Mechanisms of JP-8 Jet Fuel Toxicity. I. Induction of Apoptosis in Rat Lung Epithelial Cells

2001 ◽  
Vol 171 (2) ◽  
pp. 94-106 ◽  
Author(s):  
Bogdan A. Stoica ◽  
A.Hamid Boulares ◽  
Dean S. Rosenthal ◽  
Sudha Iyer ◽  
Ivan D.G. Hamilton ◽  
...  
2009 ◽  
Vol 23 (5) ◽  
pp. 333-344 ◽  
Author(s):  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Bindu Sadanandan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  

2013 ◽  
Vol 27 (5) ◽  
pp. 286-286 ◽  
Author(s):  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Bindu Sadanandan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  

2006 ◽  
Vol 291 (4) ◽  
pp. L725-L733 ◽  
Author(s):  
Ulrich Sydlik ◽  
Katrin Bierhals ◽  
Maria Soufi ◽  
Josef Abel ◽  
Roel P. F. Schins ◽  
...  

Apoptosis and proliferation are important causes of adverse health effects induced by inhaled ultrafine particles. The molecular mechanisms of particle cell interactions mediating these end points are therefore a major topic of current particle toxicology and molecular preventive medicine. Initial studies revealed that ultrafine particles induce apoptosis and proliferation in parallel in rat lung epithelial cells, dependent on time and dosage. With these end points, two antagonistic reactions seem to be induced by the same extracellular stimulus. It was therefore investigated whether proliferation is induced directly by the particles or as a compensation of particle-caused cell death. Experimental conditions excluding compensatory proliferation demonstrated that both end points are induced independently by specific signaling pathways. Events eliciting signaling cascades leading to apoptosis and proliferation were studied with specific inhibitors of membrane receptors. Epidermal growth factor receptor (EGF-R) kinase activity was identified as essential for apoptosis as well as for proliferation. As ultrafine particle-induced proliferation alone was dependent on the activation of β1-integrins, these membrane receptors are suggested to mediate the specificity of EGF-R signaling concerning the decision as to whether apoptosis or proliferation is triggered. Accordingly, MAP kinase signaling downstream of EGF-R showed comparable specificity with regard to receptor-dependent induction of apoptosis and proliferation. As key mediators of signaling cascades, the activation of extracellular signal-regulated kinases 1 and 2 proved to be specific for proliferation in a β1-integrin-dependent manner, whereas phosphorylation of c-Jun NH2-terminal kinases 1 and 2 was correlated with the induction of apoptosis.


Toxicology ◽  
1999 ◽  
Vol 133 (1) ◽  
pp. 43-58 ◽  
Author(s):  
B.A. Hart ◽  
C.H. Lee ◽  
G.S. Shukla ◽  
A. Shukla ◽  
M. Osier ◽  
...  

1991 ◽  
Vol 27 (8) ◽  
pp. 625-632 ◽  
Author(s):  
D. Jassal ◽  
R. N. N. Han ◽  
I. Caniggia ◽  
M. Post ◽  
A. K. Tanswell

2004 ◽  
Vol 5 (1) ◽  
pp. 11 ◽  
Author(s):  
Jin Hyuk Choi ◽  
Jun Sung Kim ◽  
Young Chul Kim ◽  
Yoon Shin Kim ◽  
Nam Hyun Chung ◽  
...  

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