title: Induction of cardiac fibrosis and transforming growth factor-β1 by motorcycle exhaust in rats.
abstract: Motorcycle exhaust (ME) is a major source of air pollution and a potential health hazard in urban areas where motorcycles are a popular means of transportation. The main objectives of this study were to determine the ability of ME to cause cardiotoxicity in rats and investigate the possible mechanisms of toxicity. Male rats were exposed to 1:10 diluted ME by inhalation 2 h daily and Monday through Friday for 8 weeks. Exposure to ME increased heart weight and decreased cardiac antioxidant enzymes glutathione S-transferase (GST), superoxide dismutase and glutathione peroxidase activities in a concentration- and time-dependent manner. Analysis of echocardiographic parameters indicated that ME increased left ventricle posterior wall thickness, interventricular septum thickness and left ventricle mass. Histopathological examinations of the hearts revealed that ME exposure caused focal cardial degeneration and necrosis, mononuclear cell infiltration, and fibrosis. The results of reverse transcriptase-polymerase chain reaction studies showed that ME decreased GST-M1 and GST-P1 mRNA expression and increased the expression of proinflammatory cytokine interleukin-1β, hypertrophy marker atrial natriuretic peptide, fibrosis markers type I and III collagen, profibrotic cytokine connective tissue growth factor, and hypertrophy and fibrosis mediator transforming growth factor (TGF)-β1 in the heart. The data of Western blot analysis showed that cardiac TGF-β1 protein was induced by ME. These findings demonstrate that subchronic ME exposure caused hypertrophy and fibrosis, and modulated GST and TGF-β1 expression in rat heart possibly by mechanisms involving oxidative stress and inflammation.
authors.affiliation: Department of Anesthesiology, Taipei Medical University Hospital, Taipei, Taiwan, ROC.
authors.forename: Ta-Liang
authors.initials: TL
authors.lastname: Chen
authors.forename: Jiunn-Wang
authors.initials: JW
authors.lastname: Liao
authors.forename: Wei-Hung
authors.initials: WH
authors.lastname: Chan
authors.forename: Chiung-Yuan
authors.initials: CY
authors.lastname: Hsu
authors.forename: Jr-Di
authors.initials: JD
authors.lastname: Yang
authors.forename: Tzuu-Huei
authors.initials: TH
authors.lastname: Ueng
mesh_terms: D015660:7-Alkoxycoumarin O-Dealkylase / Q000378:metabolism; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D002248:Carbon Monoxide / Q000633:toxicity; D006332:Cardiomegaly / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D024042:Collagen Type I / Q000235:genetics; D024043:Collagen Type II / Q000235:genetics; D005355:Fibrosis; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics; D015227:Lipid Peroxidation; D008297:Male; D009049:Motorcycles; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D024042:Collagen Type I; D024043:Collagen Type II; D053583:Interleukin-1beta; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D001335:Vehicle Emissions; D002248:Carbon Monoxide; D009320:Atrial Natriuretic Factor; D005979:Glutathione Peroxidase; D015660:7-Alkoxycoumarin O-Dealkylase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase