Prolonged, but not acute, glutathione depletion promotes fas -mediated mitochondrial permeability transition and apoptosis in mice

Hepatology

Volumn 33, Issue 5, 2001, Pages 1181-1188

  Haouzi, Delphine ^a   Lekehal, Mounia ^a   Tinel, Marina ^a   Vadrot, Nathalie ^b   Caussanel, Laure ^a   Lettéron, Philippe ^a   Moreau, Alain ^b   Feldmann, Gérard ^b   Fau, Daniel ^a   Pessayre, Dominique ^a  

^a BEAUJON HOSPITAL   (France)

^b INSERM   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ALANINE AMINOTRANSFERASE; CASPASE 3; CYCLOSPORIN A; CYTOCHROME C; DNA FRAGMENT; FAS ANTIBODY; FAS LIGAND; GLUTATHIONE; PHORONE; PROTEIN BAX; PROTEIN BCL X; PROTEIN P53; RECEPTOR; SULFUR AMINO ACID; THIOL;

ALANINE AMINOTRANSFERASE BLOOD LEVEL; AMINO ACID DEFICIENCY; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CHRONICITY; CONTROLLED STUDY; DIET RESTRICTION; ELECTRON MICROSCOPY; ENZYME ACTIVATION; LIVER MITOCHONDRION; LIVER TOXICITY; MALE; MEMBRANE DEPOLARIZATION; MEMBRANE PERMEABILITY; MEMBRANE RUPTURE; MORTALITY; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN LOCALIZATION;

EID: 0035029170     PISSN: 02709139     EISSN: None     Source Type: Journal    
DOI: 10.1053/jhep.2001.24235     Document Type: Article

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