Mansoor, SGupta, NFalatoonzadeh, PKuppermann, B DKenney, M C2015-01-272015-01-272014-01Mansoor S, Gupta N, Falatoonzadeh P, Kuppermann B D, Kenney M C. 2-ethylpyridine, a cigarette smoke component, causes mitochondrial damage in human retinal pigment epithelial cells in vitro. Indian Journal of Ophthalmology. 2014 Jan ; 62 (1): 16-22.http://imsear.searo.who.int/handle/123456789/155500Purpose: 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 fl uorochrome assays. The production of reactive oxygen/nitrogen species (ROS/RNS) was detected with a 2’,7’-dichlorodihydrofl uorescein diacetate dye assay. The JC-1 assay was used to measure mitochondrial membrane potential (m). Mitochondrial redox potential was measured using a RedoxSensor Red kit and mitochondria were evaluated with Mitotracker dye. Results: Aft er 2-EP exposure, ARPE-19 cells showed signifi cantly decreased CV, increased caspase-3/7 and caspase-9 activities, elevated ROS/RNS levels, decreased m value and decreased redox fl uorescence 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.en2-ethylpyridineapoptosisARPE-19 cellscigarett e smoke toxicantmitochondrial membrane potentialreactive oxygen/nitrogen speciesArticle