Aminoguanidine, an inducible nitric oxide synthase inhibitor, plus N-acetylcysteine treatment reduce the lipopolysaccharide-augmented hepatotoxicity in rats with cirrhosis.
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.
Doğru-Abbasoğlu
S
S
Department of Biochemistry, Istanbul Faculty of Medicine, University of Istanbul, Turkey.
Balkan
J
J
Kanbağli
O
O
Cevikbaş
U
U
Aykaç-Toker
G
G
Uysal
M
M
D000111:Acetylcysteine / Q000627:therapeutic use*; D000704:Analysis of Variance; D000818:Animals; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006146:Guanidines / Q000627:therapeutic use*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000633:toxicity*; D008106:Liver Cirrhosis, Experimental / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D016166:Free Radical Scavengers; D006146:Guanidines; D008070:Lipopolysaccharides; D019001:Nitric Oxide Synthase; C004479:pimagedine; D000111:Acetylcysteine