The shark bile salt 5 beta-scymnol abates acetaminophen toxicity, but not covalent binding.
作者： Angela Lucas Slitt , Lee Naylor , J. Hoivik , Jose E. Manautou , Theo Macrides
DOI: 10.1016/J.TOX.2004.06.002
关键词: Antioxidant 、 Biochemistry 、 Analgesic 、 Free radical scavenger 、 Antipyretic 、 Pharmacology 、 Chemistry 、 Acetaminophen 、 Toxicity 、 Oxidative phosphorylation 、 In vitro
摘要: 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 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), (100 mg/kg) was at 0 2 h after APAP. Plasma SDH 12 alone 1630 U/l BUN 19 mg/dl versus 20 10 mg/dl, respectively, controls. Either simultaneous delayed treatment with significantly decreased the increase while only pretreatment prevented elevation. did not liver glutathione content. Western analysis of covalent binding using anti-APAP antibodies indicated alter protein arylation qualitatively quantitatively. These results suggest that impair activation are consistent protection likely from its activity.
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