| Literature DB >> 24316006 |
Jun-Ho Jang1, Shannon Bruse2, Yushi Liu2, Veronica Duffy2, Chunyu Zhang2, Nathaniel Oyamada2, Scott Randell3, Akiko Matsumoto4, David C Thompson4, Yong Lin2, Vasilis Vasiliou4, Yohannes Tesfaigzi2, Toru Nyunoya5.
Abstract
Aldehyde dehydrogenase 3A1 (ALDH3A1), an ALDH superfamily member, catalyzes the oxidation of reactive aldehydes, highly toxic components of cigarette smoke (CS). Even so, the role of ALDH3A1 in CS-induced cytotoxicity and DNA damage has not been examined. Among all of the ALDH superfamily members, ALDH3A1 mRNA levels showed the greatest induction in response to CS extract (CSE) exposure of primary human bronchial epithelial cells (HBECs). ALDH3A1 protein accumulation was accompanied by increased ALDH enzymatic activity in CSE-exposed immortalized HBECs. The effects of overexpression or suppression of ALDH3A1 on CSE-induced cytotoxicity and DNA damage (γH2AX) were evaluated in cultured immortalized HBECs. Enforced expression of ALDH3A1 attenuated cytotoxicity and downregulated γH2AX. SiRNA-mediated suppression of ALDH3A1 blocked ALDH enzymatic activity and augmented cytotoxicity in CSE-exposed cells. Our results suggest that the availability of ALDH3A1 is important for cell survival against CSE in HBECs. Published by Elsevier Inc.Entities:
Keywords: ALDH3A1; Airway epithelial cells; Chronic obstructive pulmonary disease; Cigarette smoke; Cytotoxicity; DNA damage; FANCD2; Free radicals; Reactive aldehydes
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Year: 2013 PMID： 24316006 PMCID： PMC3941192 DOI： 10.1016/j.freeradbiomed.2013.11.028
Source DB: PubMed Journal: Free Radic Biol Med ISSN： 0891-5849 Impact factor: 7.376