Are standardized diesel exhaust particles (DEP) representative of ambient particles in air pollution toxicological studies?

2021 ◽  
pp. 147854
Author(s):  
Vahid Jalali Farahani ◽  
Milad Pirhadi ◽  
Constantinos Sioutas
Keyword(s):  
Air Pollution ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Ambient Particles ◽  
Toxicological Studies ◽  
Exhaust Particles

scholarly journals Prolonged Pulmonary Exposure to Diesel Exhaust Particles Exacerbates Renal Oxidative Stress, Inflammation and DNA Damage in Mice with Adenine-Induced Chronic Renal Failure

2016 ◽  
Vol 38 (5) ◽  
pp. 1703-1713 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Turan Karaca ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Kidney Weight ◽  
Pulmonary Exposure ◽  
Exhaust Particles

Background/Aims: Epidemiological evidence indicates that patients with chronic kidney diseases have increased susceptibility to adverse outcomes related to long-term exposure to particulate air pollution. However, mechanisms underlying these effects are not fully understood. Methods: Presently, we assessed the effect of prolonged exposure to diesel exhaust particles (DEP) on chronic renal failure induced by adenine (0.25% w/w in feed for 4 weeks), which is known to involve inflammation and oxidative stress. DEP (0.5m/kg) was intratracheally (i.t.) instilled every 4th day for 4 weeks (7 i.t. instillation). Four days following the last exposure to either DEP or saline (control), various renal endpoints were measured. Results: While body weight was decreased, kidney weight increased in DEP+adenine versus saline+adenine or DEP. Water intake, urine volume, relative kidney weight were significantly increased in adenine+DEP versus DEP and adenine+saline versus saline. Plasma creatinine and urea increased and creatinine clearance decreased in adenine+DEP versus DEP and adenine+saline versus saline. Tumor necrosis factor α, lipid peroxidation and reactive oxygen species were significantly increased in adenine+DEP compared with either DEP or adenine+saline. The antioxidant calase was significantly decreased in adenine+DEP compared with either adenine+saline or DEP. Notably, renal DNA damage was significantly potentiated in adenine+DEP compared with either adenine+saline or DEP. Similarly, systolic blood pressure was increased in adenine+DEP versus adenine+saline or DEP, and in DEP versus saline. Histological evaluation revealed more collagen deposition, higher number of necrotic cell counts and dilated tubules, cast formation and collapsing glomeruli in adenine+DEP versus adenine+saline or DEP. Conclusion: Prolonged pulmonary exposure to diesel exhaust particles worsen renal oxidative stress, inflammation and DNA damage in mice with adenine-induced chronic renal failure. Our data provide biological plausibility that air pollution aggravates chronic renal failure.

scholarly journals The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 99
Author(s):  
Abderrahim Nemmar ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Salem Alblooshi ◽  
Saleh Alseiari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Diesel Exhaust ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Diesel Exhaust Particles ◽  
Cardiovascular Toxicity ◽  
Particulate Air Pollution ◽  
Exhaust Particles

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution—induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1β) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.

Abstract P312: Tracheal Instillation of Diesel Exhaust Particles Exacerbates Myocardial Ischaemia and Reperfusion Injury in Rats

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Sarah Robertson ◽  
Ashleigh L Thomson ◽  
Catherine A Shaw ◽  
Mark R Miller ◽  
David E Newby ◽  
...  
Keyword(s):  
Air Pollution ◽  
Infarct Size ◽  
Systemic Inflammation ◽  
Myocardial Ischaemia ◽  
Diesel Exhaust ◽  
Ex Vivo ◽  
Diesel Exhaust Particles ◽  
Autonomic Activation ◽  
Exhaust Particles

