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Li, N., Xia, T. & Nel, A. E. The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. Free Radic. Biol. Med. 44, 1689-1699

Division of NanoMedicine, Department of Medicine, University of California, Los Angeles, CA 90095, USA.
Free Radical Biology and Medicine (Impact Factor: 5.71). 06/2008; 44(9):1689-99. DOI: 10.1016/j.freeradbiomed.2008.01.028
Source: PubMed

ABSTRACT Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The proinflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered nanoparticles (NP) may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effects of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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    • "The use of DF confirmed that trace elements play a significant role in ROS formation in vitro. Transition metal ions associated with PM can produce ROS or catalyze the formation of hydroxyl radical from hydrogen peroxide through Fenton and Haber–Weiss reactions (Li et al., 2008). PACs, such as quinone and hydroquinones , can produce the superoxide ion that act as a catalyst for the Fenton and Haber–Weiss reactions (Akhtar et al., 2010; Balakrishna et al., 2009). "
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    • "Total cellular inflammation in BALF from this acute study did not significantly correlate with the ability of PM to exacerbate allergic airway inflammation; pulmonary HO-1 levels, however, demonstrated a strong positive correlation with total cellular inflammation, as well as lymphocyte and eosinophil specific recruitment in the allergic model. This finding is in agreement with the hypotheses that PM adjuvant effects are mediated through PM-induced oxidative stress in the lung and, specifically, increased intracellular ROS in antigen presenting cells (Li et al., 2008). Pulmonary HO-1 levels were reported to be an effective marker of oxidative stress (Ayres et al., 2008; Li et al., 2009), and prior in vitro research indicated HO-1 as a biomarker of exposure to quantum dot nanoparticles, which elicit their acute toxicity via generation of reactive oxygen intermediates (McConnachie et al., 2013). "
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    • "At an intermediate level of oxidative stress (Tier 2), activation of MAPK and NF-κB cascades induces pro-inflammatory responses, e.g., cytokines and chemokines. Finally, at a high level of oxidative stress (established as Tier 3), perturbation of the mitochondrial permeability transition pore and disruption of electron transfer result in cellular apoptosis or necrosis (Xia et al. 2008; Li et al. 2008). The expression of two enzymes involved in tier 1 response (Ho1 and Sod2) was evaluated in this study. "
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