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

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