Effects Of Particulate Air Pollution On The Development Of Autoimmune Disease: Studies Of Ambient Urban Particulates And Diesel Exhaust Particles In The NOD Mouse Model Of Type 1 Diabetes

2010 ◽  
Author(s):  
Stacey Ritz ◽  
Catherine Brummer
Keyword(s):  
Air Pollution ◽  
Type 1 Diabetes ◽  
Autoimmune Disease ◽  
Mouse Model ◽  
Diesel Exhaust ◽  
Nod Mouse ◽  
Diesel Exhaust Particles ◽  
Particulate Air Pollution ◽  
Exhaust Particles

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.

Influence of experimental type 1 diabetes on the pulmonary effects of diesel exhaust particles in mice

2013 ◽  
Vol 217 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-salam ◽  
Deepa Subramaniyan ◽  
Javed Yasin ◽  
Priya Yuvaraju ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Experimental Type ◽  
Exhaust Particles

scholarly journals Pancreatic Effects of Diesel Exhaust Particles in Mice with Type 1 Diabetes Mellitus

2014 ◽  
Vol 33 (2) ◽  
pp. 413-422 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Exhaust Particles

scholarly journals Thioreductase-Containing Epitopes Inhibit the Development of Type 1 Diabetes in the NOD Mouse Model

2016 ◽  
Vol 7 ◽  
Author(s):  
Elin Malek Abrahimians ◽  
Luc Vander Elst ◽  
Vincent A. Carlier ◽  
Jean-Marie Saint-Remy
Keyword(s):  
Type 1 Diabetes ◽  
Mouse Model ◽  
Nod Mouse

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.

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