Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 12, Issue -, Pages 1238-1246Publisher
BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/2142
Keywords
particulate matter (PM); ROS; apoptosis; oxidative stress; mitochondria; PT pore; review
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Funding
- NIAID NIH HHS [P01 AI50495] Funding Source: Medline
- NIEHS NIH HHS [R01 ES10553, R01 ES13432, R01 ES10253] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI050495] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES013432, R01ES010553] Funding Source: NIH RePORTER
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Increasing evidence suggests that reactive oxygen species ( ROS) and oxidative stress are involved in PM-mediated lung and cardiovascular injury. The physical characteristics and the chemical composition of particulate matter ( PM) play a key role in ROS generation in vitro and in vivo. The mitochondria are major subcellular targets for PM as well as a source of ROS production. ROS production is due to interference in mitochondrial electron transfer and PT pore opening by pro-oxidative PM components. Another possible mechanism is direct physical targeting by ambient ultrafine particles that lodge in and destroy mitochondrial structure. An understanding of the mitochondrial effects of PM is key in understanding the mechanisms of PM-induced adverse health effects.
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