Fas receptor-deficient lpr mice are protected against acetaminophen hepatotoxicity due to higher glutathione synthesis and enhanced detoxification of oxidant stress-Reference-Cited by-同舟云学术

Fas receptor-deficient lpr mice are protected against acetaminophen hepatotoxicity due to higher glutathione synthesis and enhanced detoxification of oxidant stress

Published:2013-08 Issue: Volume:58 Page:228-235
ISSN:0278-6915
Container-title:Food and Chemical Toxicology
language:en
Short-container-title:Food and Chemical Toxicology

Author:

Williams C. David,McGill Mitchell R.,Farhood Anwar,Jaeschke Hartmut

Funder

the National Institutes of Health

the National Center for Research Resources

the National Institute of General Medical Sciences

the National Institute of General Medical Sciences of the National Institutes of Health

Publisher

Elsevier BV

Subject

Toxicology,General Medicine,Food Science

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3. High-mobility group box-1 protein and keratin-18, circulating serum proteins informative of acetaminophen-induced necrosis and apoptosis in vivo;Antoine;Toxicol. Sci.,2009

4. Diet restriction inhibits apoptosis and HMGB1 oxidation and promotes inflammatory cell recruitment during acetaminophen hepatotoxicity;Antoine;Mol. Med.,2010

5. Nuclear translocation of endonuclease G and apoptosis-inducing factor during acetaminophen-induced liver cell injury;Bajt;Toxicol. Sci.,2006

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