Health and Cellular Impacts of Air Pollutants: From Cytoprotection to Cytotoxicity
Figure 1
ROS-dependent and -independent apoptosis induced by particulate pollutants. Particulate matter (PM) or their compounds (PAHs and metals) provoke apoptotic cell death through ROS-dependent (pink zone) or ROS-independent (blue zone) pathways. Actually, particulate pollutants are considered as potent ROS generators from organic (i.e., PAHs) or metallic compounds (1) and leading to oxidative stress as the result of the unbalance between ROS production and activation of antioxidant defenses. Senft et al. demonstrated that AhR activation might regulate the mitochondrial respiratory chain function and induce production of and H2O2 from mitochondria ([83], (2)). As a consequence of oxidative stress, mitochondria are harmed by ROS that are responsible for damage of mitochondrial DNA (3), mitochondrial lipid peroxidation, and opening of PTP complex (PTP open. (4)). Mitochondrial membrane permeabilization (MMP) and PTP opening might also be a direct effect of diesel particles on isolated mitochondria ([84], (5)). As an additional pathway of the ROS-dependant apoptosis induced by air pollutants, the apoptogenic activity of AIF might be enhanced by xenobiotics, air pollutants, or their ROS derivatives (6). Some other ROS-independent signaling pathways have been identified such as the upregulation of proapoptotic proteins and/or the repression of prosurvival Bcl-2 family proteins (7). Recent publications also demonstrated a new mechanism of apoptosis triggered by PAHs through alterations of lipid rafts’ composition and remodeling of the plasma membrane (8). Illustrations carried out thanks to Servier Medical Art.
