Abonnement à la biblothèque: Guest
Portail numérique Bibliothèque numérique eBooks Revues Références et comptes rendus Collections
Journal of Environmental Pathology, Toxicology and Oncology
Facteur d'impact: 1.625 Facteur d'impact sur 5 ans: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Imprimer: 0731-8898
ISSN En ligne: 2162-6537

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

RÉSUMÉ

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.


Articles with similar content:

Protective Effect of Bacoside A on Cigarette Smoking-Induced Brain Mitochondrial Dysfunction in Rats
Journal of Environmental Pathology, Toxicology and Oncology, Vol.24, 2005, issue 3
Ganapathy Vani, Chennam Srinivasulu Shyamala Devi
Nephroprotective Effect of Jaggery against Acute and Subchronic Toxicity of Acetaminophen in Wistar Rats
Journal of Environmental Pathology, Toxicology and Oncology, Vol.31, 2012, issue 3
Vinay Sharma, Chandra Kant Sharma
Reversal of Carbon Tetrachloride-Induced Hepatic Injury by Aqueous Extract of Artemisia absinthium in Sprague-Dawley Rats
Journal of Environmental Pathology, Toxicology and Oncology, Vol.31, 2012, issue 4
Monika Sharma, Sangeeta Shukla
Bioenergetics for Hepatocyte Polarization: Coordination of Multiple Cellular Organelles and the Master Regulator AMPK
Critical Reviews™ in Eukaryotic Gene Expression, Vol.29, 2019, issue 5
Sun Woo Sophie Kang, Dong Fu
In Vivo Toxicity of the Culturable Marine Cyanobacterium Geitlerinema pseudacutissimum CNP 1019 Extract on Male Swiss Albino Mice (Mus musculus)
Journal of Environmental Pathology, Toxicology and Oncology, Vol.33, 2014, issue 2
Veerabadhran Maruthanayagam, Manivel Nagarajan, Sundararaman Muthuraman