Oxidative stress, apoptosis, and cell cycle arrest are induced in primary fetal alveolar type II epithelial cells exposed to fine particulate matter from cooking oil fumes

2015 ◽  
Vol 22 (13) ◽  
pp. 9728-9741 ◽  
Author(s):  
Ying Liu ◽  
Yan-Yan Chen ◽  
Ji-Yu Cao ◽  
Fang-Biao Tao ◽  
Xiao-Xia Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Alveolar Type ◽  
Type Ii ◽  
Cooking Oil ◽  
Cooking Oil Fumes ◽  
Cycle Arrest ◽  
Fine Particulate

The injury of fine particulate matter from cooking oil fumes on umbilical cord blood vessels in vitro

2017 ◽  
Vol 49 ◽  
pp. 65-73 ◽  
Author(s):  
Lijuan Hou ◽  
Jian Zhang ◽  
Chao Zhang ◽  
Yachun Xu ◽  
Xiaoxia Zhu ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Cord Blood ◽  
Blood Vessels ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Fine Particulate Matter ◽  
Cooking Oil ◽  
Cooking Oil Fumes ◽  
Fine Particulate

scholarly journals Effects of ambient PM2.5and 9-nitroanthracene on DNA damage and repair, oxidative stress and metabolic enzymes in the lungs of rats

2017 ◽  
Vol 6 (5) ◽  
pp. 654-663 ◽  
Author(s):  
Ruijin Li ◽  
Lifang Zhao ◽  
Li Zhang ◽  
Minghui Chen ◽  
Jing Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Dna Damage ◽  
Particulate Matter ◽  
Cancer Risk ◽  
Lung Cancer Risk ◽  
Fine Particulate Matter ◽  
Complex Mixture ◽  
Dna Damage And Repair ◽  
Fine Particulate

Ambient fine particulate matter (PM2.5) is a complex mixture associated with lung cancer risk.

scholarly journals Fine Particulate Matter Leads to Unfolded Protein Response and Shortened Lifespan by Inducing Oxidative Stress in C. elegans

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Yunli Zhao ◽  
Ling Jin ◽  
Yuxin Chi ◽  
Jing Yang ◽  
Quan Zhen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Metabolic Enzyme ◽  
C Elegans ◽  
Unfolded Protein ◽  
Fine Particulate ◽  
Underlying Mechanisms ◽  
Protein Response ◽  
Phenylbutyric Acid

Oxidative stress has been proven as one of the most critical regulatory mechanisms involved in fine Particulate Matter- (PM2.5-) mediated toxicity. For a better understanding of the underlying mechanisms that enable oxidative stress to participate in PM2.5-induced toxic effects, the current study explored the effects of oxidative stress induced by PM2.5 on UPR and lifespan in C. elegans. The results implicated that PM2.5 exposure induced oxidative stress response, enhanced metabolic enzyme activity, activated UPR, and shortened the lifespan of C. elegans. Antioxidant N-acetylcysteine (NAC) could suppress the UPR through reducing the oxidative stress; both the antioxidant NAC and UPR inhibitor 4-phenylbutyric acid (4-PBA) could rescue the lifespan attenuation caused by PM2.5, indicating that the antioxidant and moderate proteostasis contribute to the homeostasis and adaptation to oxidative stress induced by PM2.5.

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