Arsenic induces mitochondria-dependent apoptosis by reactive oxygen species generation rather than glutathione depletion in Chang human hepatocytes

Archives of Toxicology

Volumn 83, Issue 10, 2009, Pages 899-908

  Wang, Yi ^a   Xu, Yuanyuan ^a   Wang, Huihui ^a   Xue, Peng ^a   Li, Xin ^a   Li, Bing ^a   Zheng, Quanmei ^a   Sun, Guifan ^a  

^a CHINA MEDICAL UNIVERSITY   (China)

Author keywords

Apoptosis; Arsenic; Glutathione; Mitochondria; Reactive oxygen species

Indexed keywords

ACETYLCYSTEINE; ARSENITE SODIUM; CASPASE 3; CYTOCHROME C; GLUTATHIONE; MALONALDEHYDE; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PHOSPHATIDYLSERINE; REACTIVE OXYGEN METABOLITE;

APOPTOSIS; ARTICLE; CELL ASSAY; CELL DISRUPTION; CELL VIABILITY; CONCENTRATION (PARAMETERS); CONTROLLED STUDY; CYTOSOL; HUMAN; HUMAN CELL; INTRACELLULAR SPACE; LIVER MITOCHONDRION; MITOCHONDRIAL MEMBRANE POTENTIAL; PRIORITY JOURNAL; PROTEIN CLEAVAGE; PROTEIN SECRETION;

ACETYLCYSTEINE; APOPTOSIS; ARSENIC; ARSENITES; CELL SURVIVAL; CELLS, CULTURED; CYTOCHROMES C; GLUTATHIONE; HEPATOCYTES; HUMANS; MALONDIALDEHYDE; MEMBRANE POTENTIAL, MITOCHONDRIAL; MITOCHONDRIA; REACTIVE OXYGEN SPECIES; SODIUM COMPOUNDS;

EID: 70349626975     PISSN: 03405761     EISSN: None     Source Type: Journal    
DOI: 10.1007/s00204-009-0451-x     Document Type: Article

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