Relationehips between lipid peroxidation and vitamin E levela in bronchoalveolar lavage fluid and rat lungs after acute exposure to nitrogen dioxide

1995 ◽  
Vol 78 ◽  
pp. 43
Author(s):  
J Jajte ◽  
E. Rajkowska ◽  
K. Rydzyn̈ski ◽  
B. Opalska
2020 ◽  
Vol 382 (8) ◽  
pp. 697-705 ◽  
Author(s):  
Benjamin C. Blount ◽  
Mateusz P. Karwowski ◽  
Peter G. Shields ◽  
Maria Morel-Espinosa ◽  
Liza Valentin-Blasini ◽  
...  

2001 ◽  
Vol 91 (4) ◽  
pp. 1694-1700 ◽  
Author(s):  
Nancy C. Long ◽  
Jung Suh ◽  
Jason D. Morrow ◽  
Robert H. Schiestl ◽  
G. G. Krishna Murthy ◽  
...  

Ozone (O3), a major component of urban air pollution, is a strong oxidizing agent that can cause lung injury and inflammation. In the present study, we investigated the effect of inhalation of O3 on levels of F2-isoprostanes in bronchoalveolar lavage fluid (BALF) and on levels of antioxidants in the BALF and plasma of hamsters. Because antioxidants, including urate, ascorbate, GSH, and vitamin E, defend the lungs by reacting with oxidizing agents, we expected to find a decrease in antioxidant levels after O3exposure. Similarly, we expected an increase in the levels of F2-isoprostanes, which are lipid peroxidation products. Exposure to 1.0 or 3.0 parts/million (ppm) O3 for 6 h resulted in an increase in BALF neutrophil numbers, an indicator of acute inflammation, as well as elevation of BALF F2-isoprostanes. The higher dose of O3 caused an increase in the BALF level of urate and a decrease in the plasma level of ascorbate, but 1.0 ppm O3 had no effect on BALF or plasma antioxidant levels. Exposure to 0.12 ppm O3 had no effect on BALF neutrophils or F2-isoprostanes nor on BALF and plasma antioxidants. We also investigated the effect of O3 exposure of hamsters during exercise on F2-isoprostane and antioxidant levels. We found that exposure to 1.0 ppm O3 during 1 h of exercise on a laddermill increased BALF levels of F2-isoprostanes but had no effect on BALF neutrophils or on BALF and plasma antioxidants. These results indicate that O3 induces inflammation and biomolecule oxidation in the lungs, whereas extracellular antioxidant levels are relatively unchanged.


2007 ◽  
Vol 115 (5) ◽  
pp. 756-763 ◽  
Author(s):  
John A. Lewis ◽  
K. Murali Krishna Rao ◽  
Vince Castranova ◽  
Val Vallyathan ◽  
William E. Dennis ◽  
...  

1994 ◽  
Vol 76 (3) ◽  
pp. 1232-1241 ◽  
Author(s):  
C. L. Bryan ◽  
A. J. Patefield ◽  
D. Cohen ◽  
J. L. Nielsen ◽  
B. Emanuel ◽  
...  

Single-lung transplantation after 3 h of hypothermic storage produces bilateral lung injury [pulmonary reimplantation response (PRR)]. We hypothesized that glutathione (GSH) hypothermic storage would protect both lungs from PRR for extended preservation times and that differences in injury and protection would be realized between the graft and the nontransplanted lung. Mongrel dogs underwent left single-lung autotransplantation after preservation for 5–6 h in Euro-Collins (EC) solution, EC plus exogenous GSH (EC+GSH), or Viaspan (VIA) at 4 degrees C. Lung injury was measured in both lungs after 1 h of reperfusion. EC dogs demonstrated significant increases in lung edema, lipid peroxidation, and alveolar neutrophil recruitment in the lung graft and to a less extent in the nontransplanted right lung compared with control dogs (P < 0.05). Edema, lipid peroxidation, and alveolar neutrophils were significantly reduced in both lungs from EC+GSH and VIA dogs compared with lungs from EC dogs (P < 0.05). An increase in large-pore permeability was measured in the lung graft from EC dogs compared with all other lungs. Bronchoalveolar lavage fluid lactate dehydrogenase and total protein concentrations were elevated in both lungs from all three groups of tranplanted dogs compared with those of control dogs (P < 0.05). These data suggest that GSH-containing solutions attenuate the PRR after 6 h of ischemic hypothermic storage but that the protection is incomplete. Mechanisms of injury affecting the lung graft during the PRR appear to differ from those affecting the nontransplanted lung.


1998 ◽  
Vol 6 (3) ◽  
pp. 177-185 ◽  
Author(s):  
Abdellaziz Ben-Jebria ◽  
Laju Satchithanandam ◽  
Rebecca J Gusic ◽  
Thomas R Gervais ◽  
James S Ultman

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