In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 5 ( 2001-02-27), p. 2622-2627
Abstract:
A wealth of evidence supports increased NO (NO ⋅ ) in asthma,
but its roles are unknown. To investigate how NO participates in inflammatory airway events in asthma, we measured NO ⋅ and
NO ⋅ chemical reaction products [nitrite, nitrate, S -nitrosothiols (SNO), and nitrotyrosine] before, immediately and 48 h after bronchoscopic antigen (Ag) challenge of
the peripheral airways in atopic asthmatic individuals and nonatopic healthy controls. Strikingly, NO \documentclass[12pt]{minimal} \usepackage{amsmath}
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\begin{document} \begin{equation*}{\mathrm{_{3}^{-}}}\end{equation*}\end{document} was the only
NO ⋅ derivative to increase during the immediate Ag-induced
asthmatic response and continued to increase over 2-fold at 48 h after Ag challenge in contrast to controls [ P 〈 0.05]. NO \documentclass[12pt]{minimal} \usepackage{amsmath}
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\begin{document} \begin{equation*}{\mathrm{_{2}^{-}}}\end{equation*}\end{document} was not affected by Ag challenge at 10
min or 48 h after Ag challenge. Although SNO was not detectable in asthmatic airways at baseline or immediately after Ag, SNO increased
during the late response to levels found in healthy controls. A model of NO ⋅ dynamics derived from the current findings predicts that
NO ⋅ may have harmful effects through formation of peroxynitrite,
but also subserves an antioxidant role by consuming reactive oxygen species during the immediate asthmatic response, whereas nitrosylation
during the late asthmatic response generates SNO, safe reservoirs for removal of toxic NO ⋅ derivatives.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.051629498
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
2001
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
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