GdCl3 induced hep G2 cell death through mitochondrial and external death pathways without significant elevation of ROS generation

Biological Trace Element Research

Volumn 151, Issue 1, 2013, Pages 148-155

  Ye, Lihua ^a   Shi, Zhe ^b   Liu, Huixue ^b   Yang, Xiaoda ^a   Wang, Kui ^a  

^a PEKING UNIVERSITY   (China)

^b PEKING UNIVERSITY HEALTH SCIENCE CENTER   (China)

Author keywords

Apoptosis; Gadolinium chloride; MAPK; Mitochondria

Indexed keywords

APOPTOSIS INDUCING FACTOR; CASPASE 3; CASPASE 8; CYTOCHROME C; GADOLINIUM CHLORIDE; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN BAX; PROTEIN BID; REACTIVE OXYGEN METABOLITE; STRESS ACTIVATED PROTEIN KINASE; GADOLINIUM;

APOPTOSIS; ARTICLE; CELL STRAIN HEPG2; CONTROLLED STUDY; DRUG MECHANISM; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; HEPATOBLASTOMA; HUMAN; HUMAN CELL; MITOCHONDRIAL MEMBRANE POTENTIAL; PROTEIN CLEAVAGE; PROTEIN SECRETION; PROTEIN TRANSPORT; BIOLOGICAL MODEL; CELL SURVIVAL; CONFOCAL MICROSCOPY; DOSE RESPONSE; DRUG EFFECT; FLOW CYTOMETRY; HEPG2 CELL LINE; METABOLISM; MITOCHONDRION; PHYSIOLOGY; SECRETION (PROCESS); SIGNAL TRANSDUCTION; TIME; WESTERN BLOTTING;

APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; BH3 INTERACTING DOMAIN DEATH AGONIST PROTEIN; BLOTTING, WESTERN; CASPASE 3; CASPASE 8; CELL SURVIVAL; CYTOCHROMES C; DOSE-RESPONSE RELATIONSHIP, DRUG; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; FLOW CYTOMETRY; GADOLINIUM; HEP G2 CELLS; HUMANS; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MEMBRANE POTENTIAL, MITOCHONDRIAL; MICROSCOPY, CONFOCAL; MITOCHONDRIA; MODELS, BIOLOGICAL; REACTIVE OXYGEN SPECIES; SIGNAL TRANSDUCTION; TIME FACTORS;

EID: 84871923982     PISSN: 01634984     EISSN: 15590720     Source Type: Journal    
DOI: 10.1007/s12011-012-9538-y     Document Type: Article

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