Lipopolysaccharide-induced hepatic oxidative injury is not potentiated by knockout of GPX1 and SOD1 in mice

Biochemical and Biophysical Research Communications

Volumn 404, Issue 1, 2011, Pages 559-563

  Zhu, Jian Hong ^a,b   Lei, Xin Gen ^b  

^a WENZHOU MEDICAL UNIVERSITY   (China)

^b Cornell University ^*  (United States)

Author keywords

Glutathione peroxidase; Lipopolysaccharide; Oxidative injury; Superoxide dismutase

Indexed keywords

ALANINE AMINOTRANSFERASE; BACTERIUM LIPOPOLYSACCHARIDE; COPPER ZINC SUPEROXIDE DISMUTASE; GLUTATHIONE; GLUTATHIONE PEROXIDASE 1; NITRIC OXIDE; SODIUM CHLORIDE;

ALANINE AMINOTRANSFERASE BLOOD LEVEL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; GENOTYPE; GLUTATHIONE METABOLISM; KNOCKOUT MOUSE; LIVER INJURY; LIVER METABOLISM; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; PROTEIN DEPLETION; PROTEIN METABOLISM; PROTEIN NITRATION; STRAIN DIFFERENCE; WILD TYPE;

ANIMALS; ENDOTOXEMIA; GENE KNOCKOUT TECHNIQUES; GLUTATHIONE; GLUTATHIONE PEROXIDASE; LIPOPOLYSACCHARIDES; LIVER; MICE; OXIDATIVE STRESS; SUPEROXIDE DISMUTASE;

BACTERIA (MICROORGANISMS); MUS;

EID: 78650911980     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2010.12.025     Document Type: Article

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