Pharmacological levels of copper exert toxic effects in Caco-2 cells.

Copper might be toxic to human intestinal cells because of its ability to catalyze the formation of free radicals. The aim of the present study was to quantify toxicological effects of increasing copper concentrations in preconfluent, colonic cancerous cells as well as in postconfluent, differentiating Caco-2 cells. Our results indicate that postconfluent cells might be more sensitive to copper toxicity. A significant rise of lactate dehydrogenase (LDH) release (150 microM or above) and decrease of cell proliferation (100 microM or above) with increasing copper levels was found, as compared to the control. To the contrary, preconfluent cells were not significantly affected by copper (LDH release) or, if so, only at a concentration of 250 microM (proliferation). Loss of viability and morphological changes, including loss of adherence and cell rounding, were visible after incubation with 250 microM copper in both groups. Superoxide dismutase (SOD) activities were not affected by copper. Glutathione peroxidase (GSH-Px) and catalase activities were higher in copper-treated cells, especially in the postconfluent ones (nevertheless, the results were not significant because of high standard deviations). In conclusion, we demonstrated that copper exerts intracellular, toxicological effects on both groups of Caco-2 cells, although the effects seem to be more evident in the postconfluent (enterocytelike) group. Risk assessment, especially for high concentrations, might be of special interest.