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Beneficial effect of nitric oxide synthase inhibitor on hepatotoxicity induced by allyl alcohol
Author(s) -
Alam Khurshid,
Nagi Mahmoud N.,
AlShabanah Othman A.,
AlBekairi Abdullah M.
Publication year - 2001
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.10008
Subject(s) - allyl alcohol , chemistry , glutathione , alcohol , nitric oxide synthase , toxicity , alcohol dehydrogenase , liver injury , nitric oxide , pharmacology , ethanol , metabolism , biochemistry , in vivo , enzyme , medicine , biology , organic chemistry , catalysis , microbiology and biotechnology
The effect of aminoguanidine (a selective inhibitor of inducible nitric oxide synthase) on allyl alcohol‐induced liver injury was assessed by the measurement of serum ALT and AST activities and histo‐ pathological examination. When aminoguanidine (50–300 mg/kg, i.p.) was administered to mice 30 min before a toxic dose of allyl alcohol (75 μL/kg, i.p.), significant changes related to liver injury were observed. In the presence of aminoguanidine the level of ALT and AST enzymes were significantly decreased. All symptoms of liver necrosis produced by allyl alcohol toxicity almost completely disappeared when animals were pretreated with aminoguanidine at 300 mg/kg. Depletion of hepatic glutathione as a consequence of allyl alcohol metabolism was minimal in mice pretreated with aminoguanidine at 300 mg/kg. It was found that the inhibition of toxicity was not due to alteration in allyl alcohol metabolism since aminoguanidine did not effect alcohol dehydrogenase activity both in vivo and in vitro. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:317–321, 2001