Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO2 inhalation exposure

Li, Hongyan; Han, Ming; Guo, Lin; Li, Guangke; Sang, Nan

doi:10.1016/j.chemosphere.2010.11.055

Cited by 55 publications

(38 citation statements)

References 31 publications

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“…Using exposures lasting from hours to days, recent mechanistic animal studies show: protein S-glutathionylation in the lung at 25 ppm NO 2 (Aesif et al, 2009); a decrease in aggregating activity of surfactant-protein D at 10 ppm or 20 ppm (Matalon et al, 2009); and increases in markers of oxidative stress, endothelial dysfunction, inflammation and apoptosis in the hearts of rats from exposures of 2.7 ppm to 10.6 ppm (Li H et al, 2011). Zhu et al (2012) found that 2.6 ppm NO 2 delayed recovery from stroke (slowed reduction in infarct volume) in a rat stroke model and increased behavioural deficits.…”

Section: Toxicological Studies On Short-term Exposure (Hours To Days)mentioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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Section: Toxicological Studies On Short-term Exposure (Hours To Days)mentioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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“…4 shows the concentration-dependent cell apoptosis after 24 h of treatment with either the spring or winter samples, in which significant differences occurred after exposure to 3 or 10 mg/mL samples of the heavy metal-containing PM 2.5 . Previous studies have demonstrated that decreased expression of the anti-apoptotic protein bcl-2 and elevated expression of the pro-apoptotic proteins bax and p53 could collaboratively trigger an evolutionarily conserved process, cell apoptosis (Li et al, 2011;Yun et al, 2010b). Therefore, our results imply that the heavy metals associated with the PM 2.5 derived from coal burning caused H9C2 cell apoptosis even at a low dose.…”

Section: Effects Of Heavy Metal-containing Pm 25 On H9c2 Cell Apoptosismentioning

confidence: 60%

“…Specifically, the iNOS expression increased 2.17-and 4.64-fold relative to the control levels, and the ICAM-1 expression increased 1.78-and 2.24-fold relative to the control levels after 24 h of treatment with the highest concentrations of the spring and winter samples. Over-expression of ICAM-1 contributes to the process of leukocyte recruitment to the sites of inflammation (Li et al, 2011). During the development of inflammation, endothelial cells actively participate in this process by regulating the leukocyte recruitment by enhancing the expression of proinflammatory enzymes, such as iNOS (Yun et al, 2010a).…”

Section: Effects Of Heavy Metal-containing Pm 25 On H9c2 Cell Apoptosismentioning

confidence: 99%

“…Previous studies have shown that a decrease in the bcl-2/bax ratio is partially regulated by a sustained generation of nitric oxide (NO) by iNOS, which is critical for apoptosis (Semmler et al, 2005). ICAM-1 is an endothelial celland leukocyte-associated transmembrane protein that has long been known to be important in stabilizing cell-cell interactions and is also a factor closely associated with cell apoptosis (Li et al, 2011;Pan et al, 2012). To explore the possible mechanism of the H9C2 cell apoptosis induced by the heavy metal-containing PM 2.5 , we evaluated the expression of the inflammatory mediators, including iNOS and ICAM-1.…”

Section: Effects Of Heavy Metal-containing Pm 25 On H9c2 Cell Apoptosismentioning

confidence: 99%

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Heavy metals bound to fine particulate matter from northern China induce season-dependent health risks: A study based on myocardial toxicity

Zhang

et al. 2016

Environmental Pollution

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130

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Substantial epidemiological evidence has consistently reported that fine particulate matter (PM2.5) is associated with an increased risk of cardiovascular outcomes. PM2.5 is a complex mixture of extremely small particles and liquid droplets composed of multiple components, and there has been high interest in identifying the specific health-relevant physical and/or chemical toxic constituents of PM2.5. In the present study, we analyzed 8 heavy metals (Cr, Ni, Cu, Cd, Pb, Zn, Mn and Co) in the PM2.5 collected during four different seasons in Taiyuan, a typical coal-burning city in northern China. Our results indicated that total concentrations of the 8 heavy metals differed among the seasons. Zn and Pb, which are primarily derived from the anthropogenic source, coal burning, were the dominant elements, and high concentrations of these two elements were observed during the spring and winter. To clarify whether these heavy metals in the locally collected PM2.5 were associated with health effects, we conducted health risk assessments using validated methods. Interestingly, Pb was responsible for greater potential health risks to children. Because cardiovascular disease (CVD) is a main contributor to the mortality associated with PM2.5 exposure, we performed experimental assays to evaluate the myocardial toxicity. Our in vitro experiments showed that the heavy metal-containing PM2.5 induced season-dependent apoptosis in rat H9C2 cells through a reactive oxygen species (ROS)-mediated inflammatory response. Our findings suggested that heavy metals bound to PM2.5 produced by coal burning play an important role in myocardial toxicity and contribute to season-dependent health risks.

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“…In the study, rats (n = 6/group) were exposed for 6 h/d for 7 d to fresh air, 5, 10 or 20 mg/m 3 NO 2 using protocol of dynamic inhalation based on our previous studies [25,26]. During exposure period, the four groups of rats were placed in 1 m 3 exposure chambers simultaneously.…”

Section: Animal Exposure and Treatment Protocolsmentioning

confidence: 99%

Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO2 inhalation exposure

Cited by 55 publications

References 31 publications

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Heavy metals bound to fine particulate matter from northern China induce season-dependent health risks: A study based on myocardial toxicity

In vivo screening to determine neurological hazards of nitrogen dioxide (NO2) using Wistar rats

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