Abstract:
:The administration of 3'-hydroxyacetanilide, a regioisomer of acetaminophen, to mice failed to produce hepatotoxicity even after the administration of diethyl maleate. In contrast, hepatotoxicity did occur when 3'-hydroxyacetanilide was administered to buthionine sulfoximine pretreated mice. Although the administration of 3'-hydroxyacetanilide in conjunction with either diethyl maleate or buthionine sulfoximine depleted total hepatic glutathione, only the combined buthionine sulfoximine-3'-hydroxyacetanilide treatment decreased hepatic mitochondrial glutathione concentrations to below 20% of control values. In addition, pretreatment with buthionine sulfoximine increased the amount of 3'-hydroxyacetanilide bound to mitochondrial proteins. These results, in conjunction without previous results on the involvement of mitochondrial damage in the pathogenesis of hepatotoxicity caused by acetaminophen, suggest a probable relationship between mitochondrial damage caused by the buthionine sulfoximine-3'-hydroxyacetanilide treatment and hepatotoxicity caused by this treatment.
journal_name
Chem Res Toxicoljournal_title
Chemical research in toxicologyauthors
Tirmenstein MA,Nelson SDdoi
10.1021/tx00020a014subject
Has Abstractpub_date
1991-03-01 00:00:00pages
214-7issue
2eissn
0893-228Xissn
1520-5010journal_volume
4pub_type
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