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Exhaled breath condensate: a promising source for biomarkers of lung disease.

Liang Y, Yeligar SM, Brown LA - ScientificWorldJournal (2012)

Bottom Line: Substances measured in EBC include oxidative stress and inflammatory mediators, such as arachidonic acid derivatives, reactive oxygen/nitrogen species, reduced and oxidized glutathione, and inflammatory cytokines.Although EBC is viewed as a noninvasive method for sampling airway lining fluid (ALF), validation is necessary to confirm that EBC truly represents the ALF.Likewise, a dilution factor for the EBC is needed in order to compare across subjects and determine changes in the ALF.

View Article: PubMed Central - PubMed

Affiliation: Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Emory University and Emory+Children's Healthcare of Atlanta Center for Developmental Lung Biology, Atlanta, GA 30322, USA.

ABSTRACT
Exhaled breath condensate (EBC) has been increasingly studied as a noninvasive research method for sampling the alveolar and airway space and is recognized as a promising source of biomarkers of lung diseases. Substances measured in EBC include oxidative stress and inflammatory mediators, such as arachidonic acid derivatives, reactive oxygen/nitrogen species, reduced and oxidized glutathione, and inflammatory cytokines. Although EBC has great potential as a source of biomarkers in many lung diseases, the low concentrations of compounds within the EBC present challenges in sample collection and analysis. Although EBC is viewed as a noninvasive method for sampling airway lining fluid (ALF), validation is necessary to confirm that EBC truly represents the ALF. Likewise, a dilution factor for the EBC is needed in order to compare across subjects and determine changes in the ALF. The aims of this paper are to address the characteristics of EBC; strategies to standardize EBC sample collection and review available analytical techniques for EBC analysis.

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Related in: MedlinePlus

Metabolism of arachidonic acid. Arachidonic acid is released from phospholipids by the action of phospholipase A2 (PLA2). Arachidonic acid is metabolized by cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450 (CYP). COXs metabolize arachidonic acid to prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs). Leukotrienes (LTs) are the final arachidonic acid metabolites in the 5-lipoxygenase- (5-LO-) mediated pathway. CYP epoxygenases (CYP-EO) metabolize arachidonic acid to epoxyeicosatrienoic acid (EETs), and CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). 8-Isoprostane (8-IP) can be generated in vivo by the free radical-catalyzed peroxidation of arachidonic acid.
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fig2: Metabolism of arachidonic acid. Arachidonic acid is released from phospholipids by the action of phospholipase A2 (PLA2). Arachidonic acid is metabolized by cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450 (CYP). COXs metabolize arachidonic acid to prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs). Leukotrienes (LTs) are the final arachidonic acid metabolites in the 5-lipoxygenase- (5-LO-) mediated pathway. CYP epoxygenases (CYP-EO) metabolize arachidonic acid to epoxyeicosatrienoic acid (EETs), and CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). 8-Isoprostane (8-IP) can be generated in vivo by the free radical-catalyzed peroxidation of arachidonic acid.

Mentions: Arachidonic acid (AA) is a polyunsaturated omega-6 fatty acid present in the phospholipids of cell membranes. Arachidonic acid is released by the activation of the enzyme phospholipase A2 (PLA2) but can be further metabolized by cyclooxygenases (COX), 5-lipoxygenases (5-LO) and cytochrome P450 (CYP) [19–22]. A detailed scheme is presented in Figure 2 for arachidonic acid metabolism, where intracellular interactions control arachidonic acid conversion and activity. Cyclooxygenases generate prostanoids which can be further subdivided into three main groups: the prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs), each of which is involved in some aspect of the inflammatory response. Arachidonate 5-lipoxygenase converts AA to yield leukotrienes (LTs). CYP epoxygenases (CYP-EO) convert arachidonic acid to epoxyeicosatrienoic acids (EETs). CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). Airway epithelial cells are sensitive to arachidonate metabolites and have abundant arachidonic acid and novel cyclooxygenases and lipoxygenases at increased levels relative to other cell types [23]. However, arachidonate metabolites can be synthesized by and have potent biologic effects on other airway cells such as leukocytes, smooth muscle, nerves, mucus glands, and platelets. 8-Isoprostane (8-IP), a prostaglandin (PG)-F2-like compound, belongs to the F2 isoprostane class that is produced in vivo by the free radical-catalyzed peroxidation of arachidonic acid [24]. Because of the transcellular feature of arachidonic acid metabolism and function, airway lining fluid is the critical medium for these actions. Significant amounts of arachidonic acid and its derivatives are present in ALF. 8-Isoprostane, LTs, and prostanoids have been detected in EBC and used as biomarkers for oxidative stress and respiratory infection. Methods used to detect arachidonic acid derivatives in the EBC include gas chromatography/mass spectrometry (GC/MS), liquid chromatography/mass spectrometry (LC/MS), radioimmunoassay (RIA), and enzyme immunoassay (EIA).


Exhaled breath condensate: a promising source for biomarkers of lung disease.

