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Title:

Protection against acetaminophen toxicity in CYP1A2 and CYP2E1 double-null mice.

Document type:
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Article
Author(s):
Zaher, H; Buters, JT; Ward, JM; Bruno, MK; Lucas, AM; Stern, ST; Cohen, SD; Gonzalez, FJ
Abstract:
Acetaminophen (APAP) hepatotoxicity is due to its biotransformation to a reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI), that is capable of binding to cellular macromolecules. At least two forms of cytochrome P450, CYP2E1 and CYP1A2, have been implicated in this reaction in mice. To test the combined roles of CYP1A2 and CYP2E1 in an intact animal model, a double-null mouse line lacking functional expression of CYP1A2 and CYP2E1 was produced by cross-breeding Cyp1a2-/- mice with Cyp2e...     »
Journal title abbreviation:
Toxicol Appl Pharmacol
Year:
1998
Journal volume:
152
Journal issue:
1
Pages contribution:
193-9
Language:
eng
Fulltext / DOI:
doi:10.1006/taap.1998.8501
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/9772215
Print-ISSN:
0041-008X
TUM Institution:
Molekulare Allergologie (Prof. Schmidt-Weber)
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