225
Views
20
CrossRef citations to date
0
Altmetric
Research Article

N-acetylcysteine protects alveolar epithelial cells from hydrogen peroxide–induced apoptosis through scavenging reactive oxygen species and suppressing c-Jun N-terminal kinase

, , , &
Pages 352-361 | Received 18 May 2009, Accepted 04 Feb 2010, Published online: 24 Jul 2010
 

ABSTRACT

The production of reactive oxygen species (ROS) during hyperoxia contribute to alveolar epithelial apoptosis. In the present study, the molecular mechanisms of oxidative stress–induced alveolar epithelial cell apoptosis were investigated. The cytoprotective effects of N-acetylcysteine (NAC) were evaluated. Treatments using 500 μM H2O2 can induce primary alveolar type II epithelial cell apoptosis. During this procedure, c-Jun N-terminal kinase (JNK) was activated. SP600125, a specific inhibitor of JNK, can partially block H2O2-induced alveolar type II epithelial cells (ATII cells). SP600125 also attenuated Bax protein content and p53 nuclear accumulation induced by H2O2. NAC (5 mM) pretreatment decreased H2O2-induced ATII cell apoptosis. The high level of intracellular reactive oxygen species (ROS) induced by H2O2 was also attenuated by NAC pretreatment. Taken together, H2O2 can induce primary ATII cells apoptosis and increase JNK phosphorylation. NAC, a precursor of glutathione (GSH) synthesis, can protect ATII cells from H2O2-induced apoptosis through scavenging ROS.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.