Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells

Toxicon

Volumn 52, Issue 2, 2008, Pages 361-368

  Chen, Ku Chung ^a   Lin, Shinne Ren ^b   Chang, Long Sen ^a  

^a NATIONAL SUN YAT SEN UNIVERSITY   (Taiwan)

^b KAOHSIUNG MEDICAL UNIVERSITY   (Taiwan)

Author keywords

Cardiotoxin; Cytotoxicity; Mitochondrial alteration; Reactive oxygen species generation

Indexed keywords

ACETYLCYSTEINE; CARDIOTOXIN; CASPASE 3; CASPASE 9; CYCLOSPORIN A; CYTOCHROME C; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DEHYDROGENASE (UBIQUINONE); ROTENONE; SNAKE VENOM;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; DRUG MECHANISM; ENZYME ACTIVATION; HUMAN; HUMAN CELL; MITOCHONDRIAL MEMBRANE POTENTIAL; NEUROBLASTOMA CELL; PRIORITY JOURNAL; PROTEIN FAMILY; RESPIRATORY CHAIN;

ACETYLCYSTEINE; APOPTOSIS; CASPASES; CELL LINE, TUMOR; COBRA CARDIOTOXIN PROTEINS; COBRA VENOMS; CYCLOSPORINE; CYTOCHROMES C; ENZYME ACTIVATION; FREE RADICAL SCAVENGERS; HUMANS; MEMBRANE POTENTIAL, MITOCHONDRIAL; MITOCHONDRIA; NEUROBLASTOMA; REACTIVE OXYGEN SPECIES; ROTENONE; UNCOUPLING AGENTS;

NAJA ATRA;

EID: 49449110179     PISSN: 00410101     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.toxicon.2008.06.013     Document Type: Article

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