Abstract: Iron is an essential trace element in vertebrates, involved in critical biological processes like oxygen transport and energy metabolism. This study focused on Ctenopharyngodon idella, investigating the damaging effects of dietary iron overload. Healthy C. idella weighing 50-80 g were fed a diet supplemented with 0, 400, and 800 mg/kg of ferrous fumarate for 60 days. Growth performance results indicated that excessive iron intake significantly reduced the fish's length growth rate. Iron ion content analysis showed that ferrous fumarate supplementation significantly increased iron levels in serum and liver. ELISA results indicated that dietary iron overload led to an increase in hematocrit, along with significantly elevated activities of ALT, AST, and GPX4 in serum and liver. qRT-PCR results revealed that iron metabolism-related genes Tf, DMT1, Hepcidin, FPN, and NOCA4 were significantly upregulated in the ferrous fumarate group, while TfR1 and Ferritin were significantly downregulated. Furthermore, antioxidant-related genes HO-1, GPX4, and Nrf2 were significantly upregulated in the ferrous fumarate group. In vitro experiments showed that FAC incubation of L8824 cells resulted in a significant increase in intracellular iron and ROS; qRT-PCR analysis revealed significant increases in inflammatory genes P65, TNF-α, NF-κB, TLR4, and P38-MAPK, along with significant rises in oxidative stress-related genes Keap1a, Nrf2, and HO-1. In conclusion, this study suggests that dietary iron overload leads to an imbalance in iron metabolism and oxidative stress in C. idella, accompanied by inflammatory responses, providing a theoretical basis for understanding iron metabolism-related diseases and their prevention in C. idella.