Document Detail


Formaldehyde induces apoptosis through decreased Prx 2 via p38 MAPK in lung epithelial cells.
MedLine Citation:
PMID:  20347000     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Formaldehyde (FA) is an important substance that induces sick house syndrome and diseases, such as asthma and allergies. Oxidative stress is involved in the development of respiratory disease, and diverse antioxidants may protect respiratory tract cells from apoptosis. Peroxiredoxin is a pivotal endogenous antioxidant. In the present study, FA induced death in A549 cells, a lung epithelial cell line, in a dose-dependent manner. FA also increased lipid peroxide formation (LPO) in A549 cells, suggesting a role for oxidative stress. Additionally, FA decreased peroxiredoxin 2 (Prx 2) protein levels after a 24 or 48h exposure to FA. We also examined whether the FA-induced decrease in Prx 2 was associated with apoptosis. Prx 2 overexpression protected against FA-induced cell apoptosis but not necrosis. Prx 2 overexpression blocked FA-induced increase in Bax, a pro-apoptotic molecule, and a decrease in Bcl-2, an anti-apoptotic molecule. Prx 2 overexpression also protected against FA-induced activation of some special apoptosis-associated proteins [caspase-3, caspase-9, and polypeptide poly (ADP-ribose) polymerase (PARP)]. Furthermore, we examined the signaling molecules involved in the FA-induced decrease in Prx 2 expression. The FA-induced decrease in Prx 2 and increase in cell apoptosis was restored by treatment with SB203580 [a p38 mitogen activated protein kinase (MAPK) inhibitor], but not by SP600125 [a c-jun-N-terminal kinase (JNK) inhibitor]. Also, FA-induced events were blocked by treatment with p38 siRNA, but not by scrambled siRNA. Indeed, FA increased p38 MAPK activation, suggesting a role for p38 MAPK in FA action. In conclusion, FA mediated apoptosis in lung epithelial cells by decreasing Prx 2 via p38 MAPK.
Authors:
Seul Ki Lim; Jong Chun Kim; Chang Jong Moon; Gye Yeop Kim; Ho Jae Han; Soo Hyun Park
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-25
Journal Detail:
Title:  Toxicology     Volume:  271     ISSN:  1879-3185     ISO Abbreviation:  Toxicology     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-10     Completed Date:  2010-05-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0361055     Medline TA:  Toxicology     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  100-6     Citation Subset:  IM    
Affiliation:
Bio-therapy Human Resources Center, College of Veterinary Medicine, Chonnam National University, Yongbongdong 300 Bukgu, Gwangju 500-757, Republic of Korea.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Diphosphate Ribose / metabolism
Apoptosis / physiology*
Caspase 3 / metabolism
Caspase 9 / metabolism
Cell Death
Cell Line, Tumor
Epithelial Cells / metabolism*
Formaldehyde / metabolism*
Genes, bcl-2
Humans
Lung / metabolism,  pathology
Oxidative Stress
Peroxiredoxins / metabolism*
Poly(ADP-ribose) Polymerases / metabolism
bcl-2-Associated X Protein / metabolism
p38 Mitogen-Activated Protein Kinases / metabolism*
Chemical
Reg. No./Substance:
0/bcl-2-Associated X Protein; 20762-30-5/Adenosine Diphosphate Ribose; 50-00-0/Formaldehyde; EC 1.11.1.15/Peroxiredoxins; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9

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