Inhibition of fatty acid oxidation by etomoxir impairs NADPH production and increases reactive oxygen species resulting in ATP depletion and cell death in human glioblastoma cells

Biochimica et Biophysica Acta - Bioenergetics

Volumn 1807, Issue 6, 2011, Pages 726-734

  Pike, Lisa S ^a   Smift, Amy L ^a   Croteau, Nicole J ^b   Ferrick, David A ^a   Wu, Min ^a  

^a Seahorse Bioscience   (United States)

^b DANA FARBER CANCER INSTITUTE   (United States)

Author keywords

Fatty acid oxidation; Mitochondrial dysfunction; NADPH; Oxidative stress; ROS

Indexed keywords

ADENOSINE TRIPHOSPHATE; ETOMOXIR; FATTY ACID; GLUTATHIONE; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE; TIRON;

ACIDIFICATION; ARTICLE; CANCER GROWTH; CANCER INHIBITION; CANCER SURVIVAL; CELL DEATH; CELL METABOLISM; CELL PROLIFERATION; CELL VIABILITY; CONTROLLED STUDY; DRUG INHIBITION; FATTY ACID OXIDATION; GLIOBLASTOMA; GLYCOLYSIS; HUMAN; HUMAN CELL; MITOCHONDRIAL ENERGY TRANSFER; OXIDATIVE PHOSPHORYLATION; OXIDATIVE STRESS; OXYGEN CONSUMPTION; PRIORITY JOURNAL; TREATMENT OUTCOME;

EID: 79955601028     PISSN: 00052728     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bbabio.2010.10.022     Document Type: Article

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