Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins

Jin, Hongjun; Webb-Robertson, Bobbie-Jo M; Peterson, Elena S; Tan, Ruimin; Bigelow, Diana J; Scholand, Mary Beth; Hoidal, John R; Pounds, Joel G; Zangar, Richard C

doi:10.1289/ehp.1103745

Title: Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins

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Abstract

BACKGROUND: Nitric oxide is a physiologically regulator of endothelial function and hemodynamics. Oxidized products of nitric oxide can form nitrotyrosine, which is a marker of nitrative stress. Cigarette smoking decreases exhaled nitric oxide, and the underlying mechanism may be important in the cardiovascular toxicity of cigarette smoke, although it is not clear if this effect results from decreased nitric oxide production or oxidation of nitric oxide to reactive, nitrating, species. These processes would be expected to have opposite effects on nitrotyrosine levels, a marker of nitrative stress. OBJECTIVE: In this study, we determine the effects of smoking and chronic obstructive pulmonary disease (COPD) on circulating levels of nitrotyrosine, and thereby gain insight into the processes regulating nitrotyrosine formation. METHODS: A custom antibody microarray platform was used to analyze the levels of 3-nitrotyrosine modifications on 24 proteins in plasma. Plasma samples from 458 individuals were analyzed. RESULTS: Nitrotyrosine levels in circulating proteins were uniformly reduced in smokers but increased in COPD patients. We also observed a persistent suppression of nitrotyrosine in former smokers. CONCLUSIONS: Smoking broadly suppresses the levels of 3-nitrotyrosine in plasma proteins, suggesting that cigarette smoke suppresses endothelial nitric oxide production. In contrast, the increase in nitrotyrosine levels inmore »« less

Authors:: Jin, Hongjun; Webb-Robertson, Bobbie-Jo M; Peterson, Elena S; Tan, Ruimin; Bigelow, Diana J; Scholand, Mary Beth; Hoidal, John R; Pounds, Joel G; Zangar, Richard C

Publication Date:: Thu Sep 01 00:00:00 EDT 2011

Research Org.:: Pacific Northwest National Lab. (PNNL), Richland, WA (United States)

Sponsoring Org.:: USDOE

OSTI Identifier:: 1025066

Report Number(s):: PNNL-SA-73870
Journal ID: ISSN 0091-6765; EVHPAZ; 400412000; TRN: US201120%%250

DOE Contract Number:: AC05-76RL01830

Resource Type:: Journal Article

Journal Name:: Environmental Health Perspectives, 119(9):1314-1320

Additional Journal Information:: Journal Volume: 119; Journal Issue: 9; Journal ID: ISSN 0091-6765

Country of Publication:: United States

Language:: English

Subject:: 59 BASIC BIOLOGICAL SCIENCES; 60 APPLIED LIFE SCIENCES; CARDIOVASCULAR DISEASES; DISEASES; ELASTICITY; MODIFICATIONS; NITRIC OXIDE; OXIDATION; PATIENTS; PLASMA; PRODUCTION; PROTEINS; TOXICITY; cigarette smoke; ELISA; nitrotyrosine; COPD; eNOS

Citation Formats


                    Jin, Hongjun, Webb-Robertson, Bobbie-Jo M, Peterson, Elena S, Tan, Ruimin, Bigelow, Diana J, Scholand, Mary Beth, Hoidal, John R, Pounds, Joel G, and Zangar, Richard C. Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins.  United States: N. p., 2011. 
        Web.  doi:10.1289/ehp.1103745.

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                    Jin, Hongjun, Webb-Robertson, Bobbie-Jo M, Peterson, Elena S, Tan, Ruimin, Bigelow, Diana J, Scholand, Mary Beth, Hoidal, John R, Pounds, Joel G, & Zangar, Richard C. Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins.  United States.  https://doi.org/10.1289/ehp.1103745

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                    Jin, Hongjun, Webb-Robertson, Bobbie-Jo M, Peterson, Elena S, Tan, Ruimin, Bigelow, Diana J, Scholand, Mary Beth, Hoidal, John R, Pounds, Joel G, and Zangar, Richard C. 2011.  
        "Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins".  United States.  https://doi.org/10.1289/ehp.1103745.

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@article{osti_1025066,

  title        = {Smoking, COPD and 3-Nitrotyrosine Levels of Plasma Proteins},

  author       = {Jin, Hongjun and Webb-Robertson, Bobbie-Jo M and Peterson, Elena S and Tan, Ruimin and Bigelow, Diana J and Scholand, Mary Beth and Hoidal, John R and Pounds, Joel G and Zangar, Richard C},

  abstractNote = {BACKGROUND: Nitric oxide is a physiologically regulator of endothelial function and hemodynamics. Oxidized products of nitric oxide can form nitrotyrosine, which is a marker of nitrative stress. Cigarette smoking decreases exhaled nitric oxide, and the underlying mechanism may be important in the cardiovascular toxicity of cigarette smoke, although it is not clear if this effect results from decreased nitric oxide production or oxidation of nitric oxide to reactive, nitrating, species. These processes would be expected to have opposite effects on nitrotyrosine levels, a marker of nitrative stress. OBJECTIVE: In this study, we determine the effects of smoking and chronic obstructive pulmonary disease (COPD) on circulating levels of nitrotyrosine, and thereby gain insight into the processes regulating nitrotyrosine formation. METHODS: A custom antibody microarray platform was used to analyze the levels of 3-nitrotyrosine modifications on 24 proteins in plasma. Plasma samples from 458 individuals were analyzed. RESULTS: Nitrotyrosine levels in circulating proteins were uniformly reduced in smokers but increased in COPD patients. We also observed a persistent suppression of nitrotyrosine in former smokers. CONCLUSIONS: Smoking broadly suppresses the levels of 3-nitrotyrosine in plasma proteins, suggesting that cigarette smoke suppresses endothelial nitric oxide production. In contrast, the increase in nitrotyrosine levels in COPD patients most likely results from inflammatory processes. This study provides the first evidence that smoking has irreversible effects on endothelial production of nitric oxide, and provides insight into how smoking could induce a loss of elasticity in the vasculature and a long-term increase in the risk of cardiovascular disease.},

  doi          = {10.1289/ehp.1103745},

  url          = {https://www.osti.gov/biblio/1025066},
  journal      = {Environmental Health Perspectives, 119(9):1314-1320},

  issn         = {0091-6765},

  number       = 9,

  volume       = 119,

  place        = {United States},

  year         = {Thu Sep 01 00:00:00 EDT 2011},

  month        = {Thu Sep 01 00:00:00 EDT 2011}

}

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