Document Detail


Radon-induced reduced apoptosis in human bronchial epithelial cells with knockdown of mitochondria DNA.
MedLine Citation:
PMID:  22891884     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Radon and radon progeny inhalation exposure are recognized to induce lung cancer. To explore the role of mitochondria in radon-induced carcinogenesis in humans, an in vitro partially depleted mitochondrial DNA (mtDNA) cell line (ρ-) was generated by treatment of human bronchial epithelial (HBE) cells (ρ+) with ethidium bromide (EB). The characterization of ρ- cells indicated the presence of dysfunctional mitochondria and might thus serve a reliable model to investigate the role of mitochondria. In a gas inhalation chamber, ρ- and ρ+ cells were exposed to radon gas produced by a radium source. Results showed that apoptosis was significantly increased both in ρ- and ρ+ cells irradiated by radon. Moreover, apoptosis in ρ- cells showed a lower level than in ρ+ cells. Radon was further found to depress mitochondrial membrane potential (MMP) of HBE cells with knockdown mtDNA. Production of reactive oxygen species (ROS) was markedly elevated both in ρ- and ρ+ cells exposed to radon. The distribution of phases of cell cycle was different in ρ- compared to ρ+ cells. Radon irradiation induced a rise in G2/M and decrease in S phase in ρ+ cells. In ρ- cells, G1, G2/M, and S populations remained similar to cells exposed to radon. In conclusion, radon-induced changes in ROS generation, MMP and cell cycle are all attributed to reduction of apoptosis, which may trigger and promote cell transformation, leading to carcinogenesis. Our study indicates that the use of the ρ- knockdown mtDNA HBE cells may serve as a reliable model to study the role played by mitochondria in carcinogenic diseases.
Authors:
Bing-Yan Li; Jing Sun; Hong Wei; Yu-Zhi Cheng; Lian Xue; Zhi-Hai Cheng; Jian-Mei Wan; Ai-Qing Wang; Tom K Hei; Jian Tong
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of toxicology and environmental health. Part A     Volume:  75     ISSN:  1528-7394     ISO Abbreviation:  J. Toxicol. Environ. Health Part A     Publication Date:  2012  
Date Detail:
Created Date:  2012-08-15     Completed Date:  2012-10-22     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  100960995     Medline TA:  J Toxicol Environ Health A     Country:  England    
Other Details:
Languages:  eng     Pagination:  1111-9     Citation Subset:  IM    
Affiliation:
Department of Toxicology, School of Public Health, Soochow University, Suzhou, China.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects,  radiation effects*
Bronchi / drug effects,  metabolism,  radiation effects*
Carcinogens, Environmental / toxicity*
Cell Cycle / radiation effects
Cell Line
Cell Transformation, Neoplastic / radiation effects
DNA, Mitochondrial / antagonists & inhibitors*,  metabolism
Ethidium / pharmacology
Gene Knockdown Techniques
Humans
Intercalating Agents / pharmacology
Membrane Potential, Mitochondrial / radiation effects
Mitochondria / drug effects,  metabolism,  radiation effects*
Radon / toxicity*
Radon Daughters / toxicity
Reactive Oxygen Species / metabolism
Respiratory Mucosa / drug effects,  metabolism,  radiation effects*
Toxicity Tests, Chronic / methods
Grant Support
ID/Acronym/Agency:
CA49062/CA/NCI NIH HHS; ES05786/ES/NIEHS NIH HHS; P01 CA049062/CA/NCI NIH HHS; P42 ES010349/ES/NIEHS NIH HHS; P42 ES10349/ES/NIEHS NIH HHS; R01 ES005786/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Carcinogens, Environmental; 0/DNA, Mitochondrial; 0/Intercalating Agents; 0/Radon Daughters; 0/Reactive Oxygen Species; 10043-92-2/Radon; 3546-21-2/Ethidium
Comments/Corrections

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