Asymmetric Dimethylarginine Is Increased in Asthma
Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models. To test the hypothesis...
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Published in | American journal of respiratory and critical care medicine Vol. 184; no. 7; pp. 779 - 785 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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New York, NY
American Thoracic Society
01.10.2011
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Abstract | Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models.
To test the hypothesis that ADMA is increased in asthma and that NOS inhibition by ADMA contributes to airways obstruction.
We assessed alterations of L-arginine, ADMA, and symmetric dimethylarginine (SDMA) levels in a murine model of allergic airways inflammation using LC-tandem mass spectrometry. Based on the levels of ADMA observed in the murine model, we further tested the direct effects of nebulized inhaled ADMA on airways responsiveness in naive control mice. We also assessed alterations of L-arginine, ADMA, and SDMA in humans in adult lung specimens and sputum samples from pediatric patients with asthma.
ADMA was increased in lungs from the murine model of allergic airways inflammation. Exogenous administration of ADMA to naive mice, at doses consistent with the levels observed in the allergically inflamed lungs, resulted in augmentation of the airways responsiveness to methacholine. ADMA levels were also increased in human asthma lungs and sputum samples.
ADMA levels are increased in asthma and contribute to NOS-related pathophysiology. |
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AbstractList | Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models.
To test the hypothesis that ADMA is increased in asthma and that NOS inhibition by ADMA contributes to airways obstruction.
We assessed alterations of L-arginine, ADMA, and symmetric dimethylarginine (SDMA) levels in a murine model of allergic airways inflammation using LC-tandem mass spectrometry. Based on the levels of ADMA observed in the murine model, we further tested the direct effects of nebulized inhaled ADMA on airways responsiveness in naive control mice. We also assessed alterations of L-arginine, ADMA, and SDMA in humans in adult lung specimens and sputum samples from pediatric patients with asthma.
ADMA was increased in lungs from the murine model of allergic airways inflammation. Exogenous administration of ADMA to naive mice, at doses consistent with the levels observed in the allergically inflamed lungs, resulted in augmentation of the airways responsiveness to methacholine. ADMA levels were also increased in human asthma lungs and sputum samples.
ADMA levels are increased in asthma and contribute to NOS-related pathophysiology. RATIONALEAsymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models.OBJECTIVESTo test the hypothesis that ADMA is increased in asthma and that NOS inhibition by ADMA contributes to airways obstruction.METHODSWe assessed alterations of L-arginine, ADMA, and symmetric dimethylarginine (SDMA) levels in a murine model of allergic airways inflammation using LC-tandem mass spectrometry. Based on the levels of ADMA observed in the murine model, we further tested the direct effects of nebulized inhaled ADMA on airways responsiveness in naive control mice. We also assessed alterations of L-arginine, ADMA, and SDMA in humans in adult lung specimens and sputum samples from pediatric patients with asthma.MEASUREMENTS AND MAIN RESULTSADMA was increased in lungs from the murine model of allergic airways inflammation. Exogenous administration of ADMA to naive mice, at doses consistent with the levels observed in the allergically inflamed lungs, resulted in augmentation of the airways responsiveness to methacholine. ADMA levels were also increased in human asthma lungs and sputum samples.CONCLUSIONSADMA levels are increased in asthma and contribute to NOS-related pathophysiology. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models. To test the hypothesis that ADMA is increased in asthma and that NOS inhibition by ADMA contributes to airways obstruction. We assessed alterations of L-arginine, ADMA, and symmetric dimethylarginine (SDMA) levels in a murine model of allergic airways inflammation using LC-tandem mass spectrometry. Based on the levels of ADMA observed in the murine model, we further tested the direct effects of nebulized inhaled ADMA on airways responsiveness in naive control mice. We also assessed alterations of L-arginine, ADMA, and SDMA in humans in adult lung specimens and sputum samples from pediatric patients with asthma. ADMA was increased in lungs from the murine model of allergic airways inflammation. Exogenous administration of ADMA to naive mice, at doses consistent with the levels observed in the allergically inflamed lungs, resulted in augmentation of the airways responsiveness to methacholine. ADMA levels were also increased in human asthma lungs and sputum samples. ADMA levels are increased in asthma and contribute to NOS-related pathophysiology. |
Author | BELIK, Jaques GRASEMANN, Hartmut SUBBARAO, Padmaja PENCHARZ, Paul NORTH, Michelle L SCOTT, Jeremy A HAILU HUANG RAFII, Mahroukh |
Author_xml | – sequence: 1 givenname: Jeremy A surname: SCOTT fullname: SCOTT, Jeremy A organization: Division of Occupational Medicine, University of Toronto, Toronto, Ontario, Canada – sequence: 2 givenname: Michelle L surname: NORTH fullname: NORTH, Michelle L organization: Division of Occupational Medicine, University of Toronto, Toronto, Ontario, Canada – sequence: 3 givenname: Mahroukh surname: RAFII fullname: RAFII, Mahroukh organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada – sequence: 4 surname: HAILU HUANG fullname: HAILU HUANG organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada – sequence: 5 givenname: Paul surname: PENCHARZ fullname: PENCHARZ, Paul organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada – sequence: 6 givenname: Padmaja surname: SUBBARAO fullname: SUBBARAO, Padmaja organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada – sequence: 7 givenname: Jaques surname: BELIK fullname: BELIK, Jaques organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada – sequence: 8 givenname: Hartmut surname: GRASEMANN fullname: GRASEMANN, Hartmut organization: Program in Physiology and Experimental Medicine, Research Institute, University of Toronto, Toronto, Ontario, Canada |
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Keywords | Lung disease Intensive care Arginine Respiratory disease Aminoacid Bronchus disease Obstructive pulmonary disease Metabolism biomarker Resuscitation Asthma airways hyperresponsiveness |
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References | Grasemann H (bib17) 2010; 181 Kenyon NJ (bib37) 2010; 181 bib14 bib36 bib15 bib12 bib34 bib13 bib35 bib10 bib32 bib11 bib33 bib30 bib31 bib29 bib27 bib28 Amin R (bib16) 2009; 209 bib25 bib26 bib23 bib24 bib21 bib22 bib20 bib9 bib7 bib8 bib5 bib18 bib6 bib19 bib3 bib38 bib4 bib39 bib1 bib2 |
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SubjectTerms | Adolescent Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Arginine - analogs & derivatives Arginine - metabolism Asthma Asthma - metabolism Biological and medical sciences Biomarkers - metabolism Bronchial Hyperreactivity - metabolism Case-Control Studies Child Chronic obstructive pulmonary disease, asthma Competition Disease Female Humans Inflammation Intensive care medicine Lungs Male Mass spectrometry Medical sciences Metabolism Metabolites Mice Mice, Inbred BALB C Nitric oxide Nitric Oxide Synthase - metabolism Pathophysiology Patients Pediatrics Pneumology Scientific imaging Smooth muscle Sputum - metabolism Steroids |
Title | Asymmetric Dimethylarginine Is Increased in Asthma |
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