Generation of Reactive Oxygen Species during Interaction of Diesel Exhaust Particle Components with NADPH-Cytochrome p450 Reductase and Involvement of the Bioactivation in the DNA Damage

Kumagai, Yoshito; Arimoto, Toyoko; Shinyashiki, Masaru; Shimojo, Naoki; Nakai, Yoshinobu; Yoshikawa, Toshikazu; Sagai, Masaru

doi:10.1016/s0891-5849(96)00341-3

Cited by 237 publications

(196 citation statements)

References 34 publications

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“…Thus, the extent of cellular toxicity is directly related to these organic chemical compounds. It is possible to assess the pro-oxidant activity of PM by using the dithiothreitol (DTT) assay that reflects the particle content of redox cycling chemical groups such as quinones [22,23]. This assay is premised on the interaction of redox cycling chemical quinones (Q) with DTT:…”

Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

“…Studies using fractionated organic DEP extract have demonstrated that quinones and PAHs are representative organic chemical groups that could contribute to the oxidant injury in the lung [23][24][25]. PAHs can be converted to quinones via biotransformation, e.g.…”

Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

“…DEP, one of the major sources of ambient UFP, has been used as a model particulate pollutant to elucidate the mechanisms by which ambient PM may contribute to asthma. This includes some evidence that the generation of oxidative stress by organic DEP chemicals could be responsible for the pro-inflammatory and adjuvant effects of these particles in the respiratory tract [23,[49][50][51]. Redox-active PM chemicals can exert non-specific pro-inflammatory as well as allergic inflammatory effects in the nose depending on whether the challenge is performed in a non-atopic or an atopic individual.…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

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The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

821

529

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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 pro-inflammatory 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 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 effect 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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Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

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The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

821

529

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“…RT was performed at 42°C in a total volume of 20 l containing 5 g total RNA; 0.5 g oligo(dT) [12][13][14][15][16][17][18] ; 10 mM DTT; 0.5 mM each of dATP, dGTP, dCTP, and dTTP; and 10 U Moloney murine leukemia virus reverse transcriptase (15). HO-1 primers for PCR amplification of a 350-bp human HO-1 fragment (36) were obtained from Life Technologies.…”

Section: Rt-pcr Analysismentioning

confidence: 99%

“…While NAC could increase basal GSH/GSSG ratios in THP-1 An organic DEP extract was fractionated by silica gel chromatography as previously described (15). The presence of alkenes, PAHs, and quinones in these respective fractions were confirmed by chemical analysis as previously described (15). The indicated amounts of the crude methanol extract as well as each fraction were incubated with THP-1 and BEAS-2B cells for 5 h before Western blotting.…”

Section: Organic Dep Extracts Induce Ros Production and Oxidative Strmentioning

confidence: 99%

Comparison of the Pro-Oxidative and Proinflammatory Effects of Organic Diesel Exhaust Particle Chemicals in Bronchial Epithelial Cells and Macrophages

Wang

Oberley

et al. 2002

The Journal of Immunology

288

231

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Inhaled diesel exhaust particles (DEP) exert proinflammatory effects in the respiratory tract. This effect is related to the particle content of redox cycling chemicals and is involved in the adjuvant effects of DEP in atopic sensitization. We demonstrate that organic chemicals extracted from DEP induce oxidative stress in normal and transformed bronchial epithelial cells, leading to the expression of heme oxygenase 1, activation of the c-Jun N-terminal kinase cascade, IL-8 production, as well as induction of cytotoxicity. Among these effects, heme oxygenase 1 expression is the most sensitive marker for oxidative stress, while c-Jun N-terminal kinase activation and induction of apoptosis-necrosis require incremental amounts of the organic chemicals and increased levels of oxidative stress. While a macrophage cell line (THP-1) responded in similar fashion, epithelial cells produced more superoxide radicals and were more susceptible to cytotoxic effects than macrophages. Cytotoxicity is the result of mitochondrial damage, which manifests as ultramicroscopic changes in organelle morphology, a decrease in the mitochondrial membrane potential, superoxide production, and ATP depletion. Epithelial cells also differ from macrophages in not being protected by a thiol antioxidant, N-acetylcysteine, which effectively protects macrophages against cytotoxic DEP chemicals. These findings show that epithelial cells exhibit a hierarchical oxidative stress response that differs from that of macrophages by more rapid transition from cytoprotective to cytotoxic responses. Moreover, epithelial cells are not able to convert N-acetylcysteine to cytoprotective glutathione.

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Air Pollution and Other Environmental Modulators of Cardiac Function

Gorr

Falvo

Wold

2017

Comprehensive Physiology

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Cardiovascular disease (CVD) is the leading cause of death in developed regions and a worldwide health concern. Multiple external causes of CVD are well known, including obesity, diabetes, hyperlipidemia, age, and sedentary behavior. Air pollution has been linked with the development of CVD for decades, though the mechanistic characterization remains unknown. In this comprehensive review, we detail the background and epidemiology of the effects of air pollution and other environmental modulators on the heart, including both short- and long-term consequences. Then, we provide the experimental data and current hypotheses of how pollution is able to cause the CVD, and how exposure to pollutants is exacerbated in sensitive states. Published 2017. Compr Physiol 7:1479-1495, 2017.

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Generation of Reactive Oxygen Species during Interaction of Diesel Exhaust Particle Components with NADPH-Cytochrome p450 Reductase and Involvement of the Bioactivation in the DNA Damage

Cited by 237 publications

References 34 publications

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Comparison of the Pro-Oxidative and Proinflammatory Effects of Organic Diesel Exhaust Particle Chemicals in Bronchial Epithelial Cells and Macrophages

Air Pollution and Other Environmental Modulators of Cardiac Function

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