Impairment of mitochondrial function by particulate matter (PM) and their toxic components: implications for PM-induced cardiovascular and lung disease

被引:107
作者
Xia, Tian [1 ]
Kovochich, Michael [1 ]
Nel, Andre E. [1 ]
机构
[1] Univ Calif Los Angeles, Sch Med, Dept Med, Div Clin Immunol & Allergy,So Calif Particle Ctr, Los Angeles, CA 90095 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
particulate matter (PM); ROS; apoptosis; oxidative stress; mitochondria; PT pore; review; PERMEABILITY TRANSITION PORE; DIESEL EXHAUST PARTICLES; OXIDATIVE STRESS; AIR-POLLUTION; FREE-RADICALS; OXIDIZED LDL; DNA-DAMAGE; CELL-DEATH; APOPTOSIS; DYSFUNCTION;
D O I
10.2741/2142
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1238 / 1246
页数:9
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