Liang Y, Yeligar SM, Brown LA - ScientificWorldJournal (2012)

Metabolism of arachidonic acid. Arachidonic acid is released from phospholipids by the action of phospholipase A2 (PLA2). Arachidonic acid is metabolized by cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450 (CYP). COXs metabolize arachidonic acid to prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs). Leukotrienes (LTs) are the final arachidonic acid metabolites in the 5-lipoxygenase- (5-LO-) mediated pathway. CYP epoxygenases (CYP-EO) metabolize arachidonic acid to epoxyeicosatrienoic acid (EETs), and CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). 8-Isoprostane (8-IP) can be generated in vivo by the free radical-catalyzed peroxidation of arachidonic acid.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539342&req=5

fig2: Metabolism of arachidonic acid. Arachidonic acid is released from phospholipids by the action of phospholipase A2 (PLA2). Arachidonic acid is metabolized by cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450 (CYP). COXs metabolize arachidonic acid to prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs). Leukotrienes (LTs) are the final arachidonic acid metabolites in the 5-lipoxygenase- (5-LO-) mediated pathway. CYP epoxygenases (CYP-EO) metabolize arachidonic acid to epoxyeicosatrienoic acid (EETs), and CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). 8-Isoprostane (8-IP) can be generated in vivo by the free radical-catalyzed peroxidation of arachidonic acid.
Mentions: Arachidonic acid (AA) is a polyunsaturated omega-6 fatty acid present in the phospholipids of cell membranes. Arachidonic acid is released by the activation of the enzyme phospholipase A2 (PLA2) but can be further metabolized by cyclooxygenases (COX), 5-lipoxygenases (5-LO) and cytochrome P450 (CYP) [19–22]. A detailed scheme is presented in Figure 2 for arachidonic acid metabolism, where intracellular interactions control arachidonic acid conversion and activity. Cyclooxygenases generate prostanoids which can be further subdivided into three main groups: the prostaglandins (PGs), prostacyclin (PGI2), and thromboxanes (TXs), each of which is involved in some aspect of the inflammatory response. Arachidonate 5-lipoxygenase converts AA to yield leukotrienes (LTs). CYP epoxygenases (CYP-EO) convert arachidonic acid to epoxyeicosatrienoic acids (EETs). CYP hydroxylases (CYP-HO) metabolize arachidonic acid to hydroxyeicosatetraenoic acids (HETEs). Airway epithelial cells are sensitive to arachidonate metabolites and have abundant arachidonic acid and novel cyclooxygenases and lipoxygenases at increased levels relative to other cell types [23]. However, arachidonate metabolites can be synthesized by and have potent biologic effects on other airway cells such as leukocytes, smooth muscle, nerves, mucus glands, and platelets. 8-Isoprostane (8-IP), a prostaglandin (PG)-F2-like compound, belongs to the F2 isoprostane class that is produced in vivo by the free radical-catalyzed peroxidation of arachidonic acid [24]. Because of the transcellular feature of arachidonic acid metabolism and function, airway lining fluid is the critical medium for these actions. Significant amounts of arachidonic acid and its derivatives are present in ALF. 8-Isoprostane, LTs, and prostanoids have been detected in EBC and used as biomarkers for oxidative stress and respiratory infection. Methods used to detect arachidonic acid derivatives in the EBC include gas chromatography/mass spectrometry (GC/MS), liquid chromatography/mass spectrometry (LC/MS), radioimmunoassay (RIA), and enzyme immunoassay (EIA).

Bottom Line: Substances measured in EBC include oxidative stress and inflammatory mediators, such as arachidonic acid derivatives, reactive oxygen/nitrogen species, reduced and oxidized glutathione, and inflammatory cytokines.Although EBC is viewed as a noninvasive method for sampling airway lining fluid (ALF), validation is necessary to confirm that EBC truly represents the ALF.Likewise, a dilution factor for the EBC is needed in order to compare across subjects and determine changes in the ALF.

View Article: PubMed Central - PubMed

Affiliation: Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Emory University and Emory+Children's Healthcare of Atlanta Center for Developmental Lung Biology, Atlanta, GA 30322, USA.

ABSTRACT
Exhaled breath condensate (EBC) has been increasingly studied as a noninvasive research method for sampling the alveolar and airway space and is recognized as a promising source of biomarkers of lung diseases. Substances measured in EBC include oxidative stress and inflammatory mediators, such as arachidonic acid derivatives, reactive oxygen/nitrogen species, reduced and oxidized glutathione, and inflammatory cytokines. Although EBC has great potential as a source of biomarkers in many lung diseases, the low concentrations of compounds within the EBC present challenges in sample collection and analysis. Although EBC is viewed as a noninvasive method for sampling airway lining fluid (ALF), validation is necessary to confirm that EBC truly represents the ALF. Likewise, a dilution factor for the EBC is needed in order to compare across subjects and determine changes in the ALF. The aims of this paper are to address the characteristics of EBC; strategies to standardize EBC sample collection and review available analytical techniques for EBC analysis.

Show MeSH
Related in: MedlinePlus