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Human & Experimental Toxicology
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Aminoguanidine, an inducible nitric oxide synthase inhibitor, plus N-acetylcysteine treatment reduce the lipopolysaccharideaugmented hepatotoxicity in rats with cirrhosis

S DogÏru-AbbasogÏlu

J Balkan

Ö KanbagÏlõ

Department of Biochemistry, Istanbul Faculty of Medicine, University of Istanbul, Capa 34390, Istanbul, Turkey

U Cevikbas

Department of Pathology, Istanbul Faculty of Medicine, University of Istanbul, Capa 34390, Istanbul, Turkey

G Aykac-Toker

Department of Biochemistry, Istanbul Faculty of Medicine, University of Istanbul, Capa 34390, Istanbul, Turkey

M Uysal

Department of Biochemistry, Istanbul Faculty of Medicine, University of Istanbul, Capa 34390, Istanbul, Turkey; mujdatuysal{at}hotmail.com

Hepatic cirrhosis is produced in rats by administration of thioacetamide (TAA) (0.3 g/L tap water for a period of three months). This treatment caused an increase in oxidative stress in the liver. Lipopolysaccharide (LPS) administration (5 mg/kg) to rats with cirrhosis was observed to increase hepatotoxicity as well as oxidative stress according to biochemical and histopathological findings. However, aminoguanidine (AG), an inducible nitric oxide synthase (iNOS) inhibitor, plus N-acetylcysteine (NAC) treatment reduced the LPS-augmented hepatotoxicity in rats with cirrhosis without making any changes in oxidative stress in the liver.

Key Words: inducible nitric oxide synthase inhibitor • lipopolysaccharide • liver cirrhosis • N-acetylcysteine • oxidative stress • thioacetamide

Human & Experimental Toxicology, Vol. 21, No. 7, 359-364 (2002)
DOI: 10.1191/0960327102ht256oa
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