Mice with a homozygous null mutation for the most abundant glutathione peroxidase, Gpx1, show increased susceptibility to the oxidative stress- inducing agents paraquat and hydrogen peroxide

Journal of Biological Chemistry

Volumn 273, Issue 35, 1998, Pages 22528-22536

  De Haan, Judy B ^a   Bladier, Cécile ^a   Griffiths, Peter ^a   Kelner, Michael ^a,b   O'Shea, Ross D ^c   Cheung, Nam Sang ^c   Bronson, R T ^d   Silvestro, Mary J ^a   Wild, Steven ^a   Zheng, Shao Shan ^a   Beart, Philip M ^c   Hertzog, Paul J ^a   Kola, Ismail ^a  

^a MONASH MEDICAL CENTRE   (Australia)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c MONASH UNIVERSITY   (Australia)

^d TUFTS UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GLUTATHIONE PEROXIDASE; HYDROGEN PEROXIDE; PARAQUAT; REACTIVE OXYGEN METABOLITE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANTIOXIDANT ACTIVITY; ARTICLE; CELL VIABILITY; CONTROLLED STUDY; DOSE RESPONSE; ENZYME ACTIVITY; GENE MUTATION; KNOCKOUT MOUSE; LETHALITY; MOUSE; NERVE CELL DEGENERATION; NEUROPROTECTION; NONHUMAN; OXIDATIVE STRESS; PARAQUAT POISONING; PRIORITY JOURNAL; TRANSCRIPTION REGULATION;

ANIMALS; CELLS, CULTURED; GLUTATHIONE PEROXIDASE; HOMOZYGOTE; HYDROGEN PEROXIDE; MICE; MICE, KNOCKOUT; OXIDATIVE STRESS; PARAQUAT; PROMOTER REGIONS (GENETICS); TRANSCRIPTION, GENETIC;

ANIMALIA;

EID: 14444271790     PISSN: 00219258     EISSN: None     Source Type: Journal    
DOI: 10.1074/jbc.273.35.22528     Document Type: Article

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