title: Myocardial mitochondrial injury induced by pulmonary exposure to particulate matter in rats.
abstract: Exposure to air pollution has been associated with acute myocardial ischemia, impaired myocardrial function, and ST-segment depression. Particulate matter (PM)-associated metals, especially vanadium and nickel, have been implicated in observed cardiovascular impairments. We aimed to assess the effect of single intratracheal pulmonary exposure to vanadium-rich respirable oil combustion PM (HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats. The authors subjected isolated heart tissue slices derived from saline or PM-exposed rats to low glucose low oxygen induced ischemia followed by oxygenated condition with glucose supplementation. Mitochondrial structural integrity was determined by TEM (transmission electron microscopy) and functionality by the 3-(4, 5 dimethylthiazol-2yl)-2, 5 diphenyltetrazolium bromide (MTT) assay. Rats exposed to PM exhibited no apparent inhibition of mitochondrial dehydrogenase activity in oxygenated conditions at 24 or 48 hr post-PM exposure. However, in conditions of simulated ischemia/reoxygenation, these heart slices showed a delayed but consistent and significant decrease in dehydrogenase activity compared to controls at 48 hr after exposure to PM. Electron microscopy revealed significant myocardial mitochondrial injury upon exposure to PM characterized by mitochondrial swelling and fusion. The authors conclude that exposure to soluble vanadium-rich PM induces mitochondrial functional impairment and structural abnormality, which compromises mitochondrial respiration and results in decreased tolerance to ischemia/reoxygenation in rats.
authors.affiliation: Department of Pathology, Shaare Zedek Medical Center, Hebrew University School of Medicine, Jerusalem, Israel.
authors.forename: Eliahu
authors.initials: E
authors.lastname: Golomb
authors.forename: Didi
authors.initials: D
authors.lastname: Matza
authors.forename: Connie A
authors.initials: CA
authors.lastname: Cummings
authors.forename: Herzl
authors.initials: H
authors.lastname: Schwalb
authors.forename: Urmila P
authors.initials: UP
authors.lastname: Kodavanti
authors.forename: Aviva
authors.initials: A
authors.lastname: Schneider
authors.forename: Esther
authors.initials: E
authors.lastname: Houminer
authors.forename: Amit
authors.initials: A
authors.lastname: Korach
authors.forename: Abraham
authors.initials: A
authors.lastname: Nyska
authors.forename: Oz M
authors.initials: OM
authors.lastname: Shapira
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D006335:Heart Injuries / Q000473:pathology; D007511:Ischemia / Q000473:pathology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D009206:Myocardium / Q000473:pathology*; D009532:Nickel / Q000633:toxicity; D010084:Oxidation-Reduction; D010100:Oxygen / Q000097:blood; D052638:Particulate Matter / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014639:Vanadium / Q000633:toxicity
chemical_list: D001786:Blood Glucose; D052638:Particulate Matter; D014639:Vanadium; D009532:Nickel; D010100:Oxygen