The subject of acute injury, apoptosis and canceration of animals induced by heavy metal ions has been one of the hotspots studied worldwide. However, the exact molecular mechanism of Cd-induced carcinogenicity remains largely unclear, and how to relieve the toxicity in vivo has rarely been reported. For this paper, we have investigated the mechanism of Cd2+ on DNA cleavage and Ca2+ on DNA repair in the liver of silver crucian carp (Carassius auratus gibelio) by agarose gel electrophoresis methods and by estimating biochemical indexes. Our results show that Cd2+ induces the classical laddering degradation of DNA in vivo and that DNA cleavage is repaired after injection with Ca2+ under various Cd2+ concentrations. DNA cleavage caused by Cd2+ is due to the activation of deoxyribonuclease (DNase) and the accumulation of reactive oxygen species (ROS). Furthermore, Cd2+ destroys the antioxidant system, which diminishes the activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD), causing an increase of the lipid peroxidation (LPO) level, respectively. However, after the liver is injected with Ca2+ under various Cd2+ concentrations, the DNase activity, the ROS generating rate and the LPO level are obviously reduced, the activities of SOD, CAT, and POD are greatly increased. At the same time, ROS production and removal recoves its balance. The results show that Ca2+ can relieve the toxicity of Cd2+ in silver crucian carp.