Abstract View
Chemical and Cellular Superoxide Generation upon Respiratory Deposition of Quinones and Secondary Organic Aerosols
TING FANG, Yu-Kai Huang, Jinlai Wei, Jessica Monterrosa, Pascale Lakey, Michael Kleinman, Michelle Digman, Manabu Shiraiwa, University of California, Irvine
Abstract Number: 152
Working Group: Health-Related Aerosols
Abstract
Deposition of particulate matter (PM) in the respiratory tract causes formation of reactive oxygen species (ROS) which can trigger oxidative stress and inflammation leading to cardiorespiratory disease. PM can form ROS through chemical reactions such as redox cycling and decomposition of organic species, or can stimulate macrophages to release ROS biologically in lung fluid. However, the relative contributions of chemical and cellular ROS are seldom quantified and the mechanisms linking them to adverse health effects remain uncertain. Here we apply a chemiluminescence assay calibrated with an Electron Paramagnetic Resonance spectrometer coupled with a spin trapping technique to quantify superoxide production. We measure cellular ROS release by RAW 264.7 macrophage cells and chemical superoxide generation in vitro by PM components including quinone and biogenic and anthropogenic secondary organic aerosols (SOA). We show that atmospherically-relevant doses of quinone activate macrophages to release massive cellular superoxide and cause lipid oxidation, as revealed by fluorescence lifetime imaging (FLIM) coupled with a phasor approach, while higher doses trigger cellular antioxidant response elements that protect against further oxidative damages. We find that chemical ROS is more important for SOA as macrophages remain mostly inactive after exposures to atmospherically-relevant SOA.