Episodes of increased air pollution are associated with higher cardiovascular mortality. The adverse effects of air pollution have been attributed to particulate matter, especially ultrafine particles. This study addresses the hypothesis that ultrafine diesel exhaust particles (DEP) exacerbate myocardial ischaemia reperfusion (I/R) injury secondary to induction of a systemic inflammatory response. Wistar rats (n=5–6/group) received DEP (0.5 mg) or saline vehicle by intratracheal instillation. 6h later I/R was induced either in vivo or ex vivo in isolated buffer perfused hearts. Lung inflammation was confirmed 6h after DEP instillation by increased levels of neutrophils, total protein and IL-6 in bronchoalveolar lavage fluid. However, there was no evidence for systemic inflammation as assessed by plasma cytokine levels (IL-6, TNF-α, and CRP) or by neutrophil priming (CD11b expression) or activation (CD62L expression). In vivo , systolic blood pressure was significantly higher in DEP-instilled rats (129 ± 7 mmHg) than in saline controls (92 ± 3 mmHg, P<0.01), consistent with increased autonomic activation. Arrhythmias occurred intermittently after induction of ischaemia (in total 8.2±1.2 s in the saline group) and were more prevalent in DEP-instilled rats (32.9±5.0s, P<0.001). Fatal arrhythmias occurred in 60% of rats receiving DEP but not at all in saline controls. Following reperfusion, infarct size (extent of triphenyltetrazolium chloride staining) was significantly increased after DEP (34.7 ± 1.2% left ventricle) vs saline-instilled (10.3 ± 1.2%, P<0.001). Infarct size was similarly potentiated in hearts isolated from DEP instilled rats and perfused ex-vivo . Histological examination confirmed the absence of inflammatory infiltrate in hearts prior to I/R. Prior exposure to pollution in vivo thus renders the heart more vulnerable to I/R injury, either in situ in the body or ex vivo when the heart is isolated from systemic mediators and cells. Systemic inflammation does not appear to be necessary for this ‘priming’ effect of DEP. The role of autonomic activation in promoting cardiac arrythmia in vivo after DEP instillation and in determining the ability of the heart to withstand subsequent I/R injury merits further investigation.

The Use of Standardized Diesel Exhaust Particles in Alzheimer’s Disease Research

2021 ◽  
pp. 1-2
Author(s):  
Michelle L. Block ◽  
Urmila P. Kodavanti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Particulate Matter ◽  
Diesel Exhaust ◽  
Disease Risk ◽  
Urban Air Pollution ◽  
Diesel Exhaust Particles ◽  
Urban Air ◽  
Exhaust Particles

The mechanisms underlying how urban air pollution exposure conveys Alzheimer’s disease risk and affects plaque pathology is largely unknown. Because particulate matter, the particle component of urban air pollution, varies across location, pollution source, and time, a single model representative of all ambient particulate matter is unfeasible for research investigating the role of ar pollution in central nervous system diseases. More specifically, the investigation of several models of particulate matter with enrichment of source-specific components are essential to employ, in order to more fully understand what characteristics of particulate matter affects Alzheimer’s disease, including standardized diesel exhaust particles.

scholarly journals Study of the Antioxidant Effects of Coffee Phenolic Metabolites on C6 Glioma Cells Exposed to Diesel Exhaust Particles

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1169
Author(s):  
Laura Botto ◽  
Alessandra Bulbarelli ◽  
Elena Lonati ◽  
Emanuela Cazzaniga ◽  
Michele Tassotti ◽  
...  
Keyword(s):  
Air Pollution ◽  
Diesel Exhaust ◽  
Glioma Cells ◽  
C6 Glioma ◽  
Diesel Exhaust Particles ◽  
C6 Glioma Cells ◽  
Major Constituent ◽  
Heme Oxygenase 1 ◽  
Phenolic Metabolites ◽  
Exhaust Particles

The contributing role of environmental factors to the development of neurodegenerative diseases has become increasingly evident. Here, we report that exposure of C6 glioma cells to diesel exhaust particles (DEPs), a major constituent of urban air pollution, causes intracellular reactive oxygen species (ROS) production. In this scenario, we suggest employing the possible protective role that coffee phenolic metabolites may have. Coffee is a commonly consumed hot beverage and a major contributor to the dietary intake of (poly) phenols. Taking into account physiological concentrations, we analysed the effects of two different coffee phenolic metabolites mixes consisting of compounds derived from bacterial metabolization reactions or phase II conjugations, as well as caffeic acid. The results showed that these mixes were able to counteract DEP-induced oxidative stress. The cellular components mediating the downregulation of ROS included extracellular signal-regulated kinase 1/2 (ERK1/2), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and uncoupling protein 2 (UCP2). Contrary to coffee phenolic metabolites, the treatment with N-acetylcysteine (NAC), a known antioxidant, was found to be ineffective in preventing the DEP exposure oxidant effect. These results revealed that coffee phenolic metabolites could be promising candidates to protect against some adverse health effects of daily exposure to air pollution.

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