The effects of astaxanthin on liver histopathology and expression of superoxide dismutase in rat aflatoxicosis.

The metabolism of aflatoxin B (AFB) 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-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 groups were gavaged by water for 7 days followed by a single DMSO and 1 mg/kg AFB, respectively. The AXL+ AFB and AXH+ AFB groups were given of 5 mg/kg and 100 mg/kg AX for 7 days before 1 mg/kg AFB administration. The result showed significantly elevated liver weight per 100 g body weight in AFB group. The histopathological finding revealed vacuolar degeneration, necrosis, megalocytosis and binucleation of hepatocytes with bile duct hyperplasia in AFB group. The severities of pathological changes were sequentially reduced in AXL+AFB and AXH+AFB groups. Most rats in AXH+AFB 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 group than solely treated AFB and AXL+AFB groups. In conclusion, AX alleviated AFB-induced liver damage in rat by stimulating SOD1 expression and transdifferentiation of cholangiocytes in dose dependent manner.