scholarly journals Hydrogen Peroxide Causes Cell Death via Increased Transcription of HOXB13 in Human Lung Epithelial A549 Cells

Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 78
Author(s):  
Naoki Endo ◽  
Takashi Toyama ◽  
Akira Naganuma ◽  
Yoshiro Saito ◽  
Gi-Wook Hwang
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Human Lung ◽  
A549 Cells ◽  
Protein Levels ◽  
Intracellular Ros ◽  
Lung Epithelial ◽  
Homeobox Protein

Although homeobox protein B13 (HOXB13) is an oncogenic transcription factor, its role in stress response has rarely been examined. We previously reported that knockdown of HOXB13 reduces the cytotoxicity caused by various oxidative stress inducers. Here, we studied the role of HOXB13 in cytotoxicity caused by hydrogen peroxide in human lung epithelial A549 cells. The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)). This suggests that HOXB13 may be involved in the cytotoxicity caused by hydrogen peroxide via the production of reactive oxygen species (ROS). Hydrogen peroxide also increased both the mRNA and protein levels of HOXB13. However, these increases were rarely observed in the presence of a transcriptional inhibitor, which suggests that hydrogen peroxide increases protein levels via increased transcription of HOXB13. Furthermore, cell death occurred in A549 cells that highly expressed HOXB13. However, this cell death was mostly inhibited by treatment with antioxidants. Taken together, our findings indicate that HOXB13 may be a novel factor involved in the induction of oxidative stress, which causes cell death via intracellular ROS production.

scholarly journals Aqueous areca nut extract induces oxidative stress in human lung epithelial A549 cells: Probable role of p21 in inducing cell death

Gene Reports ◽  
2017 ◽  
Vol 6 ◽  
pp. 103-111 ◽  
Author(s):  
Rashmi Nagesh ◽  
K. M Kiran Kumar ◽  
M Naveen Kumar ◽  
Rajeshwari H. Patil ◽  
K Kavya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Human Lung ◽  
A549 Cells ◽  
Areca Nut ◽  
Lung Epithelial ◽  
Probable Role

scholarly journals Hydrogen Sulfide Attenuates Hydrogen Peroxide-Induced Injury in Human Lung Epithelial A549 Cells

2019 ◽  
Vol 20 (16) ◽  
pp. 3975 ◽  
Author(s):  
Mingqi Wang ◽  
Xinyu Cao ◽  
Chang Luan ◽  
Zhengqiang Li
Keyword(s):  
Hydrogen Peroxide ◽  
Hydrogen Sulfide ◽  
Lung Injury ◽  
Er Stress ◽  
Human Lung ◽  
A549 Cells ◽  
Mapk Signaling ◽  
Protective Mechanism ◽  
Lung Epithelial ◽  
Pre Treatment

Lung tissues are frequently exposed to a hyperoxia environment, which leads to oxidative stress injuries. Hydrogen sulfide (H2S) is widely implicated in physiological and pathological processes and its antioxidant effect has attracted much attention. Therefore, in this study, we used hydrogen peroxide (H2O2) as an oxidative damage model to investigate the protective mechanism of H2S in lung injury. Cell death induced by H2O2 treatment could be significantly attenuated by the pre-treatment of H2S, resulting in a decrease in the Bax/Bcl-2 ratio and the inhibition of caspase-3 activity in human lung epithelial cell line A549 cells. Additionally, the results showed that H2S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H2O2 in mitochondria energy-producing and cell metabolism. Pre-treatment of H2S also decreased H2O2-induced suppression of endogenous H2S production enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H2S attenuated [Ca2+] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H2S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H2O2-induced lung injury.

scholarly journals Role of the MAPK pathway in human lung epithelial-like A549 cells apoptosis induced by paraquat

2020 ◽  
Vol 43 (2) ◽  
Author(s):  
Da-Zhuang Sun ◽  
Chun-Qing Song ◽  
Yong-Min Xu ◽  
Xue-Song Dong
Keyword(s):  
Human Lung ◽  
Mapk Pathway ◽  
A549 Cells ◽  
Lung Epithelial

scholarly journals Flavonoid Fraction of Orange and Bergamot Juices Protect Human Lung Epithelial Cells from Hydrogen Peroxide-Induced Oxidative Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Nadia Ferlazzo ◽  
Giuseppa Visalli ◽  
Antonella Smeriglio ◽  
Santa Cirmi ◽  
Giovanni Enrico Lombardo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Human Lung ◽  
Antioxidant Properties ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Food Sources ◽  
Plant Metabolites ◽  
Lung Epithelial ◽  
Flavonoid Fraction

