Cadmium (Cd), a potent toxic heavy metal, is a widespread environmental contaminant. Its cellular traffic via pathways dedicated to transition metals contributes to the toxicity mechanisms. Zinc (Zn) homeostasis is complex , involving both zinc importers (Zip) and zinc exporters (ZnT). Cellular signal transduction pathways are influenced by Zn and redox status of the cell. The aim of the present study is to examine if the accumulation of Cd in the human lymphocyte B cell line BJAB and its capacity to promote oxidative stress and adverse effects could result from changes in the mRNA expression pattern of Zn transporters and metallothioneins. Cells were exposed to 5, 10, 20 and 40 μMofCdCl 2 equivalent to 0.91, 1.83, 3.66 and 7.33 μg/ml respectively, for 24 h. Cd significantly reduced the viability of BJAB cells and induced a dose-dependent increase in DNA damage. Cd also induced the formation of 8-hydroxy-2′-deoxyguanosine adducts and augmented MTF1 expression in BJAB cells. We observed interesting responses in relative gene expression to Cd exposure among the seven transporters we analyzed. Cd exposure increased the expression of DMT1 and caused an up-regulation of ZnT1. However, the T calcium channel alpha1G subunit could not be detected. A change in expression of ZnTs and Zips in response to Cd exposure emphasizes the involvement of Zn transporters in Cd cellular metabolism and induced oxidative stress.