Eriodictyol attenuates arsenic trioxide-induced liver injury by activation of Nrf2

Arsenic, a well-known human carcinogen, has been reported to induce hepatic oxidative stress and hepatic injury. Eriodictyol, a flavonoid found in citrus fruits, has been reported to have antioxidant effects. In this study, we aimed to investigate the protective effects of eriodictyol on arsenic trioxide (As(2)O(3))-induced liver injury and to clarify the molecular mechanism. Male Wistar rats were administrated 3mg/kg As(2)O(3) intravenous injection at days 1, 4, 5, and 7. Eriodictyol was given 1 h before or after As(2)O(3) treatment. The results showed that eriodictyol prevented As(2)O(3)-induced liver reactive oxygen species (ROS) and malonaldehyde (MDA) levels. Eriodictyol abrogated As(2)O(3)-induced decrease of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activity. Eriodictyol also attenuated As(2)O(3)-induced hepatic pathological damage. In addition, eriodictyol promoted the expression of nuclear factor erythroid 2 p45 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) up-regulated by As(2)O(3). In conclusion, our results demonstrated that eriodictyol exhibited a protective effect on As(2)O(3)-induced liver injury and the possible mechanism is involved in activating Nrf2 signaling pathway.