Ambient Particulate Matter Exhibits Direct Inhibitory Effects on Oxidative Stress Enzymes (original) (raw)
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Environmental Science & Technology, 2008
Recent atmospheric particulate matter health studies have suggested that the redox activity is an important factor in particulate matter toxicology, and that reactive oxygen species (ROS) activity may be an important characteristic of particulate matter that is associated with adverse health effects. In this study, associations between atmospheric particulate matter sources and in vitro ROS activities are investigated. Ambient concentrations of fine particle water-soluble elements and total organic and elemental carbon were measured daily in Denver for the 2003 calendar year. The data were used in a multivariate factor analysis source apportionment model, positive matrix factorization (PMF), to determine the contributions of nine sources or factors: a mobile source factor, a water soluble carbon factor, a sulfate factor, a soil dust source, an iron source, two point sources characterized by water soluble toxic metals, a pyrotechnique factor, and a platinum group metal factor. Aqueous leachates, including water soluble and colloidal components, as well as insoluble particles that pass through a 0.2 µm pore size filter, of 45 randomly selected PM samples, were assayed to quantify ROS activity using an in vitro rat alveolar macrophage assay. Results show that PM-stimulated in vitro ROS production was significantly positively correlated with the contributions from three sources: the iron source, the soil dust source and the water soluble carbon factor. The iron source accounted for the greatest fraction of the measured variability in redox activity, followed by the soil dust and the water-soluble carbon factor. Seventy-seven percent of the in vitro ROS activity was explained by a linear combination of these three source contributions.
Roles of oxidative stress in signaling and inflammation induced by particulate matter
Cell Biology and Toxicology, 2010
This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca 2+ influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.
Review-evaluating the molecular assays for measuring the oxidative potential of particulate matter
• The available methodologies for the measurements of the OP of particles are reviewed • Atmospheric particles show higher OP than particles emitted from individual combustion sources • To have the most realistic values of OP several assays should be used simultaneously • A uniform way of reporting the results should be implemented Abstract Several cell-free assays are currently used to quantify and detect the reactive oxygen species (ROS). All of them have certain limitations, do not provide direct comparison of results and, to date, none of these assays have been acknowledged as the most suitable acellular assay and none has yet been adopted for investigation of potential PM toxicity. These assays include DTT, ascorbic acid, DCFH-DA and PFN assays which have been used in measurements of the particles generated from various combustion sources such as diesel engine, wood smoke (or biomass burning) and cigarette smoke, as well as for outdoor measurements. All the probes use different units for expressing redox properties of PM. Also, their reactivity is being triggered by different types of ROS. This limits the direct comparison of the results that are reporting the toxicity of the same aerosol type measured with various probes. This study is evaluating and comparing the various assays in order to develop deeper understanding of their capabilities, selectivity as well as improve understanding of the underlying chemical mechanisms.
The role of reactive oxygen species and oxidative stress in mediating particulate matter injury
Clinics in occupational and environmental medicine, 2006
Numerous reports link oxidative stress to particulate matter (PM)-induced adverse health effects. Increasing evidence is being collected that reactive oxygen species and oxidative stress are involved in PM-mediated injury. The physical characteristics and the chemical composition of PM play a key role in reactive oxygen species generation in vitro and in vivo. According to the hierarchical oxidative stress hypothesis, antioxidant phase II enzymes protect against PM-induced inflammation and cytotoxicity. This concept is useful in understanding PM-induced disease models, susceptibility, and biomaker development to access exposures outcomes and is useful for developing therapeutic intervention in PM-induced adverse health effects.
Biomolecules, 2015
Inflammation is considered to play a central role in a diverse range of disease outcomes associated with exposure to various types of inhalable particulates. The initial mechanisms through which particles trigger cellular responses leading to activation of inflammatory responses are crucial to clarify in order to understand what physico-chemical characteristics govern the inflammogenic activity of particulate matter and why some particles are more harmful than others. Recent research suggests that molecular triggering mechanisms involved in activation of proinflammatory genes and onset of inflammatory reactions by particles or soluble particle components can be categorized into direct formation of reactive oxygen species (ROS) with subsequent oxidative stress, interaction with the lipid layer of cellular membranes, activation of cell surface receptors, and direct interactions with intracellular molecular targets. The present review focuses on the immediate effects and responses in cells exposed to particles and central down-stream signaling mechanisms involved in regulation of proinflammatory genes, with special emphasis on the role of oxidant and non-oxidant triggering mechanisms. Importantly, ROS act as a central second-messenger in a variety of signaling pathways. Even non-oxidant mediated triggering mechanisms are therefore also likely to activate downstream redox-regulated events.
