Document Detail


The decrease of mitochondrial NADH dehydrogenease and drug induced apoptosis in doxorubicin resistant A431 cells.
MedLine Citation:
PMID:  10954045     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Doxorubicin (DOX) resistant A10A cells derived from human squamous carcinoma A431 cells were found to exhibit a smaller degree of apoptosis after DOX treatment as compared to their parent cells. Induction of reactive oxygen species (ROS) formation and mitochondrial depolarization by DOX were more pronounced in the parent cells than in the A10A cells. The fact that catalase suppressed the DOX effect on ROS induction, mitochondrial depolarization and apoptosis in both cell lines suggests an involvement of ROS in the DOX-induced apoptosis. To investigate the underlying mechanisms for DOX resistance in A10A cells, RT-PCR based differential display was used. One of the clones, which was down-regulated in the A10A cells, had sequence homology with part of the mitochondrial NADH dehydrogenase III (ND3) gene. NADH dehydrogenase plays an important role in generating ROS during DOX treatment. The results indicate that down-regulation of ND3 may at least in part contribute to the mechanism for A10A cells resistant to DOX-induced apoptosis.
Authors:
T W Wong; H Y Yu; S K Kong; K P Fung; T T Kwok
Related Documents :
10494335 - Role and mechanisms of secondary mitochondrial failure.
23166045 - Cell viability and angiogenic potential of a bioartificial adipose substitute.
12608435 - Oxidative stress in lung epithelial cells from patients with idiopathic interstitial pn...
22612335 - Pho1 expression in guard cells mediates the stomatal response to abscisic acid in arabi...
1416265 - Bronchial inflammation in mite-sensitive asthmatic subjects after 5 years of specific i...
22742535 - Synthesized pheophorbide a-mediated photodynamic therapy induced apoptosis and autophag...
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Life sciences     Volume:  67     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2000  
Date Detail:
Created Date:  2000-09-06     Completed Date:  2000-09-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1111-8     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, The Chinese University of Hong Kong, Shatin.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects*,  physiology
Carcinoma, Squamous Cell / drug therapy,  enzymology*,  pathology
Catalase / metabolism
DNA Probes
DNA, Complementary / genetics
Dose-Response Relationship, Drug
Doxorubicin / pharmacology*
Drug Resistance, Neoplasm
Gene Expression Profiling
Humans
Isoenzymes / biosynthesis,  genetics,  metabolism
Mitochondria / drug effects,  enzymology*
NADH Dehydrogenase / biosynthesis,  genetics,  metabolism*
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/DNA Probes; 0/DNA, Complementary; 0/Isoenzymes; 0/Reactive Oxygen Species; 23214-92-8/Doxorubicin; EC 1.11.1.6/Catalase; EC 1.6.99.3/NADH Dehydrogenase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Production of nitric oxide from endothelial cells by 31-amino-acid-length endothelin-1, a novel vaso...
Next Document:  Lymphocyte subpopulations, cytokines and trace elements in asymptomatic atopic women exposed to an u...