Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 2668
  • Home
  • Print this page
  • Email this page
ORIGINAL ARTICLE
Year : 2014  |  Volume : 62  |  Issue : 1  |  Page : 16-22

2-ethylpyridine, a cigarette smoke component, causes mitochondrial damage in human retinal pigment epithelial cells in vitro


1 Gavin Herbert Eye Institute, School of Medicine, University of California Irvine, Irvine; Department of Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, GA, USA
2 Gavin Herbert Eye Institute, School of Medicine, University of California Irvine, Irvine CA, USA; Department of Ophthalmology, Lotus Eye Care Hospital, Coimbatore, TN, India
3 Gavin Herbert Eye Institute, School of Medicine, University of California Irvine, Irvine CA; Drexel University, College of Medicine, Philadelphia, PA, USA
4 Gavin Herbert Eye Institute, School of Medicine, University of California Irvine, Irvine CA, USA
5 Gavin Herbert Eye Institute, School of Medicine; Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA, USA

Correspondence Address:
M C Kenney
Gavin Herbert Eye Institute, Ophthalmology Research Laboratory, University of California Irvine, Hewitt Hall, Room 2028, 843 Health Science Rd., Irvine, CA 92697, USA

Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.126168

Rights and Permissions

Purpose: Our goal was to identify the cellular and molecular effects of 2-ethylpyridine (2-EP, a component of cigarette smoke) on human retinal pigment epithelial cells (ARPE-19) in vitro. Materials and Methods: ARPE-19 cells were exposed to varying concentrations of 2-EP. Cell viability (CV) was measured by a trypan blue dye exclusion assay. Caspase-3/7 and caspase-9 activities were measured by fluorochrome assays. The production of reactive oxygen/nitrogen species (ROS/RNS) was detected with a 2',7'-dichlorodihydrofluorescein diacetate dye assay. The JC-1 assay was used to measure mitochondrial membrane potential (ΔΨm). Mitochondrial redox potential was measured using a RedoxSensor Red kit and mitochondria were evaluated with Mitotracker dye. Results: After 2-EP exposure, ARPE-19 cells showed significantly decreased CV, increased caspase-3/7 and caspase-9 activities, elevated ROS/RNS levels, decreased ΔΨm value and decreased redox fluorescence when compared with control samples. Conclusions: These results show that 2-EP treatment induced cell death by caspase-dependent apoptosis associated with an oxidative stress and mitochondrial dysfunction. These data represent a possible mechanism by which smoking contributes to age-related macular degeneration and other retinal diseases and identify mitochondria as a target for future therapeutic interventions.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed1794    
    Printed33    
    Emailed0    
    PDF Downloaded192    
    Comments [Add]    

Recommend this journal