It has been reported that oxidant/antioxidant imbalance triggers cell damage that in turn causes a number of lung diseases. Flavonoids are known for their health benefits, andCitrusfruits juices are one of the main food sources of these secondary plant metabolites. The present study was designed to evaluate the effect of the flavonoid fraction of bergamot and orange juices, on H2O2-induced oxidative stress in human lung epithelial A549 cells. First we tested the antioxidant properties of both extracts in cell-free experimental models and then we assayed their capability to prevent the cytotoxic effects induced by H2O2. Our results demonstrated that bothCitrusjuice extracts reduce the generation of reactive oxygen species and membrane lipid peroxidation, improve mitochondrial functionality, and prevent DNA-oxidative damage in A549 cells incubated with H2O2. Our data indicate that the mix of flavonoids present in both bergamot and orange juices may be of use in preventing oxidative cell injury and pave the way for further research into a novel healthy approach to avoid lung disorders.

Oxidative stress-induced regulation of the methionine metabolic pathway in human lung epithelial-like (A549) cells

2009 ◽  
Vol 674 (1-2) ◽  
pp. 23-30 ◽  
Author(s):  
Mihalis I. Panayiotidis ◽  
Sally P. Stabler ◽  
Robert H. Allen ◽  
Aglaia Pappa ◽  
Carl W. White
Keyword(s):  
Oxidative Stress ◽  
Metabolic Pathway ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Epithelial

scholarly journals Induction of Apoptotic Cell Death by Synthetic Naringenin Derivatives in Human Lung Epithelial Carcinoma A549 Cells

2007 ◽  
Vol 30 (12) ◽  
pp. 2394-2398 ◽  
Author(s):  
Eung-Ryoung Lee ◽  
Yong-Jin Kang ◽  
Hye-Yeon Choi ◽  
Geun-Ho Kang ◽  
Jung-Hyun Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Human Lung ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Apoptotic Cell Death ◽  
Lung Epithelial

Mechanism of thorium-nitrate and thorium-dioxide induced cytotoxicity in normal human lung epithelial cells (WI26): Role of oxidative stress, HSPs and DNA damage

2021 ◽  
Vol 281 ◽  
pp. 116969
Author(s):  
Sourav Kumar Das ◽  
Manjoor Ali ◽  
Neena G. Shetake ◽  
Rama Mohan R. Dumpala ◽  
Badri N. Pandey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Thorium Nitrate ◽  
Thorium Dioxide ◽  
Lung Epithelial ◽  
Normal Human ◽  
Human Lung Epithelial Cells

scholarly journals Oxidative stress induces cell death partially by decreasing both mRNA and protein levels of nicotinamide phosphoribosyltransferase in PC12 cells

2020 ◽  
Author(s):  
Cuiyan Zhou ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Pc12 Cells ◽  
Mrna Levels ◽  
Salvage Pathway ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Protein Levels ◽  
Pathological Conditions ◽  
Important Enzyme

AbstractNumerous studies have indicated critical roles of NAD+ deficiency in both aging and multiple major diseases. It is critical to investigate the mechanisms underlying the NAD+ deficiency under the pathological conditions. It has been reported that there was a decreased level of Nicotinamide phosphoribosyltransferase (Nampt) – an important enzyme in the salvage pathway of NAD+ synthesis – under certain pathological conditions, while the mechanisms underlying the Nampt decrease require investigation. In this study we used differentiated PC12 cells as a cellular model to investigate the effects of oxidative stress on both the mRNA and protein levels of Nampt, as well as the role of this effect in oxidative stress-induced cell death: First, Nampt plays significant roles in both the NAD+ synthesis and survival of the cells under basal conditions; second, H2O2 produced significant decreases in both the mRNA levels and the protein levels of Nampt; and third, H2O2 induced cell death partially by producing the decreases in the mRNA and protein levels of Nampt, since the Nampt inhibitor or the Nampt activator significantly exacerbated or attenuated the H2O2-induced cell death, respectively. Collectively, our study has indicated that oxidative stress can decrease both the mRNA and protein levels of Nampt, which has indicated a novel mechanism underlying the NAD+ deficiency in aging and under multiple pathological conditions. Our study has also indicated that the decreased Nampt levels contribute to the H2O2-induced cell death, suggesting a new mechanism underlying oxidative cell death.

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