Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage.

By Ning Li, C. Sioutas, A. Cho, D. Schmitz, Chandan Misra, J. Sempf, Meiying Wang, T. Oberley, J. Froines, A. Nel. Environmental Health Perspectives, 2002

2,086 citations recorded by the source corpus.

The objectives of this study were to determine whether differences in the size and composition of coarse (2.5-10 micro m), fine (< 2.5 microm), and ultrafine (< 0.1 microm) particulate matter (PM) are related to their uptake in macrophages and epithelial cells and their ability to induce oxidative stress. The premise for this study is the increasing awareness that various PM components induce pulmonary inflammation through the generation of oxidative stress. Coarse, fine, and ultrafine particles (UFPs) were collected by ambient particle concentrators in the Los Angeles basin in California and used to study their chemical composition in parallel with assays for generation of reactive oxygen species (ROS) and ability to induce oxidative stress in macrophages and epithelial cells. UFPs were most potent toward inducing cellular heme oxygenase-1 (HO-1) expression and depleting intracellular glutathione. HO-1 expression, a sensitive marker for oxidative stress, is directly correlated with the high organic carbon and polycyclic aromatic hydrocarbon (PAH) content of UFPs. The dithiothreitol (DTT) assay, a quantitative measure of in vitro ROS formation, was correlated with PAH content and HO-1 expression. UFPs also had the highest ROS activity in the DTT assay. Because the small size of UFPs allows better tissue penetration, we used electron microscopy to study subcellular localization. UFPs and, to a lesser extent, fine particles, localize in mitochondria, where they induce major structural damage. This may contribute to oxidative stress. Our studies demonstrate that the increased biological potency of UFPs is related to the content of redox cycling organic chemicals and their ability to damage mitochondria.

Subfields: Health, Toxicology and Mutagenesis, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e7042d195efe7fd31e75e53e70732960ae0a1392

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Citations in the corpus

Size-dependent toxicity of metal oxide particles--a comparison between nano- and micrometer size. (2009, background): “The depolarization may be due to structural damage following particle interactions, which has been shown by ultrafine particles that lodge in the mitochondria (Li et al., 2003b).”
Ultrafine Particles Cross Cellular Membranes by Nonphagocytic Mechanisms in Lungs and in Cultured Cells (2005, background): “In vitro experiments revealed penetration of UFPs into mitochondria of macrophages and epithelial cells that was associated with oxidative stress and mitochondrial damage (Li et al. 2003).”
Oxidative Stress and Air Pollution Exposure (2011, background): “5 and UFPs adsorbed on their surface and are capable of ROS formation by Fenton’s reaction [35].”
Airborne Particulate Matter and Human Health: Toxicological Assessment and Importance of Size and Composition of Particles for Oxidative Damage and Carcinogenic Mechanisms (2008, background): “Electron microscopy showed that ultrafine particles are localized inside damaged mitochondria (107).”
Understanding biophysicochemical interactions at the nano-bio interface. (2009, background): “Although it is difficult at present to quantify reactive surface areas accurately, studies of the pro-oxidative potentials of ambient ultrafine particles under abiotic and cellular conditions and how they relate to pro-oxidative pathogenic events (for example atherosclerosis) in animals are examples”
Applications and implications of nanotechnologies for the food sector (2008, background): “Such concerns have arisen from a growing body of scientific evidence which indicates that free engineered nanoparticles can cross cellular barriers and that exposure to some forms can lead to increased production of oxyradicals and, consequently, oxidative damage to the cell (Li et al. 2003; Donalds”
Nanotoxicology: An Emerging Discipline Evolving from Studies of Ultrafine Particles (2005, background): “…and UFPs, especially under concomitant exposure to light, UV, or transition metals (Brown et al. 2000, 2001; Derfus et al. 2004; Joo et al. 2004; Li et al. 2003; Nagaveni et al. 2004; Oberdörster E 2004a; Rancan et al. 2002; Sayes et al. 2004; Shvedova et al. 2004a, 2004b; Wilson et al. 2002;…”
The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. (2008, methodology): “In particular, it was demonstrated that the biological activity and oxidant potential of CAPs are determined by the content of redox cycling chemicals [22] (Table 1).”
Principles for characterizing the potential human health effects from exposure to nanomaterials: elements of a screening strategy (2005, background): “Nanoparticles of various sizes and chemical compositions are able to preferentially localize in mitochondria where they induce major structural damage and can contribute to oxidative stress [65].”
Exposure Assessment for Atmospheric Ultrafine Particles (UFPs) and Implications in Epidemiologic Research (2005, background): “Other studies showed that UFPs contain the largest fraction of polycyclic aromatic hydrocarbons (PAHs) by mass (Eiguren-Fernandez et al. 2003; Li et al. 2003).”
Toxicology of nanoparticles: A historical perspective (2007, background): “…particles in mitochondria after entry into cells following in vivo exposure in the 1970s (DeLorenzo 1970; Gopinath et al. 1978) and recently demonstrated in vitro in macrophages with ambient ultrafine particles, thereby inducing oxidative stress and severe mitochondrial damage (Li et al. 2003).”