Oxidative Stress and Lung Cancer

2014 ◽  
pp. 245-257 ◽  
Author(s):  
Aditya Jindal ◽  
Navneet Singh
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer

TWIST2 inhibits EMT and induces oxidative stress in lung cancer cells by regulating the FGF21-mediated AMPK/mTOR pathway

2021 ◽  
pp. 112661
Author(s):  
Yingjian Song ◽  
Wei Zhang ◽  
Jiuxu Zhang ◽  
Zhaolei You ◽  
Tao Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Mtor Pathway ◽  
Lung Cancer Cells

Toxicity of Cerium Oxide Nanoparticles in Human Lung Cancer Cells

2006 ◽  
Vol 25 (6) ◽  
pp. 451-457 ◽  
Author(s):  
Weisheng Lin ◽  
Yue-wern Huang ◽  
Xiao-Dong Zhou ◽  
Yinfa Ma
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Lactate Dehydrogenase ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cerium Oxide ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

With the fast development of nanotechnology, the nanomaterials start to cause people’s attention for potential toxic effect. In this paper, the cytotoxicity and oxidative stress caused by 20-nm cerium oxide (CeO2) nanoparticles in cultured human lung cancer cells was investigated. The sulforhodamine B method was employed to assess cell viability after exposure to 3.5, 10.5, and 23.3 μg/ml of CeO2 nanoparticles for 24, 48, and 72 h. Cell viability decreased significantly as a function of nanoparticle dose and exposure time. Indicators of oxidative stress and cytotoxicity, including total reactive oxygen species, glutathione, malondialdehyde, α-tocopherol, and lactate dehydrogenase, were quantitatively assessed. It is concluded from the results that free radicals generated by exposure to 3.5 to 23.3 μg/ml CeO2 nanoparticles produce significant oxidative stress in the cells, as reflected by reduced glutathione and α-tocopherol levels; the toxic effects of CeO2 nanoparticles are dose dependent and time dependent; elevated oxidative stress increases the production of malondialdehyde and lactate dehydrogenase, which are indicators of lipid peroxidation and cell membrane damage, respectively.

scholarly journals ΔNp63 targets cytoglobin to inhibit oxidative stress-induced apoptosis in keratinocytes and lung cancer

Oncogene ◽  
2015 ◽  
Vol 35 (12) ◽  
pp. 1493-1503 ◽  
Author(s):  
A Latina ◽  
G Viticchiè ◽  
A M Lena ◽  
M C Piro ◽  
M Annicchiarico-Petruzzelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Induced Apoptosis

Significance of the urinary 8-OHdG level as an oxidative stress marker in lung cancer patients

Lung Cancer ◽  
2009 ◽  
Vol 63 (1) ◽  
pp. 111-114 ◽  
Author(s):  
Tokujiro Yano ◽  
Fumihiro Shoji ◽  
Hiromitsu Baba ◽  
Tadashi Koga ◽  
Takeshi Shiraishi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Patients ◽  
Oxidative Stress Marker ◽  
Lung Cancer Patients ◽  
Stress Marker

scholarly journals BA6 Induces Apoptosis via Stimulation of Reactive Oxygen Species and Inhibition of Oxidative Phosphorylation in Human Lung Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-21 ◽  
Author(s):  
Meng-Hsuan Cheng ◽  
Hung-Ling Huang ◽  
Yen-You Lin ◽  
Kuan-Hao Tsui ◽  
Pei-Chin Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Oxygen Species ◽  
Apoptotic Pathway ◽  
Induced Apoptosis

