Protective effects of pulmonary epithelial lining fluid on oxidative stress and DNA single-strand breaks caused by ultrafine carbon black, ferrous sulphate and organic extract of diesel exhaust particles

Chuang, Hsiao-Chi; Cheng, Yi Ming; Yu, Lei; Chang, Hui-Wen; Cheng, Tsun Jen

doi:10.1016/j.taap.2012.12.004

Cited by 38 publications

(12 citation statements)

References 34 publications

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“…Wood smoke has adverse effects on surfactant48 and cilial function 49. To offset particle oxidative effects, epithelial lining fluid contains high levels of the antioxidant glutathione,50 which is up-regulated after exposure to wood smoke 51. Although incompletely studied, such redox changes will probably alter host response to infection52,53 through effects on inflammatory signalling54 and recognition of apoptotic cells 55…”

Section: Respiratory Infectionsmentioning

confidence: 99%

Respiratory risks from household air pollution in low and middle income countries

Gordon¹,

Bruce²,

Grigg³

et al. 2014

The Lancet Respiratory Medicine

758

592

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A third of the world’s population uses solid fuel derived from plant material (biomass) or coal for cooking, heating, or lighting. These fuels are smoky, often used in an open fire or simple stove with incomplete combustion, and result in a large amount of household air pollution when smoke is poorly vented. Air pollution is the biggest environmental cause of death worldwide, with household air pollution accounting for about 3·5–4 million deaths every year. Women and children living in severe poverty have the greatest exposures to household air pollution. In this Commission, we review evidence for the association between household air pollution and respiratory infections, respiratory tract cancers, and chronic lung diseases. Respiratory infections (comprising both upper and lower respiratory tract infections with viruses, bacteria, and mycobacteria) have all been associated with exposure to household air pollution. Respiratory tract cancers, including both nasopharyngeal cancer and lung cancer, are strongly associated with pollution from coal burning and further data are needed about other solid fuels. Chronic lung diseases, including chronic obstructive pulmonary disease and bronchiectasis in women, are associated with solid fuel use for cooking, and the damaging effects of exposure to household air pollution in early life on lung development are yet to be fully described. We also review appropriate ways to measure exposure to household air pollution, as well as study design issues and potential effective interventions to prevent these disease burdens. Measurement of household air pollution needs individual, rather than fixed in place, monitoring because exposure varies by age, gender, location, and household role. Women and children are particularly susceptible to the toxic effects of pollution and are exposed to the highest concentrations. Interventions should target these high-risk groups and be of sufficient quality to make the air clean. To make clean energy available to all people is the long-term goal, with an intermediate solution being to make available energy that is clean enough to have a health impact.

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Section: Respiratory Infectionsmentioning

confidence: 99%

Respiratory risks from household air pollution in low and middle income countries

Gordon¹,

Bruce²,

Grigg³

et al. 2014

The Lancet Respiratory Medicine

758

592

View full text Add to dashboard Cite

show abstract

“…Mechanistically, it was observed that reactive oxygen species (ROS) enhance DNA damage by inflammatory cells such as eosinophils and neutrophils via the helide (Cl − and Br − )-dependent formation of DNA adducts and thus enhancement of cancer (107). It is already evident that sulfate (a semi-volatile component) present in the soot particles directly induces oxidative stress in the cells (108, 109). It is also found that sulfate in DEP may involve in the tissue remodeling and fibrosis (110).…”

