Oxidative stress and antioxidant defenses in asthmatic murine model exposed to printer emissions and environmental tobacco smoke.
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, alpha-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 significant 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 significant 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.
Konga
Durga Bhavani
DB
Institute of Industrial and Environmental Medicine (IEIM), Hanyang University, Seoul, Republic of Korea.
Kim
Yoonshin
Y
Hong
Seung Cheol
SC
Roh
Young Man
YM
Lee
Cheol Min
CM
Kim
Ki Youn
KY
Lee
So Min
SM
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001249:Asthma / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D001273:Atmosphere Exposure Chambers; D004195:Disease Models, Animal; D055615:Electrical Equipment and Supplies / Q000009:adverse effects*; D045222:Electron Transport Chain Complex Proteins / Q000378:metabolism; D005260:Female; D007521:Isocitrate Dehydrogenase / Q000378:metabolism; D007655:Ketoglutarate Dehydrogenase Complex / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D052638:Particulate Matter / Q000633:toxicity*; D010758:Phosphorus / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000378:metabolism; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D000975:Antioxidants; D045222:Electron Transport Chain Complex Proteins; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D014028:Tobacco Smoke Pollution; D010758:Phosphorus; D008291:Malate Dehydrogenase; D007521:Isocitrate Dehydrogenase; D007655:Ketoglutarate Dehydrogenase Complex; D013385:Succinate Dehydrogenase; D000251:Adenosine Triphosphatases