scholarly journals Age and Gender Effects on Genotoxicity in Diesel Exhaust Particles Exposed C57BL/6 Mice

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 374
Author(s):  
Joong Won Lee ◽  
Jin Sik Kim ◽  
Hee Jae Lee ◽  
Ji-Hye Jang ◽  
Ja-Hyun Kim ◽  
...  

There is growing evidence that the accumulation of DNA damage induced by fine particulate matter (PM2.5) exposure is an underlying mechanism of pulmonary disease onset and progression. However, there is a lack of experimental evidence on whether common factors (age, gender) affect PM2.5 induced genomic damage. Here, we assessed the DNA damage potency of PM2.5 using conventional genotoxicity testing in old male and female mice aged 8 and 40 weeks. Mice were intratracheally instilled with diesel exhaust PM2.5 (DEP, NIST SRM 1650b), twice a week for 4 weeks. Exposure to DEP was not associated with an increase in the frequency of micronucleated polychromatic erythrocytes and did not induce a systemic genotoxic effect in the bone marrow. Meanwhile, the results from the comet assay showed a significant increase in DNA damage in DEP exposed mouse lung specimens. The positive relationship between DEP exposure and DNA damage is stronger in the older than in the younger group. Statistical analysis showed that there was a modifying effect of age on the association between PM2.5 exposure and DNA damage. Our results suggest that the age factor should be considered to better understand the cellular adverse effects of PM2.5.

2016 ◽  
Vol 38 (5) ◽  
pp. 1703-1713 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Turan Karaca ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Javed Yasin ◽  
...  

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.


2016 ◽  
Vol 1 (1) ◽  
pp. 85 ◽  
Author(s):  
Ankita Srivastava ◽  
Sanjay Yadav ◽  
Alok K Pandey ◽  
Uppendra N Dwivedi ◽  
Devendra Parmar

<div class="page" title="Page 1"><div class="layoutArea"><div class="column"><p><span>Attempts were made to investigate the role of cytochrome P450 1A1 (CYP1A1) on similarities in the generation of reactive oxygen species (ROS) and DNA damage in IM9, a human B lymphoblastic cell line with A549, the human lung adenocarcinoma epithelial cell line on exposure of diesel exhaust particles (DEP). </span><span>A suspension of ultrafine particles (&lt; 0.2 μM) of DEP (1mg/ml) in DMEM-F12 medium, at a concentration range of 1-100 μg/ml, was added to the cells for 6-48h. Expression studies revealed that DEP induced similar </span><span>increase in the expression of CYP1A1, generation of ROS and DNA damage in both the cells. Pre-incubation with 3-methylcholanthrene (MC), a CYP1A1 inducer resulted in higher magnitude of induction of CYP1A1, ROS </span><span>and DNA damage. This synergistic effect was lowered when α-naphthoflavone (α-NF), an inhibitor of CYP1A1 </span><span>catalysed reactions, was added to these cells. Though the magnitude of alterations was lower in IM9 cells when compared to A549 cells, similarities in the alterations in blood and lungs cells has further suggested that blood lymphocytes can be used as a surrogate to monitor toxicity of vehicular emissions.</span></p></div></div></div>


Author(s):  
Pernille Høgh Danielsen ◽  
Lotte Risom ◽  
Håkan Wallin ◽  
Herman Autrup ◽  
Ulla Vogel ◽  
...  

Author(s):  
Anne K. Müller ◽  
E.Olatunde Farombi ◽  
Peter Møller ◽  
Herman N. Autrup ◽  
Ulla Vogel ◽  
...  

Author(s):  
Nicklas Raun Jacobsen ◽  
Peter Møller ◽  
Corey Alexander Cohn ◽  
Steffen Loft ◽  
Ulla Vogel ◽  
...  

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