Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death

Free Radical Biology and Medicine

Volumn 31, Issue 2, 2001, Pages 139-152

  Hickey, E J ^a   Raje, R R ^a   Reid, V E ^a   Gross, S M ^a   Ray, S D ^a  

^a LONG ISLAND UNIVERSITY   (United States)

Author keywords

Apoptosis; Diclofenac; DNA fragmentation; Free radicals; In vivo; Nephrotoxicity; Oxidative stress

Indexed keywords

BIOLOGICAL MARKER; CALCIUM ION; CELL DNA; DICLOFENAC; DNA FRAGMENT; ENDONUCLEASE; ETODOLAC; FENOPROFEN; FREE RADICAL; IBUPROFEN; INDOMETACIN; KETOROLAC; LIPID; MAGNESIUM ION; MALONALDEHYDE; NABUMETONE; NAPROXEN; NITROGEN; NONSTEROID ANTIINFLAMMATORY AGENT; REACTIVE OXYGEN METABOLITE; SULINDAC; SUPEROXIDE DISMUTASE; TOLMETIN; UREA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BLOOD SAMPLING; CELL NUCLEUS; CELLULAR DISTRIBUTION; CONTROLLED STUDY; DNA DAMAGE; DOSE RESPONSE; DRUG ACTIVITY; DRUG EFFECT; DRUG INDUCED DISEASE; ENZYME ACTIVATION; ENZYME ACTIVITY; GEL ELECTROPHORESIS; GENOME; HISTOPATHOLOGY; IN VIVO STUDY; KIDNEY; KIDNEY INJURY; LIPID PEROXIDATION; MALE; MOUSE; NEPHROTOXICITY; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; UREA NITROGEN BLOOD LEVEL;

ANIMALS; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; APOPTOSIS; DICLOFENAC; DNA FRAGMENTATION; ENDODEOXYRIBONUCLEASES; ENZYME ACTIVATION; HUMANS; KIDNEY; LIPID PEROXIDATION; MALE; MALONDIALDEHYDE; MICE; MICE, INBRED ICR; NECROSIS; OXIDATIVE STRESS; SUPEROXIDE DISMUTASE;

ANIMALIA;

EID: 0035879827     PISSN: 08915849     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0891-5849(01)00560-3     Document Type: Article

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