Abstract

Yusuf Savran*, Turker Cavusoglu, Mehmet Kemal Tumer, Gurkan Yigitturk, Oznur Dilek Ciftci, Ahmet Cagdas Acara, Yigit Uyanıkgil and Oytun Erbas

ABSTRACT

Acetaminophen is a commonly used antipyretic and analgesic agent which may cause severe hepatic failure in overdoses. The only approved agent used in the treatment of overdoses is still N-acetylcystein. Ursodeoxycholic acid, is a well known chemical approved in the treatment of especially cholestatic liver diseases but may it also have an affect in acetaminophen intoxication? Our aim was to study the effect of ursodeoxycholic acid on outcome of acetaminophen overdose on a rat model. 32 male Sprague Dawley albino mature rats were randomly assigned into 4 groups. Group 1 (n=8) was control group and was administrated no drug. Remaining 24 rats were applied single dose 300 mg/kg paracetamol intraperitoneally and divided randomly into 3 groups (n=8). Group 2, 3 and 4 rats were applied 1 ml/kg/day of %0,9 NaCl saline, 300 mg/kg/day of N-acetylcystein and 100 mg/kg/day of ursodeoxycholic acid respectively intraperitoneally for three days. Then, the animals were decapitated and blood samples were collected by cardiac puncture for biochemical analysis and hepatectomy was performed for histopathological and biochemical examinations. Alanine aminotransferase, aspartate aminotransferase and malondialdehyde levels in group 2 were extremely increased and tissue glutathione levels depleted when compared to group 1 as expected. The alanine aminotransferase, aspartate aminotransferase and malondialdehyde levels in group 4 were decreased and tissue glutathione levels were increased significantly in a similar pattern with the group 3 when compared to group 2. According to these results we can conclude that ursodeoxycholic acid ameliorates liver function and tissue destruction in acute acetaminophen intoxication.