed by the metabolism of LTA4 and is found in human endothelial cells. Leukotrienes (LT) are a family of naturally occurring lipids that are oxygenated metabolites of arachidonic acid. Biosynthesis of the leukotrienes involves the action of a lipoxygenase on arachidonate to yield a hydroperoxy intermediate which is then dehydrated to the allylic epoxide, LTA4. LTA4 can be hydrolyzed to the dihydroxy acid, LTB4 or it can be conjugated with glutathione (GSH) to produce the parent slow reacting substance, LTC4. The leukotrienes are mediators of inflammation, hypersensitivity reactions, and respiratory disorders. On a cellular level, LTC4 and its metabolites, LTD4 and LTE4, are potent constrictors of vascular bronchial smooth muscle. LTC4 and LTD4 also induce plasma leakage from the microvasculature. LTB4 is a potent polymorphonuclear leukocyte (PMNL) chemotaxin and induces neutrophils to degranulate, generate superoxide, and adhere to vascular endothelium. Several investigations of leukotriene synthesis by blood vessels and cultured vascular cells have been undertaken. Vascular preparations have been shown to produce LTB4 and LTC4 and to metabolize LTC4 to LTD4 and LTE4. In addition, mast cells, macrophages, and PMNL, all of which may contaminate whole vessel preparations, are known to synthesize both peptide-containing and dihydroxy acid leukotrienes. Consequently, it is unclear what cells are contributing to vascular leukotriene synthesis. No evidence of isolated vascular cell leukotriene synthesis is currently available. Indeed, this report and others have been unable to detect endothelial cell conversion of arachidonic acid to the leukotrienes. The fact that vascular endothelium lacks the full complement of leukotriene biosynthetic enzymes does not preclude an active role for this tissue in leukotriene metabolism. In some cases, tissues which are not known to synthesize leukotrienes from arachidonate are able to catalyze one or more of the intermediate steps of the pathway. In the present investigation, the leukotriene metabolism of porcine aortic endothelium has been studied. Evidence is presented which indicates that endothelial cells are unable to convert arachidonic acid to LTC4 but, nevertheless, contain LTC4 synthetase. Additional experiments suggest that a neutrophil-endothelial cell interaction augments vascular LTC4 synthesis by the intercellular transfer of LTA4 from PMNL to endothelial cells (PMID: 3023351). Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 11-trans-Leukotriene C4 (11-trans-LTC4) is leukotriene derivative formed by the metabolism of LTA4 and is found in human endothelial cells. Leukotrienes (LT) are a family of naturally occurring lipids that are oxygenated metabolites of arachidonic acid. Biosynthesis of the leukotrienes involves the action of a lipoxygenase on arachidonate to yield a hydroperoxy intermediate which is then dehydrated to the allylic epoxide, LTA4. LTA4 can be hydrolyzed to the dihydroxy acid, LTB4 or it can be conjugated with glutathione (GSH) to produce the parent slow reacting substance, LTC4. The leukotrienes are mediators of inflammation, hypersensitivy reactions, and respiratory disorders. On a cellular level, LTC4 and its metabolites, LTD4 and LTE4, are potent constrictors of vascular bronchial smooth muscle. LTC4 and LTD4 also induce plasma leakage from the microvasculature. LTB4 is a potent polymorphonuclear leukocyte (PMNL) chemotaxin and induces neutrophils to degranulate, generate superoxide, and adhere to vascular endothelium. Several investigations of leukotriene synthesis by blood vessels and cultured vascular cells have been undertaken. Vascular preparations have been shown to produce LTB4 and LTC4 and to metabolize LTC4 to LTD4 and LTE4. In addition, mast cells, macrophages, and PMNL, all of which may contaminate whole vessel preparations, are known to synthesize both peptide-containing and dihydroxy acid leukotrienes. Consequently, it is unclear what cells are contributing to vascular leukotriene synthesis. No evidence of isolated vascular cell leukotriene synthesis is currently available. Indeed, this report and others have been unable to detect endothelial cell conversion of arachidonic acid to the leukotrienes. The fact that vascular endothelium lacks the full complement of leukotriene biosynthetic enzymes does not preclude an active role for this tissue in leukotriene metabolism. In some cases, tissues which are not known to synthesize leukotrienes from arachidonate are able to catalyze one or more of the intermediate steps of the pathway. In the present investigation, the leukotriene metabolism of porcine aortic endothelium has been studied. Evidence is presented which indicates that endothelial cells are unable to convert arachidonic acid to LTC4 but, nevertheless, contain LTC4 synthetase. Additional experiments suggest that a neutrophil- endothelial cell interaction augments vascular LTC4 synthesis by the intercellular transfer of LTA4 from PMNL to endothelial cells. (PMID 3023351)
11-trans Leukotriene C4
LTC4-[d5]
CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0232.mzML; PROCESSING averaging of repeated ion fragments at 30.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0232.mzML; PROCESSING averaging of repeated ion fragments at 20.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0232.mzML; PROCESSING averaging of repeated ion fragments at 10.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 30.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 20.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 10.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 40.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 30.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0000163.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ]
Leukotriene C4
A leukotriene that is (5S,7E,9E,11Z,14Z)-5-hydroxyicosa-7,9,11,14-tetraenoic acid in which a glutathionyl group is attached at position 6 via a sulfide linkage.
15S-hydroxy,14R-(S-glutathionyl)-5Z,8Z,10E,12E-eicosatetraenoic acid
(7E,9E,11E,14E)-6-[2-[(4-amino-4-carboxybutanoyl)amino]-3-(carboxymethylamino)-3-oxopropyl]sulfanyl-5-hydroxyicosa-7,9,11,14-tetraenoic acid
(5S,6R,7E,9E,11Z)-6-({(2R)-2-{[(4S)-4-azaniumyl-4-carboxylatobutanoyl]amino}-3-[(carboxylatomethyl)amino]-3-oxopropyl}sulfanyl)-5-hydroxyicosa-7,9,11-trienoate
eoxin C4
A leukotriene that is the 14R-(S-glutathionyl),15S-hydroxy derivative of (5Z,8Z,10E,12E)-icosa-7,9,11,14-tetraenoic acid.
leukotriene C3(2-)
A leukotriene anion obtained by deprotonation of the three carboxy groups and protonation of the glutamyl alpha-amino group of leukotriene C3; major species at pH 7.3.