scholarly journals The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines

2018 ◽  
Vol 37 (5) ◽  
pp. 849-864 ◽  
Author(s):  
Malgorzata Kucinska ◽  
Helena Mieszczak ◽  
Hanna Piotrowska-Kempisty ◽  
Mariusz Kaczmarek ◽  
Walter Granig ◽  
...  
Author(s):  
Kazutaka Dohmoto ◽  
Satoko Hojo ◽  
Jiro Fujita ◽  
Yu Yang ◽  
Yutaka Ueda ◽  
...  

Author(s):  
Giuseppe Giaccone ◽  
Jannette van Ark-Otte ◽  
Gonzalo J. Rubio ◽  
Adi F. Gazdar ◽  
Henk J. Broxterman ◽  
...  

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Somruethai Sumkhemthong ◽  
Eakachai Prompetchara ◽  
Pithi Chanvorachote ◽  
Chatchai Chaotham

Abstract Background Accumulated evidence demonstrates cisplatin, a recommended chemotherapy, modulating pro-survival autophagic response that contributes to treatment failure in lung cancer patients. However, distinct mechanisms involved in cisplatin-induced autophagy in human lung cancer cells are still unclear. Results Herein, role of autophagy in cisplatin resistance was indicated by a decreased cell viability and increased apoptosis in lung cancer H460 cells pre-incubated with wortmannin, an autophagy inhibitor, prior to treatment with 50 µM cisplatin for 24 h. The elevated level of hydroxyl radicals detected via flow-cytometry corresponded to autophagic response, as evidenced by the formation of autophagosomes and autolysosomes in cisplatin-treated cells. Interestingly, apoptosis resistance, autophagosome formation, and the alteration of the autophagic markers, LC3-II/LC3-I and p62, as well as autophagy-regulating proteins Atg7 and Atg3, induced by cisplatin was abrogated by pretreatment of H460 cells with deferoxamine, a specific hydroxyl radical scavenger. The modulations in autophagic response were also indicated in the cells treated with hydroxyl radicals generated via Fenton reaction, and likewise inhibited by pretreatment with deferoxamine. Conclusions In summary, the possible role of hydroxyl radicals as a key mediator in the autophagic response to cisplatin treatment, which was firstly revealed in this study would benefit for the further development of novel therapies for lung cancer.


2013 ◽  
Vol 34 (24) ◽  
pp. 3305-3314 ◽  
Author(s):  
Chiao-Yuan Fan ◽  
Hsiu-Chuan Chou ◽  
Yi-Wen Lo ◽  
Yueh-Feng Wen ◽  
Yi-Chih Tsai ◽  
...  

2017 ◽  
Vol 27 (13) ◽  
pp. 2946-2952 ◽  
Author(s):  
Manh Tuan Ha ◽  
Manh Hung Tran ◽  
Thien Thuong Phuong ◽  
Jeong Ah Kim ◽  
Mi Hee Woo ◽  
...  

Toxins ◽  
2016 ◽  
Vol 8 (2) ◽  
pp. 38 ◽  
Author(s):  
Irasema Oroz-Parra ◽  
Mario Navarro ◽  
Karla Cervantes-Luevano ◽  
Carolina Álvarez-Delgado ◽  
Guy Salvesen ◽  
...  

1996 ◽  
Vol 14 (4) ◽  
pp. 351-357 ◽  
Author(s):  
Xin-Hai Pei ◽  
Yoichi Nakanishi ◽  
Koichi Takayama ◽  
Jun Yatsunami ◽  
Feng Bai ◽  
...  

2006 ◽  
Vol 25 (6) ◽  
pp. 451-457 ◽  
Author(s):  
Weisheng Lin ◽  
Yue-wern Huang ◽  
Xiao-Dong Zhou ◽  
Yinfa Ma

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.


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