We aimed to determine whether increased levels of asymmetric dimethylarginine (ADMA) directly cause hepatic deterioration and whether it is decreased by ascorbic acid (AA) as an antioxidant. The study included three groups: Control (n = 10), ADMA (n = 10), and ADMA + AA (n = 10). ADMA was administered at 2 mg kg-1 day-1 and AA was given at 50 mg kg-1 day-1 for 10 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase, and alkaline phosphatase activities were analyzed. Histomorphological evaluation of the liver was performed based on the Ishak scoring system. When compared with the control, ALT and ALP levels of the ADMA group were significantly higher (P = 0.006 and P = 0.041, respectively). When compared with the control, interface hepatitis, confluent necrosis, focal necrosis, histological activity index, severity of hepatitis, and portal inflammation were significantly higher in the group administered ADMA. The mentioned biochemical/histopathological parameters were lower in the ADMA + AA group when compared with the ADMA group even if no significant difference was encountered (P > 0.05). The results indicate that ADMA is a factor in the formation of liver injury. Insufficient recovery in biochemical/histopathological parameters when AA was given make us consider that different factors other than prooxidant factors are effective in the formation of liver injury.