[Frontiers in Bioscience 12, 1238-1246, January 1, 2007]

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

Tian Xia, Michael Kovochich, and Andre E. Nel

Division of Clinical Immunology and Allergy, Department of Medicine; Southern California Particle Center and Supersite, University of California, Los Angeles, CA

TABLES

Table 1. PM-induced mitochondrial effects

PM components

Mitochondrial effects

Cellular consequences

Quinones

Disrupt the electron transfer chain

­ ROS, ¯ ATP

­ ROS generation

Oxidative stress

­ Ca2+-regulated PT pore opening

CsA-sensitive mitochondrial swelling and apoptosis

¯ Calcium Retention Capacity

Apoptosis

Aromatic compounds

Non-Ca2+ regulated PT pore opening

CsA-insensitive mitochondrial swelling and apoptosis

¯ Calcium Retention Capacity

¯ PT pore threshold to PT

Transition metals

¯ Psim

¯ ATP, energy crisis, necrosis

­ ROS generation

Oxidative stress

PT pore opening

Apoptosis

Ultrafine Particles

Mitochondrial localization

Mitochondrial structural damage

ROS generation

Chemical/Particle induced ROS

Oxidative stress

Phase II enzyme expression (Tier1),

Inflammation (Tier2)

Apoptosis (Tier3)

mtDNA damage

Dysfunctional mitochondria

Lipid, protein peroxidation

¯ Oxidative phosphorylation

PM induced [Ca2+]i ­

Ca2+-regulated PT pore opening

Apoptosis