The Role of Particulate Matter-Associated Zinc in Cardiac Injury in Rats

DSpace/Manakin Repository

The Role of Particulate Matter-Associated Zinc in Cardiac Injury in Rats

Show simple item record Kodavanti, Urmila P. Schladweiler, Mette C. Gilmour, Peter S. Wallenborn, J. Grace Mandavilli, Bhaskar S. Ledbetter, Allen D. Runge, Marschall S. Karoly, Edward D. Peddada, Shyamal Jaskot, Richard Richards, Judy H. Thomas, Ronald Madamanchi, Nageswara R. Nyska, Abraham Christiani, David C. Costa, Daniel L. 2011-12-24T05:25:32Z 2008
dc.identifier.citation Kodavanti, Urmila P., Mette C. Schladweiler, Peter S. Gilmour, J. Grace Wallenborn, Bhaskar S. Mandavilli, Allen D. Ledbetter, David C. Christiani, et al. 2008. The role of particulate matter-associated zinc in cardiac injury in rats. Environmental Health Perspectives 116(1): 13-20. en_US
dc.identifier.issn 0091-6765 en_US
dc.description.abstract Background: Exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity; however, causative components are unknown. Zinc is a major element detected at high levels in urban air.Objective We investigated the role of PM-associated zinc in cardiac injury. Methods: We repeatedly exposed 12- to 14-week-old male Wistar Kyoto rats intratracheally (1×/week for 8 or16 weeks) to a) saline (control); b) PM having no soluble zinc (Mount St. Helens ash, MSH); or c) whole-combustion PM suspension containing 14.5 μg/mg of water-soluble zinc at high dose (PM-HD) and d ) low dose (PM-LD), e) the aqueous fraction of this suspension (14.5 μg/mg of soluble zinc) (PM-L), or f ) zinc sulfate (rats exposed for 8 weeks received double the concentration of all PM components of rats exposed for 16 weeks). Results: Pulmonary inflammation was apparent in all exposure groups when compared with saline (8 weeks greater than 16 weeks). PM with or without zinc, or with zinc alone caused small increases in focal subepicardial inflammation, degeneration, and fibrosis. Lesions were not detected in controls at 8 weeks but were noted at 16 weeks. We analyzed mitochondrial DNA damage using quantitative polymerase chain reaction and found that all groups except MSH caused varying degrees of damage relative to control. Total cardiac aconitase activity was inhibited in rats receiving soluble zinc. Expression array analysis of heart tissue revealed modest changes in mRNA for genes involved in signaling, ion channels function, oxidative stress, mitochondrial fatty acid metabolism, and cell cycle regulation in zinc but not in MSH-exposed rats. Conclusion: These results suggest that water-soluble PM-associated zinc may be one of the causal components involved in PM cardiac effects. en_US
dc.language.iso en_US en_US
dc.publisher National Institute of Environmental Health Sciences en_US
dc.relation.isversionof doi:10.1289/ehp.10379 en_US
dc.relation.hasversion en_US
dash.license LAA
dc.subject aconitase en_US
dc.subject air pollution en_US
dc.subject cardiac gene expression profile en_US
dc.subject mitochondria en_US
dc.subject particulate matter en_US
dc.subject zinc en_US
dc.title The Role of Particulate Matter-Associated Zinc in Cardiac Injury in Rats en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Environmental Health Perspectives en_US Christiani, David C. 2011-12-24T05:25:32Z
dash.affiliation.other HMS^Medicine-Massachusetts General Hospital en_US
dash.affiliation.other SPH^Environmental+Occupational Medicine+Epi en_US

Files in this item

Files Size Format View
2199289.pdf 386.7Kb PDF View/Open

This item appears in the following Collection(s)

Show simple item record


Search DASH

Advanced Search