Oltipraz-induced amelioration of acetaminophen hepatotoxicity in hamsters: II. Competitive shunt in metabolism via glucuronidation
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2003, Journal of Biological ChemistryCitation Excerpt :It is clear from these studies of JNK activity that deletion of GSTP does not affect how the cell responds to the chemical stress induced by APAP; rather it primes the cell, through increased JNK signaling, to be better equipped to deal with such a chemical insult. Consequently the small changes in the constitutive expression of both hepatic HO-1 and UGT1A6 (genes that are known to protect against APAP hepatotoxicity (17, 24, 48–52)) will contribute to the protection observed in GstP1/P2(–/–) mice against acetaminophen hepatotoxicity. However, these changes cannot fully explain the phenotypic differences in hepatic GSH levels seen previously (27).
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1996, Fundamental and Applied Toxicology
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Current address: Bristol-Myers Squibb Co., Department of Pathology/Toxicology, Syracuse, NY 13221.