Lung cancer is the leading cause of cancer deaths in the world, with a five-year survival rate of less than 30%. Clinically effective chemotherapeutic treatments at the initial stage may eventually face the dilemma of no drug being effective due to drug resistance; therefore, finding new effective drugs for lung cancer treatment is a necessary and important issue. Compounds capable of further increasing the oxidative stress of cancer cells are considered to have anticancer potential because they possessed the ability to induce apoptosis. This study mainly investigated the effects of BA6 (heteronemin), the marine sponge sesterterpene, on lung cancer cell apoptosis, via modulation of mitochondrial reactive oxygen species (mtROS) and oxidative phosphorylation (OXPHOS). BA6 has cellular cytotoxic activities against a variety of cancer cell lines, but it has no effect on nontumor cells. The BA6-treated lung cancer cells show a significant increase in both cellular ROS and mtROS, which in turn caused the loss of mitochondrial membrane potential (MMP). The increase of oxidative stress in lung cancer cells treated with BA6 was accompanied by a decrease in the expression of antioxidant enzymes Cu/Zn SOD, MnSOD, and catalase. In addition, OXPHOS performed in the mitochondria and glycolysis in the cytoplasm were inhibited, which subsequently reduced downstream ATP production. Pretreatment with mitochondria-targeted antioxidant MitoTEMPO reduced BA6-induced apoptosis through the mitochondria-dependent apoptotic pathway, which was accompanied by increased cell viability, decreased mtROS, enhanced MMP, and suppressed expression of cleaved caspase-3 and caspase-9 proteins. In conclusion, the results of this study clarify the mechanism of BA6-induced apoptosis in lung cancer cells via the mitochondrial apoptotic pathway, suggesting that it is a potentially innovative alternative to the treatment of human lung cancer.

Lung cancer: What are the links with oxidative stress, physical activity and nutrition

Lung Cancer ◽  
2013 ◽  
Vol 82 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Edith Filaire ◽  
Carmen Dupuis ◽  
Géraud Galvaing ◽  
Sylvie Aubreton ◽  
Hélène Laurent ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Lung Cancer

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 A mono-carbonyl analog of curcumin induces apoptosis in drug-resistant EGFR-mutant lung cancer through the generation of oxidative stress and mitochondrial dysfunction

2018 ◽  
Vol Volume 10 ◽  
pp. 3069-3082 ◽  
Author(s):  
Xuanxuan Dai ◽  
Junru Zhang ◽  
Guilong Guo ◽  
Yuepiao Cai ◽  
Ri Cui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Mitochondrial Dysfunction ◽  
Drug Resistant ◽  
Egfr Mutant

scholarly journals Myrcene Exhibits Antitumor Activity Against Lung Cancer Cells by Inducing Oxidative Stress and Apoptosis Mechanisms

2020 ◽  
Vol 15 (9) ◽  
pp. 1934578X2096118
Author(s):  
Xudong Bai ◽  
Jin Tang
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Metabolic Activity ◽  
Lung Cancer Cells ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
A549 Lung

Myrcene, a natural olefinic hydrocarbon, possesses anti-inflammatory, analgesic, antibiotic, and antimutagenic properties, but its anticancer effect has not yet been elucidated. Hence, the present study was framed to investigate the molecular mechanism by which myrcene mediates the anticancer activity of A549 lung adenocarcinoma cells. In vitro, A549 lung cancer cells were cultured either with or without myrcene, and the effects on cellular metabolic activity, levels of reactive oxygen species (ROS), mitochondrial integrity, deoxyribonucleic acid (DNA) damage, and activity of caspases were analyzed. The study demonstrated that compared with control cells, myrcene induces cell death in a dose-dependent manner while inducing ROS levels. Further experiments revealed that the metabolic activity of the A549 lung adenocarcinoma cells was diminished with increased DNA damage and altered cellular integrity. In addition, increased activity of caspase-3 was also evidenced with reduced mitochondrial membrane potential synthesis in the myrcene-treated cells, which demonstrate that lung cancer cells experience signs of toxicity during myrcene treatment through the activation of the apoptosis mechanism via mitochondria-mediated cell death signaling and induction of oxidative stress. The results provide the first report on the evidence of anticancer activity and the possibility of a new drug that could be used for the treatment of lung cancer.

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