Section: The Pathological Mechanisms Of Cancer Due To Soot and Cbsmentioning

confidence: 99%

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

2017

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The environmental soot and carbon blacks (CBs) cause many diseases in humans, but their underlying mechanisms of toxicity are still poorly understood. Both are formed after the incomplete combustion of hydrocarbons but differ in their constituents and percent carbon contents. For the first time, “Sir Percival Pott” described soot as a carcinogen, which was subsequently confirmed by many others. The existing data suggest three main types of diseases due to soot and CB exposures: cancer, respiratory diseases, and cardiovascular dysfunctions. Experimental models revealed the involvement of oxidative stress, DNA methylation, formation of DNA adducts, and Aryl hydrocarbon receptor activation as the key mechanisms of soot- and CB-induced cancers. Metals including Si, Fe, Mn, Ti, and Co in soot also contribute in the reactive oxygen species (ROS)-mediated DNA damage. Mechanistically, ROS-induced DNA damage is further enhanced by eosinophils and neutrophils via halide (Cl− and Br−) dependent DNA adducts formation. The activation of pulmonary dendritic cells, T helper type 2 cells, and mast cells is crucial mediators in the pathology of soot- or CB-induced respiratory disease. Polyunsaturated fatty acids (PUFAs) were also found to modulate T cells functions in respiratory diseases. Particularly, telomerase reverse transcriptase was found to play the critical role in soot- and CB-induced cardiovascular dysfunctions. In this review, we propose integrated mechanisms of soot- and CB-induced toxicity emphasizing the role of inflammatory mediators and oxidative stress. We also suggest use of antioxidants and PUFAs as protective strategies against soot- and CB-induced disorders.

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“…The physicochemical characteristics of nanoscaled particles contribute to oxidativeinflammatory reactions. 30,31 We also elucidated the functions of proteins modulated in response to AgNPs in the lung environment; these functional categories included blood coagulation, activation of the integrin signaling pathway and ubiquitin proteasome pathway; inflammation mediation by chemokines; activation of the cytokine signaling pathway; T-cell activation; activation of the tricarboxylic acid cycle, dopamine receptor-mediated signaling pathway, plasminogen activating cascade, and Fas signaling pathway; cytoskeletal regulation by Rho GTPase; and activation of the nicotine pharmacodynamics pathway and nicotinic acetylcholine receptor signaling pathway. AgNP exposure may alter blood coagulation via platelet activation and thrombus formation, 32 oxidative-inflammatory responses, 2,3 and innate immune responses.…”

Section: Discussionmentioning

confidence: 99%

Comparative proteomics of inhaled silver nanoparticles in healthy and allergen provoked mice

Su¹,

Chen²,

Chang³

et al. 2013

IJN

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Background: Silver nanoparticles (AgNPs) have been associated with the exacerbation of asthma; however, the immunological basis for the adjuvant effects of AgNPs is not well understood. Objective: The aim of the study reported here was to investigate the allergic effects of AgNP inhalation using proteomic approaches. Methods: Allergen provoked mice were exposed to 33 nm AgNPs at 3.3 mg/m 3 . Following this, bronchoalveolar lavage fluid (BALF) and plasma were collected to determine protein profiles. Results: In total, 106 and 79 AgNP-unique proteins were identified in the BALF of control and allergic mice, respectively. Additionally, 40 and 26 AgNP-unique proteins were found in the plasma of control and allergic mice, respectively. The BALF and plasma protein profiles suggested that metabolic, cellular, and immune system processes were associated with pulmonary exposure to AgNPs. In addition, we observed 18 proteins associated with systemic lupus erythematosus that were commonly expressed in both control and allergic mice after AgNP exposure. Significant allergy responses were observed after AgNP exposure in control and allergic mice, as determined by ovalbumin-specific immunoglobulin E. Conclusion: Inhaled AgNPs may regulate immune responses in the lungs of both control and allergic mice. Our results suggest that immunology is a vital response to AgNPs.

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Protective effects of pulmonary epithelial lining fluid on oxidative stress and DNA single-strand breaks caused by ultrafine carbon black, ferrous sulphate and organic extract of diesel exhaust particles

Cited by 38 publications

References 34 publications

Respiratory risks from household air pollution in low and middle income countries

Respiratory risks from household air pollution in low and middle income countries

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

Comparative proteomics of inhaled silver nanoparticles in healthy and allergen provoked mice

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