An imbalance in the supply of Cu relates to pathogenesis of multiple severe diseases including inflammation-related disorders (1, 3, 5, 6) and cell death via oxidative stress-dependent signalling cascades (28). In this study, we indicated further systemic pro-inflammatory and toxicological effects of nCu on kidney, liver and spleen of experimental mice. The inflammatory response related to Cu over-accumulation in systemic organs is characterized by local recruitment and activation of inflammatory leukocytes and intrinsic cell apoptosis (2, 10, 11, 17, 18). It is again consistent with our finding that pro-inflammatory and pro-apoptotic effects induced by excessive Cu storage in mice dosed with 1000 mg nCu /l were detected in splenic tissue as evidenced by infiltrations of macrophages and dendritic cells and increased activation of T lymphocytes. In addition, the serum levels of biochemical markers including ALT, AST and creatinine in 1000 mg nCu/l-treated mice were restored more than those in the control mice that reflected hepatic and renal defects in the 1000 mg nCu/l-treated mice. Moreover, we observed the increased PS exposure on splenic leukocyte surface in mice supplemented with drinking water containing 1000 mg nCu/l. The evidences indicated that nCu deposition caused hepatic and renal failures and induced inflammatory response in mice.