ArticleEnvironmental health perspectives2009
One-month diesel exhaust inhalation produces hypertensive gene expression pattern in healthy rats.
Article in Environmental health perspectives, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 60 citations in OpenAlex.
- Biological effects of diesel exhaust inhalation. III cardiovascular function.Inhalation toxicology · 2024Article
- Environmental Stressors and the PINE Network: Can Physical Environmental Stressors Drive Long-Term Physical and Mental Health Risks?International journal of environmental research and public health · 2022Review
- Diesel exhaust impairs TREM2 to dysregulate neuroinflammation.Journal of neuroinflammation · 2020Article
- Oxidative stress and the cardiovascular effects of air pollution.Free radical biology & medicine · 2020Review
- Comparison of silver nanoparticle-induced inflammatory responses between healthy and metabolic syndrome mouse models.Journal of toxicology and environmental health. Part A · 2020Article
- Susceptibility Variations in Air Pollution Health Effects: Incorporating Neuroendocrine Activation.Toxicologic pathology · 2019Article
- Mitochondrial toxicity of tobacco smoke and air pollution.Toxicology · 2017Review
- Systemic metabolic derangement, pulmonary effects, and insulin insufficiency following subchronic ozone exposure in rats.Toxicology and applied pharmacology · 2016Article
- A cross-sectional analysis of polycyclic aromatic hydrocarbons and diesel particulate matter exposures and hypertension among individuals of Mexican origin.Environmental health : a global access science source · 2015Article
- Comparative cardiopulmonary toxicity of exhausts from soy-based biofuels and diesel in healthy and hypertensive rats.Inhalation toxicology · 2015Article
- Cerium Dioxide Nanoparticle Exposure Improves Microvascular Dysfunction and Reduces Oxidative Stress in Spontaneously Hypertensive Rats.Frontiers in physiology · 2015Article
- Article
- Diesel exhaust particulate induces pulmonary and systemic inflammation in rats without impairing endothelial function ex vivo or in vivo.Particle and fibre toxicology · 2012Article
- Manufactured and airborne nanoparticle cardiopulmonary interactions: a review of mechanisms and the possible contribution of mast cells.Inhalation toxicology · 2012Review
- Diesel exhaust activates and primes microglia: air pollution, neuroinflammation, and regulation of dopaminergic neurotoxicity.Environmental health perspectives · 2011Article
- Vascular and cardiac impairments in rats inhaling ozone and diesel exhaust particles.Environmental health perspectives · 2011Article
- Antiretrovirals induce endothelial dysfunction via an oxidant-dependent pathway and promote neointimal hyperplasia.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Update in environmental and occupational medicine 2009.American journal of respiratory and critical care medicine · 2010Review
- Predicting environmental chemical factors associated with disease-related gene expression data.BMC medical genomics · 2010Article
- Tungsten carbide cobalt nanoparticles exert hypoxia-like effects on the gene expression level in human keratinocytes.BMC genomics · 2010Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals.
objectiveWe hypothesized that DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive (SH) rats than in healthy Wistar Kyoto (WKY) rats. METHODS AND
resultsMale rats (12-14 weeks of age) were exposed to air or DE from a 30-kW Deutz engine at 500 or 2,000 microg/m3, 4 hr/day, 5 days/week for 4 weeks. Neutrophilic influx was noted in the lung lavage fluid of both strains, but injury markers were minimally changed. Particle-laden macrophages were apparent histologically in DE-exposed rats. Lower baseline cardiac anti-oxidant enzyme activities were present in SH than in WKY rats; however, no DE effects were noted. Cardiac mitochondrial aconitase activity decreased after DE exposure in both strains. Electron microscopy indicated abnormalities in cardiac mitochondria of control SH but no DE effects. Gene expression profiling demonstrated alterations in 377 genes by DE in WKY but none in SH rats. The direction of DE-induced changes in WKY mimicked expression pattern of control SH rats without DE. Most genes affected by DE were down-regulated in WKY. The same genes were down-regulated in SH without DE producing a hypertensive-like expression pattern. The down-regulated genes included those that regulate compensatory response, matrix metabolism, mitochondrial function, and oxidative stress response. No up-regulation of inflammatory genes was noted.
conclusionsWe provide the evidence that DE inhalation produces a hypertensive-like cardiac gene expression pattern associated with mitochondrial oxidative stress in healthy rats.
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Registered trials
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