Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v28.i4.70

pages 325-340

Oxidative Stress and Antioxidant Defenses in Asthmatic Murine Model Exposed to Printer Emissions and Environmental Tobacco Smoke

Durga Bhavani Konga

Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea

Yoonshin Kim

Hanyang University

Seung Cheol Hong

Department of Occupational Health & Engineering, Inje University, Kimhae, Republic of Korea

Young Man Roh

Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea

Cheol Min Lee

Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea

Ki Youn Kim

Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea

So Min Lee

Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea

RESUMO

Exposure to particulate emissions from printer and cigarette smoke affects the structure and function of mitochondria, which may account for the pathogenesis of respiratory diseases. The addition of charge for the pollutant aerosols may increase the toxicity by their deposition in the lower respiratory tract. The mitochondrial damage in the lung of asthmatic mice was assessed by examining the levels of reactive oxygen species (ROS), lipid peroxides, reduced glutathione, and the activities of isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, complexes I to IV, and cytochrome c. The oxidative phosphorylation (levels of adenosine triphosphatase) was evaluated for the assessment of mitochondrial functional capacity. We found highly signifi cant elevated levels of ROS, lipid peroxides, and decreased levels of mitochondrial enzymes in the mice exposed to environmental tobacco smoke and printer emissions + environmental tobacco smoke (ETS). However, mice exposed to printer emissions alone exhibited slight signifi cant variations in the parameters studied. From the results, we conclude that printer emissions exert a synergistic effect in the presence of ETS and induce intense damage to the lung mitochondria by disrupting the structural and functional integrity of the mitochondrial membrane.