The Capacity of Murine Epithelial Cell Lines with Different Degrees of Malignant Transformation to Metabolise Benzo[a]pyrene

1996 ◽  
Vol 24 (4) ◽  
pp. 541-546
Author(s):  
Cristina Viezzer ◽  
Roberto Revoltella ◽  
Lucia Celotti

Cultures of three murine cell lines derived from fetal mouse liver (FL, FLT3 and FLT5) were treated with benzo[a]pyrene to evaluate their ability to activate promutagens. DNA adducts were detected in all three cell lines when they were treated with the major active metabolite of benzo[a]pyrene, benzo[a]pyrene diolepoxide. DNA adducts were also produced in FL and FLT3 cells when they were treated with the promutagen, benzo[a]pyrene, while treatment of FLT5 cells resulted in very few DNA adducts. In treated FL and FLT3 cells, the most evident adduct spot detected showed a chromatographic position similar to that of the main adduct formed in cells treated with (±)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydro-benzo[a]pyrene.

2019 ◽  
Vol 20 (7) ◽  
pp. 1678 ◽  
Author(s):  
Yi-Chen Lee ◽  
Chun-Yu Lin ◽  
Yen-Hsu Chen ◽  
Wen-Chin Chiu ◽  
Yen-Yun Wang ◽  
...  

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.


2003 ◽  
Vol 80 (4) ◽  
pp. 444-450 ◽  
Author(s):  
Jae-Kyung Myung ◽  
Kurt Krapfenbauer ◽  
Rachel Weitzdoerfer ◽  
Andreas Peyrl ◽  
Michael Fountoulakis ◽  
...  

2007 ◽  
Vol 4 (1) ◽  
pp. 11 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Crissey L Pascale ◽  
Andrew N Pfeffer ◽  
Cassaundra Coulter ◽  
Adam Chodobski

ORL ◽  
1984 ◽  
Vol 46 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Tom Takimoto ◽  
Kazuo Morishita ◽  
Ryozo Umeda ◽  
Hisashi Ogura ◽  
Motoichi Hatano

FEBS Letters ◽  
2000 ◽  
Vol 473 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Qing-Bai She ◽  
Jagat J Mukherjee ◽  
Karan S Crilly ◽  
Zoltan Kiss

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