Gold-induced reactive oxygen species (ROS) do not mediate suppression of monocytic mitochondrial or secretory function

Toxicology in Vitro

Volumn 20, Issue 5, 2006, Pages 625-633

  Omata, Yo ^a   Lewis, Jill B ^b   Lockwood, Petra E ^b   Tseng, Wan Y ^c   Messer, Regina L ^b   Bouillaguet, Serge ^d   Wataha, John C ^b  

^a HOKKAIDO UNIVERSITY   (Japan)

^b MEDICAL COLLEGE OF GEORGIA   (United States)

^c NATIONAL TAIWAN UNIVERSITY   (Taiwan)

^d UNIVERSITY OF GENEVA   (Switzerland)

Author keywords

Metals; Mitochondrial activity; Redox; Rheumatoid arthritis

Indexed keywords

ACETYLCYSTEINE; ANTIOXIDANT; ANTIRHEUMATIC AGENT; AURANOFIN; AUROTHIOMALATE; GOLD; HYDROQUINONE DERIVATIVE; OXIDIZING AGENT; REACTIVE OXYGEN METABOLITE; SUCCINATE DEHYDROGENASE;

ARTICLE; CELL ACTIVITY; CELL LEVEL; CONCENTRATION RESPONSE; CONTROLLED STUDY; DRUG EXPOSURE; ENZYME ACTIVITY; ENZYME INHIBITION; HUMAN; HUMAN CELL; IMMUNOTOXICITY; MITOCHONDRIAL TOXICITY; MONOCYTE; OXIDATION REDUCTION REACTION; OXIDATIVE STRESS; SECRETORY CELL; TOXICITY TESTING;

AURANOFIN; CELLS, CULTURED; GOLD COMPOUNDS; GOLD SODIUM THIOMALATE; HUMANS; MITOCHONDRIA; MONOCYTES; REACTIVE OXYGEN SPECIES;

EID: 33744525323     PISSN: 08872333     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.tiv.2005.11.001     Document Type: Article

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