The shark bile salt 5 beta-scymnol abates acetaminophen toxicity, but not covalent binding
In: Toxicology, Jg. 203 (2004-10-01), S. 109-121
Online
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Zugriff:
Acetaminophen (APAP) toxicity involves both arylative and oxidative mechanisms. The shark bile salt, 5 beta-scymnol (5beta-S), has been demonstrated to act as an antioxidant and free radical scavenger in vitro. To determine if 5beta-S protects against either APAP-induced hepatic or renal toxicity, 3-4-month-old male Swiss Laca mice were given APAP (500 mg/kg), and 5beta-S (100 mg/kg) was given at 0 and 2 h after APAP. Plasma SDH at 12 h after APAP alone was 1630 U/l and BUN was 19 mg/dl versus 20 U/l and 10 mg/dl, respectively, in controls. Either simultaneous or 2 h delayed treatment with 5beta-S significantly decreased the APAP-induced SDH increase while only the simultaneous pretreatment prevented the BUN elevation. 5beta-S alone did not increase liver glutathione content. Western analysis of APAP covalent binding using anti-APAP antibodies indicated the 5beta-S did not alter protein arylation either qualitatively or quantitatively. These results suggest that 5beta-S treatment did not impair APAP activation and are consistent with 5beta-S protection that likely results from its antioxidant activity.
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The shark bile salt 5 beta-scymnol abates acetaminophen toxicity, but not covalent binding
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Autor/in / Beteiligte Person: | Hoivik, J. ; Angela Lucas Slitt ; Naylor, Lee M. ; Macrides, Theo ; Manautou, José E. ; Cohen, Steven D. |
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Zeitschrift: | Toxicology, Jg. 203 (2004-10-01), S. 109-121 |
Veröffentlichung: | Elsevier BV, 2004 |
Medientyp: | unknown |
ISSN: | 0300-483X (print) |
DOI: | 10.1016/j.tox.2004.06.002 |
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