Lead-induced cell proliferation and organ-specific tumorigenicity

Abstract

While lead acetate is a renal carcinogen in rodent studies, the mechanism by which it induces cancer has not been established. This report proposes that the enhanced susceptibility of renal tubular epithelial cells to lead-induced mitogenicity at the levels comparable to those administered in the cancer bioassay may contribute to the carcinogenic response seen in this target organ. Of relevance is that the nonresponsiveness of the liver to lead-induced carcinogenicity was associated with significantly less capacity (i.e., 675-fold) of lead to induce the mitogenic response in the rodent liver.