Early Inflammatory Response to Asbestos Exposure in Rat and Hamster Lungs: Role of Inducible Nitric Oxide Synthase

2002 ◽  
Vol 181 (2) ◽  
pp. 93-105 ◽  
Author(s):  
Martina Dörger ◽  
Anne-Marie Allmeling ◽  
Rainer Kiefmann ◽  
Silvia Münzing ◽  
Konrad Messmer ◽  
...  
2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Alenka Franko ◽  
Metoda Dodič-Fikfak ◽  
Niko Arnerić ◽  
Vita Dolžan

Asbestos, a known occupational pollutant, may upregulate the activity of inducible nitric oxide synthase (iNOS) and thus the production of nitric oxide (NO). This study investigated whetheriNOS (CCTTT)npolymorphism is associated with an increased asbestosis risk in exposed workers. The study cohort consisted of 262 cases with asbestosis and 265 controls with no asbestos-related disease. For each subject the cumulative asbestos exposure data were available. The number of CCTTT repeats was determined following PCR amplification of theiNOSpromoter region. Logistic regression was performed to estimate asbestosis risk. The OR of asbestosis was 1.20 (95%  CI = 0.85–1.69) for the LL genotype compared to the combined SL and SS genotypes and 1.26 (95%   CI = 0.86–1.85) for the LL genotype compared to the SL genotype. The results of this study are borderline significant and suggest a possible role ofiNOS (CCTTT)npolymorphism in the risk of asbestosis; however, further studies are needed.


Shock ◽  
2001 ◽  
Vol 15 (Supplement) ◽  
pp. 30
Author(s):  
S. Cuzzocrea ◽  
L. Dugo ◽  
E. Mazzon ◽  
A. De Sarro ◽  
A. P. Caputi ◽  
...  

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  

2007 ◽  
Vol 103 (3) ◽  
pp. 1045-1055 ◽  
Author(s):  
Juliann G. Kiang ◽  
Phillip D. Bowman ◽  
Xinyue Lu ◽  
Yansong Li ◽  
Brian W. Wu ◽  
...  

Hemorrhage has been shown to increase inducible nitric oxide synthase (iNOS) and deplete ATP levels in tissues and geldanamycin limits both processes. Moreover, it is evident that inhibition of iNOS reduces caspase-3 and increases survival. Thus we sought to identify the molecular events responsible for the beneficial effect of geldanamycin. Hemorrhage in mice significantly increased caspase-3 activity and protein while treatment with geldanamycin significantly limited these increases. Similarly, geldanamycin inhibited increases in proteins forming the apoptosome (a complex of caspase-9, cytochrome c, and Apaf-1). Modulation of the expression of iNOS by iNOS gene transfection or siRNA treatment demonstrated that the level of iNOS correlates with caspase-3 activity. Our data indicate that geldanamycin limits caspase-3 expression and protects from organ injury by suppressing iNOS expression and apoptosome formation. Geldanamycin, therefore, may prove useful as an adjuvant in fluids used to treat patients suffering blood loss.


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