Document Detail

Prolonged hypoxia during cell development protects mature manganese superoxide dismutase-deficient astrocytes from damage by oxidative stress.
MedLine Citation:
PMID:  11156968     Owner:  NLM     Status:  MEDLINE    
Mouse astrocytes deficient in the mitochondrial form of superoxide dismutase do not grow in culture under 20% atmospheric O2 levels. By flow cytometry, immunocytochemistry, and enzymatic analysis we have shown that the oxygen block of cell division is due to a decrease in the number of cells entering the S phase of the cell cycle and is concomitant with higher DNA oxidation and impairment of mitochondrial functions. Seeding the cells under 5% O2 until the cultures become confluent can circumvent this problem. An initial hypoxic environment increases the resistance of manganese superoxide dismutase-deficient astrocytes to superoxide radicals artificially produced by paraquat treatment, preserves respiratory activity, and allows normoxic division during a subsequent passage. DNA oxidation is then not higher than in wild-type control cells. However, the adaptation of the cells is not due to compensation by other enzymes of the antioxidant defense system and is specific to cells totally lacking manganese superoxide dismutase. Alteration of the phenotype by prior hypoxia exposure in the SOD2-deficient mutant provide a unique model to study adaptative mechanisms of cellular resistance to oxygen toxicity.
J C Copin; Y Gasche; Y Li; P H Chan
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  15     ISSN:  0892-6638     ISO Abbreviation:  FASEB J.     Publication Date:  2001 Feb 
Date Detail:
Created Date:  2001-02-22     Completed Date:  2001-03-22     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  525-34     Citation Subset:  IM    
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305-5487 USA.
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MeSH Terms
Astrocytes / cytology,  enzymology,  physiology*
Catalase / metabolism
Cell Division / physiology
Cell Hypoxia / physiology*
Cell Size
Cells, Cultured
Crosses, Genetic
DNA / biosynthesis
Glutathione Peroxidase / metabolism
Isoenzymes / deficiency,  genetics,  metabolism
Mice, Knockout
Mitochondria / metabolism*
Oxidative Stress / physiology*
Superoxide Dismutase / deficiency,  genetics,  metabolism*
Grant Support
Reg. No./Substance:
0/Isoenzymes; 9007-49-2/DNA; EC; EC Peroxidase; EC Dismutase

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