airborne particulate matter and mitochondrial damage a cross-sectional study空气中的颗粒物和线粒体损伤一个横断面研究.pdfVIP
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airborne particulate matter and mitochondrial damage a cross-sectional study空气中的颗粒物和线粒体损伤一个横断面研究
Hou et al. Environmental Health 2010, 9:48
/content/9/1/48
RESEARCH Open Access
Airborne particulate matter and mitochondrial
damage: a cross-sectional study
1,2* 3,4 1 3,5 6 7
Lifang Hou , Zhong-Zheng Zhu , Xiao Zhang , Francesco Nordio , Matteo Bonzini , Joel Schwartz ,
3 3 3 3 8 3
Mirjam Hoxha , Laura Dioni , Barbara Marinelli , Valeria Pegoraro , Pietro Apostoli , Pier Alberto Bertazzi ,
Andrea Baccarelli3,7
Abstract
Background: Oxidative stress generation is a primary mechanism mediating the effects of Particulate Matter (PM)
on human health. Although mitochondria are both the major intracellular source and target of oxidative stress, the
effect of PM on mitochondria has never been evaluated in exposed individuals.
Methods: In 63 male healthy steel workers from Brescia, Italy, studied between April and May 2006, we evaluated
whether exposure to PM was associated with increased mitochondrial DNA copy number (MtDNAcn), an
established marker of mitochondria damage and malfunctioning. Relative MtDNAcn (RMtDNAcn) was determined
by real-time PCR in blood DNA obtained on the 1st (time 1) and 4th day (time 2) of the same work week.
Individual exposures to PM , PM , coarse particles (PM -PM ) and airborne metal components of PM (chromium,
10 1 10 1 10
lead, arsenic, nickel, manganese) were estimated based on measurements in the 11 work areas and time spent by
the study subjects in each area.
Results: RMtDNAcn was higher on t
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