Key result
Copper induced a concentration-dependent decrease in viability, growth, and DNA synthesis in cultured human vascular endothelial cells, which were more susceptible to copper cytotoxicity than human fibroblasts.
Copper induces concentration-dependent cytotoxicity that is more pronounced in human vascular endothelial cells than in fibroblasts, suggesting a potential mechanism for copper-related vascular injury.
In vitro copper cytotoxicity on endothelial cells warrants caution in exposure contexts; leaves open in vivo vascular relevance.
The effect of copper sulfate (CuSO4) on cultured human vascular endothelial (HVE) cells and cultured human fibroblasts (HAIN-55) was investigated. HVE cells were collected from umbilical veins by enzymatic digestion with collagenase. The viability, subsequent growth and DNA synthesis of both cell types were inhibited concentration-dependently by the addition of copper. The cytotoxic effect of copper on the morphology of these cells was also concentration-dependent. However, the cytotoxic effect of copper on the viability, subsequent growth and DNA synthesis was greater in HVE cells than in HAIN-55 cells. These results suggest that HVE cells are more susceptible to concentration-dependent copper cytotoxicity than HAIN-55 cells are, and that copper could induce vascular endothelial injury, which may be involved in the pathogenesis of cardiovascular disease.
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Kishimoto et al. (1992) studied Endothelial injury. Copper (CuSO4) vs. Control (medium without added copper) was evaluated on Cell viability, subsequent growth, and DNA synthesis. Copper induced a concentration-dependent decrease in viability, growth, and DNA synthesis in cultured human vascular endothelial cells, which were more susceptible to copper cytotoxicity than human fibroblasts.
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