ALUMINUM SILICATE TOXICITY IN CELL-CULTURES

To assess the cytotoxicity of four clays containing an aluminum silicate-montmorillonite, bentonite, kaolinite and erionite-we used human umbilical vein endothelial, N1E-115 neuroblastoma, and ROC-1 oligodendroglial cells. Morphological examination, lactate dehydrogenase release and fatty acid release were used as indices of trauma. The clays were added in suspension to the cell cultures at concentrations of 0.1, 0.03 and 0.01 mg/ml of medium and the cells were incubated for 1, 6 and 24h. The clays did not lyse ROC-1 and N1E-115 cells and did not cause a dose-dependent increase in fatty acid levels at 24h. There were no significant increases in lactate dehydrogenase activity in N1E-115 neuroblastoma or ROC-1 oligodendroglial cells. In human umbilical vein endothelial cells, montmorillonite, kaolinite and bentonite caused a dose-dependent increase in fatty acids at 24h. All three clays caused cell lysis. We postulate that the cytotoxicity of the clays containing an aluminum silicate towards endothelial cells may disrupt the blood-brain barrier in the affected areas, allowing the entry of the clay particle into the brain. Aluminum silicate clays caused a dose-dependent release of fatty acids in human umbilical vein endothelial cells. The clays also caused lysis of these cells. ROC-1 oligodendroglia and N1E-115 neuroblastoma cells were not lysed by the clays, suggesting that this is not a general phenomenon.