Abstract
Abstract Cadmium（Cd） is a common environmental contaminant. It has been reported that the Cd causes cell growth arrest and apoptosis. In this study we investigated the roles of p53 in cadmium-induced cell damage. When human fibroblast（HF） cells were treated with 30μM Cd, p53 increased in cells. However the increased p53 protein did not enhance apoptosis or the level of proapoptotic proteins such as Bax and PIG3. Comparing to the p53 deficient HF cells（HFE6）, the HF cells showed a less degree of cell death after Cd treatment. After induction by Cd, p53 specifically stimulated its downstream targets, p21 and MDM2.The expression of p21 was related to G2/M arrest of HF cells. We further investigated whether the p53 accumulation is correlated with MAPKs activation in cadmium- treated cells. We found that JNK and p38 activation had no direct relationship with p53 protein. However, when the pathway to activate either ERK or p53 was blocked, the other one would be activated. This result indicated a compensation of two pathways during Cd treatment. In our study, we concluded that the Cd induce p53 accumulation in early phase, and the expression of p53 is closely related to cell cycle arrest, and cell death for the Cd treatment.