Mechanisms of cigarette smoke toxicity: the inactivation of human α-1-proteinase inhibitor by nitric oxide/isoprene mixtures in air

1985 ◽  
Vol 54 ◽  
pp. 171-183 ◽  
Author(s):  
William A. Pryor ◽  
Margaret M. Dooley ◽  
Daniel F. Church
1994 ◽  
Vol 266 (6) ◽  
pp. L593-L611 ◽  
Author(s):  
M. D. Evans ◽  
W. A. Pryor

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.


Author(s):  
T. B. Williams

AbstractNitric oxide in cigarette smoke was conveniently determined by non-dispersive infrared analysis (NDIR). Recoveries of 95 % were obtained with standard gas-air mixtures but recoveries from smoke increased from 87% for high-yield to 91 % for low-yield cigarettes. Relative error was about 4 %. A reduction in the dead volume of Cambridge filter cassettes, to reduce the amount of NO reacted between puffs, increased NO deliveries of cigarettes by 4%. Deliveries of NO were estimated to average 4 % lower due to oxidation, but reaction with other smoke components reduced them further depending upon concentrations. The NO deliveries of cigarettes increased as blend nitrate increased and as the flow of air around cigarettes decreased. Nitric oxide in smoke and in standard gas-air mixtures, determined by non-dispersive infrared (NDIR) spectroscopy, was substantiated by an automated colorimetric analysis. Interfering smoke species were determined and circumvented in both methods.


Lung ◽  
2014 ◽  
Vol 192 (2) ◽  
pp. 267-275 ◽  
Author(s):  
Lei Chen ◽  
Tao Wang ◽  
Lingli Guo ◽  
Yongchun Shen ◽  
Ting Yang ◽  
...  
Keyword(s):  

Nitric Oxide ◽  
2009 ◽  
Vol 20 (3) ◽  
pp. 175-181 ◽  
Author(s):  
Samuel Santos Valença ◽  
Wagner Alves Pimenta ◽  
Carlos Romualdo Rueff-Barroso ◽  
Thiago Santos Ferreira ◽  
Ângela Castro Resende ◽  
...  

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