sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_5 ;
    pav:version "1.4" .
  sub:_4 prov:value "To determine the in vivo role of cellular glutathione peroxidase (E.C.1.11.1.9, GPX1), we challenged the GPX1 knockout [GPX1(-/-)], the GPX1 overexpressing [GPX1(+)], and their respective wild-type (WT) mice of different Se and vitamin E status with acute oxidative stress. After these mice were injected with pro-oxidants paraquat or diquat at 12 to 125 mg/kg of body weight, their survival rate and time were a function of their GPX1 activity levels. The GPX1 protection was associated with attenuation of NADPH and NADH oxidation, protein carbonyl and F(2)-isoprostanes formation, and alanine transaminase release in various tissues, and was irreplaceable by high levels of dietary vitamin E or other selenoproteins. The GPX1 expression was also protective against moderate oxidative stress induced by low levels of paraquat or diquat, particularly in the Se-deficient mice. Alteration of GPX1 expression showed no impact on the expression of other selenoproteins and antioxidant enzymes in unstressed mice. Total Se content in liver of the Se-adequate GPX1(-/-) mice was reduced by 60% the WT controls. In conclusion, normal expression of GPX1 is essential and overexpression of GPX1 is beneficial to protect mice against acute oxidative stress." ;
    prov:wasQuotedFrom pubmed:11568445 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:11568445 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}