The metabolism of aflatoxin B 1 (AFB 1 ) generates reactive oxygen species (ROS) that destroys hepatocytes. Meanwhile, astaxanthin (AX) is known to have stronger antioxidative activity than other carotenoids. This study aimed to investigate hepatoprotective role of AX from AFB 1 -induced toxicity in rat by histopathological study and immunohistochemistry of Cu/Zn-SOD (SOD1) which acts as the first enzyme in antioxidative reaction against cell injury from ROS. Twenty Wistar rats were randomly divided into 4 groups. The control and AFB 1 groups were gavaged by water for 7 days followed by a single DMSO and 1 mg/kg AFB 1 , respectively. The AXL+ AFB 1 and AXH+ AFB 1 groups were given of 5 mg/kg and 100 mg/kg AX for 7 days before 1 mg/kg AFB 1 administration. The result showed significantly elevated liver weight per 100 g body weight in AFB 1 group. The histopathological finding revealed vacuolar degeneration, necrosis, megalocytosis and binucleation of hepatocytes with bile duct hyperplasia in AFB 1 group. The severities of pathological changes were sequentially reduced in AXL+AFB 1 and AXH+AFB 1 groups. Most rats in AXH+AFB 1 group owned hypertrophic hepatocytes and atypical proliferation of cholangiocytes which are adaptive responses to severe hepatocyte damage. The SOD1 expression was also significantly higher in AXH+AFB 1 group than solely treated AFB 1 and AXL+AFB 1 groups. In conclusion, AX alleviated AFB 1 -induced liver damage in rat by stimulating SOD1 expression and transdifferentiation of cholangiocytes in dose dependent manner.