Elevated metals compromise repair of oxidative DNA damage via the base excision repair pathway: Implications of pathologic iron overload in the brain on integrity of neuronal DNA

Journal of Neurochemistry

Volumn 110, Issue 6, 2009, Pages 1774-1783

  Li, Hui ^a   Swiercz, Rafal ^a   Englander, Ella W ^a  

^a University of Texas Medical Branch School of Medicine   (United States)

Author keywords

Base excision repair; Brain; Iron; Oxidative DNA damage; Primary neuronal culture; Zinc

Indexed keywords

GENOMIC DNA; HYDROGEN PEROXIDE; IRON; METAL; ZINC;

ANIMAL CELL; ARTICLE; BLOOD LEVEL; BRAIN; CELL VIABILITY; CONTROLLED STUDY; CYTOTOXICITY; DNA DAMAGE; DNA STRAND BREAKAGE; DNA SYNTHESIS; ENZYME ACTIVITY; EXCISION REPAIR; IRON OVERLOAD; MALE; MOUSE; NERVE CELL CULTURE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT;

ANIMALS; CELL SURVIVAL; CELLS, CULTURED; CEREBRAL CORTEX; COMET ASSAY; DNA DAMAGE; DNA REPAIR; ELECTROPHORETIC MOBILITY SHIFT ASSAY; HYDROGEN PEROXIDE; IRON; MALE; METALS; NEURONS; OXIDANTS; OXIDATIVE STRESS; RATS; RATS, SPRAGUE-DAWLEY; ZINC;

EID: 69949175485     PISSN: 00223042     EISSN: 14714159     Source Type: Journal    
DOI: 10.1111/j.1471-4159.2009.06271.x     Document Type: Article

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