Aminoguanidine, an inducible nitric oxide synthase inhibitor, plus N-acetylcysteine treatment reduce the lipopolysaccharide-augmented hepatotoxicity in rats with cirrhosis


Dogru-Abbasoglu S. , BALKAN J., KANBAGH O., CEVIKBAS U. , AYKAC-TOKER G., Uysal M. M.

HUMAN & EXPERIMENTAL TOXICOLOGY, cilt.21, ss.359-364, 2002 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 21 Konu: 7
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1191/0960327102ht256oa
  • Dergi Adı: HUMAN & EXPERIMENTAL TOXICOLOGY
  • Sayfa Sayıları: ss.359-364

Özet

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.