Impaired mitochondrial function and oxidative stress in rat cortical neurons: Implications for gadolinium-induced neurotoxicity

NeuroToxicology

Volumn 31, Issue 4, 2010, Pages 391-398

  Feng, Xudong ^a   Xia, Qing ^a   Yuan, Lan ^b   Yang, Xiaoda ^a   Wang, Kui ^a  

^a PEKING UNIVERSITY HEALTH SCIENCE CENTER   (China)

^b PEKING UNIVERSITY   (China)

Author keywords

Apoptosis; Gadolinium chloride; Mitochondrial dysfunction; Neurotoxicity

Indexed keywords

ADENOSINE TRIPHOSPHATE; CASPASE 3; CYTOCHROME C; GADOLINIUM CHLORIDE; REACTIVE OXYGEN METABOLITE;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BIOACCUMULATION; CELL DEATH; CELL FUNCTION; CONTROLLED STUDY; CYTOTOXICITY; DEPOLARIZATION; DNA FRAGMENTATION; ENERGY METABOLISM; ENVIRONMENTAL EXPOSURE; ENZYME ACTIVATION; ENZYME RELEASE; ENZYME SYNTHESIS; MITOCHONDRIAL MEMBRANE POTENTIAL; MITOCHONDRION; NEUROTOXICITY; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN DEPLETION; RAT;

ADENOSINE TRIPHOSPHATE; ANIMALS; APOPTOSIS; CASPASE 3; CELL CULTURE TECHNIQUES; CEREBRAL CORTEX; CYTOCHROMES C; DNA FRAGMENTATION; GADOLINIUM; MEMBRANE POTENTIAL, MITOCHONDRIAL; MITOCHONDRIA; NEURONS; OXIDATIVE STRESS; RATS; RATS, SPRAGUE-DAWLEY; REACTIVE OXYGEN SPECIES;

RATTUS;

EID: 77953538985     PISSN: 0161813X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neuro.2010.04.003     Document Type: Article

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