title: Multigenerational mitochondrial alterations in pneumocytes exposed to oil fly ash metals.
abstract: Oil fly ash (OFA), containing high amounts of transition metals, is among the most reactive airborne particulate matter emissions, which have been associated with several diseases, such as chronic obstructive pulmonary diseases (COPD), lung cancer, and cardiovascular diseases. The aim of the present study was to evaluate mitochondrial alterations in OFA-exposed cultured pneumocytes and in their progeny. Alveolar epithelial cells (A549 line) were exposed either to an OFA water solution, containing 68.8 μM vanadium (V), 110.4 μM iron (Fe), and 18.0 μM nickel (Ni), or to the individual metal solutions. Structural and functional mitochondrial parameters were determined in exposed cultures and in 3 consecutive subcultures. OFA, V and Fe solutions caused a time-dependent loss of mitochondrial enzymatic activity, glutathione depletion, generation of lipid hydroperoxides, hydrogen peroxide and other reactive oxygen species, especially in G(0)-G(1) phase cells, accompanied by a decrease in mitochondrial mass and transmembrane potential. Mitochondrial alterations were partly transmissible to daughter cells for up to 3 generations. Fe and especially V were responsible for the observed mitochondrial alterations in pneumocytes exposed to OFA. Spread of mitochondrial dysfunctions to daughter cells is expected to amplify oxidative stress in the respiratory epithelium and to play an important role in the pathogenesis of respiratory diseases.
authors.affiliation: Department of Hygiene, Public Health and Preventive Medicine, University of Messina, I-98100 Messina, Italy.
authors.forename: Angela
authors.initials: A
authors.lastname: Di Pietro
authors.forename: Giuseppa
authors.initials: G
authors.lastname: Visalli
authors.forename: Barbara
authors.initials: B
authors.lastname: Baluce
authors.forename: Rosanna T
authors.initials: RT
authors.lastname: Micale
authors.forename: Sebastiano
authors.initials: S
authors.lastname: La Maestra
authors.forename: Pasquale
authors.initials: P
authors.lastname: Spataro
authors.forename: Silvio
authors.initials: S
authors.lastname: De Flora
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects; D056809:Alveolar Epithelial Cells / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D002244:Carbon / Q000009:adverse effects* / Q000737:chemistry; D002453:Cell Cycle; D045744:Cell Line, Tumor; D060729:Coal Ash; D004781:Environmental Exposure / Q000009:adverse effects*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007220:Industrial Waste / Q000009:adverse effects; D007501:Iron / Q000009:adverse effects; D015227:Lipid Peroxidation / Q000187:drug effects; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D019216:Metals, Heavy / Q000009:adverse effects*; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D009532:Nickel / Q000009:adverse effects; D018384:Oxidative Stress / Q000187:drug effects*; D052638:Particulate Matter / Q000009:adverse effects* / Q000737:chemistry; D017382:Reactive Oxygen Species / Q000378:metabolism; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D012140:Respiratory Tract Diseases / Q000209:etiology; D028561:Transition Elements / Q000009:adverse effects; D014639:Vanadium / Q000009:adverse effects
chemical_list: D000393:Air Pollutants; D060729:Coal Ash; D007220:Industrial Waste; D019216:Metals, Heavy; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D028561:Transition Elements; D014639:Vanadium; D002244:Carbon; D009532:Nickel; D007501:Iron; D005978:Glutathione