title: Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone.
abstract: OBJECTIVE
  Acute exposure to particulate air pollution has been linked to acute cardiopulmonary events, but the underlying mechanisms are uncertain. EXPERIMENTAL APPROACH We investigated the acute (at 4 and 18 h) effects of diesel exhaust particles (DEP) on cardiopulmonary parameters in mice and the protective effect of thymoquinone, a constituent of Nigella sativa. Mice were given, intratracheally, either saline (control) or DEP (30 µg·per mouse). KEY RESULTS At 18 h (but not 4 h) after giving DEP, there was lung inflammation and loss of lung function. At both 4 and 18 h, DEP caused systemic inflammation characterized by leucocytosis, increased IL-6 concentrations and reduced systolic blood pressure (SBP). Superoxide dismutase (SOD) activity was decreased only at 18 h. DEP reduced platelet numbers and aggravated in vivo thrombosis in pial arterioles. In vitro, addition of DEP (0.1-1 µg·mL(-1)) to untreated blood-induced platelet aggregation. Pretreatment of mice with thymoquinone prevented DEP-induced decrease of SBP and leucocytosis, increased IL-6 concentration and decreased plasma SOD activity. Thymoquinone also prevented the decrease in platelet numbers and the prothrombotic events but not platelet aggregation in vitro.
  
  
  CONCLUSIONS
  At 4 h after DEP exposure, the cardiovascular changes did not appear to result from pulmonary inflammation but possibly from the entry of DEP and/or their associated components into blood. However, at 18 h, DEP induced significant changes in pulmonary and cardiovascular functions along with lung inflammation. Pretreatment with thymoquinone prevented DEP-induced cardiovascular changes.
authors.affiliation: Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE. anemmar@uaeu.ac.ae
authors.forename: Abderrahim
authors.initials: A
authors.lastname: Nemmar
authors.forename: Suhail
authors.initials: S
authors.lastname: Al-Salam
authors.forename: Shaheen
authors.initials: S
authors.lastname: Zia
authors.forename: Fatima
authors.initials: F
authors.lastname: Marzouqi
authors.forename: Amna
authors.initials: A
authors.lastname: Al-Dhaheri
authors.forename: Deepa
authors.initials: D
authors.lastname: Subramaniyan
authors.forename: Subramanian
authors.initials: S
authors.lastname: Dhanasekaran
authors.forename: Javed
authors.initials: J
authors.lastname: Yasin
authors.forename: Badreldin H
authors.initials: BH
authors.lastname: Ali
authors.forename: Elsadig E
authors.initials: EE
authors.lastname: Kazzam
mesh_terms: D000403:Airway Resistance / Q000187:drug effects; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology; D016227:Benzoquinones / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000503:physiopathology; D054022:Cerebrum / Q000098:blood supply / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D007958:Leukocyte Count; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D051379:Mice; D052638:Particulate Matter / Q000633:toxicity*; D010974:Platelet Aggregation / Q000187:drug effects; D011014:Pneumonia / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy / Q000473:pathology; D013482:Superoxide Dismutase / Q000097:blood; D013927:Thrombosis / Q000188:drug therapy / Q000503:physiopathology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000893:Anti-Inflammatory Agents; D016227:Benzoquinones; D015850:Interleukin-6; D052638:Particulate Matter; D001335:Vehicle Emissions; D013482:Superoxide Dismutase; C003466:thymoquinone