| Oxygen tolerance and coupling of mitochondrial electron transport. | |
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MedLine Citation:
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PMID: 15328348 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Oxygen is critical to aerobic metabolism, but excessive oxygen (hyperoxia) causes cell injury and death. An oxygen-tolerant strain of HeLa cells, which proliferates even under 80% O2, termed "HeLa-80," was derived from wild-type HeLa cells ("HeLa-20") by selection for resistance to stepwise increases of oxygen partial pressure. Surprisingly, antioxidant defenses and susceptibility to oxidant-mediated killing do not differ between these two strains of HeLa cells. However, under both 20 and 80% O2, intracellular reactive oxygen species (ROS) production is significantly (approximately 2-fold) less in HeLa-80 cells. In both cell lines the source of ROS is evidently mitochondrial. Although HeLa-80 cells consume oxygen at the same rate as HeLa-20 cells, they consume less glucose and produce less lactic acid. Most importantly, the oxygen-tolerant HeLa-80 cells have significantly higher cytochrome c oxidase activity (approximately 2-fold), which may act to deplete upstream electron-rich intermediates responsible for ROS generation. Indeed, preferential inhibition of cytochrome c oxidase by treatment with n-methyl protoporphyrin (which selectively diminishes synthesis of heme a in cytochrome c oxidase) enhances ROS production and abrogates the oxygen tolerance of the HeLa-80 cells. Thus, it appears that the remarkable oxygen tolerance of these cells derives from tighter coupling of the electron transport chain. |
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Authors:
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Jian Li Campian; Mingwei Qian; Xueshan Gao; John W Eaton |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2004-08-24 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 279 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2004 Nov |
Date Detail:
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Created Date: 2004-11-01 Completed Date: 2004-12-28 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 46580-7 Citation Subset: IM |
Affiliation:
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Molecular Targets Group, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky 40202, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aconitate Hydratase
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metabolism Antioxidants / pharmacology Carbonyl Cyanide m-Chlorophenyl Hydrazone / pharmacology Cell Proliferation Citrate (si)-Synthase / metabolism Edetic Acid / pharmacology Electron Transport Electron Transport Complex IV / metabolism Electrons Glucose / metabolism Glutamine / metabolism Hela Cells Humans Ionophores / pharmacology Lactates / metabolism Mitochondria / metabolism* Oxygen / metabolism* Oxygen Consumption Partial Pressure Peroxides / metabolism Protoporphyrins / metabolism Reactive Oxygen Species Spectrometry, Fluorescence Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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DK58882/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Ionophores; 0/Lactates; 0/Peroxides; 0/Protoporphyrins; 0/Reactive Oxygen Species; 50-99-7/Glucose; 555-60-2/Carbonyl Cyanide m-Chlorophenyl Hydrazone; 56-85-9/Glutamine; 60-00-4/Edetic Acid; 7782-44-7/Oxygen; EC 1.9.3.1/Electron Transport Complex IV; EC 2.3.3.1/Citrate (si)-Synthase; EC 4.2.1.3/Aconitate Hydratase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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