Environmental pollution (Barking, Essex : 1987), 2015
The association of systemic antioxidant activity with ambient air pollution has been unclear. A panel of 40 healthy college students underwent repeated blood collection for 12 occasions under three exposure scenarios before and after relocating from a suburban area to an urban area in Beijing, China in 2010-2011. We measured various air pollutants including fine particles (PM2.5) and determined circulating levels of antioxidant enzymes extracellular superoxide dismutase (EC-SOD) and glutathione peroxidase 1 (GPX1) in the laboratory. An interquartile range increase of 63.4 μg/m(3) at 3-d PM2.5 moving average was associated with a 6.3% (95% CI: 0.6, 12.4) increase in EC-SOD and a 5.5% (95% CI: 1.3, 9.8) increase in GPX1. Several PM2.5 chemical constituents, including negative ions (nitrate and chloride) and metals (e.g., iron and strontium), were consistently associated with increases in EC-SOD and GPX1. Our results support activation of circulating antioxidant enzymes following expos...
Role of air pollutants mediated oxidative stress in respiratory diseases
Pediatric Allergy and Immunology, 2022
Airborne particulate (PM) components, especially those deriving from anthropogenic activities such as the combustion of fossil fuels, can induce oxidative stress triggered by reactive oxygen species (ROS). The reported associations between asthma morbidity and exposure to air pollutants, mainly PM 2.5, could be related to the oxidative potential of PM capable of inducing oxidative stress and airways inflammation, which are the hallmarks of asthma disease. 1 However, the oxidative potential of PM may be, in part, independent of the PM mass. Therefore, a potentially small fraction of chemical components can even produce the same effects. Many aerosol components have redox activities (e.g., polycyclic aromatic hydrocarbons (IPA), transition metals), and epidemiological associations can be influenced if the analyzes are based only on mass concentrations and not on the chemical characterization of PM2.5 and/or of PM10. Few studies have addressed this possibility by characterizing the overall oxidative potential of PM2.5 and correlating it with daily changes in fractional exhaled nitric oxide (FENO), which is a pivotal biomarker of airway inflammation in children with asthma. 2 One of the most used methods to evaluate the oxidative potential of PM components in acellular mode is the dithiothreitol (DTT) assay. DTT assay is used to demonstrate the ability of PM to transfer electrons from the DTT to oxygen, resulting in the generation of superoxide. DTT is an indicator of redox activity, positively correlated to the content of IPA, organic carbon (OC), metals, and partially inhibited by metal chelators. 3 DTT consumption is highest in ultrafine PM (<0.15 µm) and combustion sources of organic chemicals and transition metals, which have a high oxidative potential. The intracellular response to exposure to PMs with high OP (oxidative potential) consists in the production of ROS, with the parallel activation of signals for the synthesis of pro-inflammatory cytokines, determining an
Airborne Aerosols and Human Health: Leapfrogging from Mass Concentration to Oxidative Potential
2020
The mass concentration of particulate matter (PM) has been systematically used in epidemiological studies as exposure indicator, to relate airborne concentrations with a wide variety of human health effects, which can be hardly explained by using this single parameter. In fact, PM is a “particle cocktail” that includes a complex mixture of compounds with a wide range of sizes, chemical compositions and emission sources. Current research hypothesizes that many of the adverse health effects are derived from oxidative stress in biological systems caused by the deposition of PM into the lungs. This emerging hypothesis is called the oxidative stress paradigm. In this commentary article we analize how this new paradigm could help to answer the as-of-yet unanswered questions related to the mechanism of action of PM pollution on human health. Acellular oxidative potential (OP) assays have been emerged as a promising approach to quantify the PM potential to induce oxidative stress and to rel...
Role of oxidative damage in toxicity of particulates
Free Radical Research, 2010
Particulates are small particles of solid or liquid suspended in liquid or air. In vitro studies show that particles generate reactive oxygen species, deplete endogenous antioxidants, alter mitochondrial function and produce oxidative damage to lipids and DNA. Surface area, reactivity and chemical composition play important roles in the oxidative potential of particulates. Studies in animal models indicate that particles from combustion processes (generated by combustion of wood or diesel oil), silicate, titanium dioxide and nanoparticles (C 60 fullerenes and carbon nanotubes) produce elevated levels of lipid peroxidation products and oxidatively damaged DNA. Biomonitoring studies in humans have shown associations between exposure to air pollution and wood smoke particulates and oxidative damage to DNA, deoxynucleotides and lipids measured in leukocytes, plasma, urine and/or exhaled breath. The results indicate that oxidative stress and elevated levels of oxidatively altered biomolecules are important intermediate endpoints that may be useful markers in hazard characterization of particulates.