Effect of the environmental pollutant bisphenol A dimethacylate (BAD) on Ca²⁺ movement and viability in OC2 human oral cancer cells

The environmental pollutant bisphenol A dimethacylate (BAD) has been used as a dental composite. The effect of BAD on cytosolic Ca²⁺ concentrations ([Ca²⁺]_i) and viability in OC2 human oral cancer cells was explored. The Ca²⁺-sensitive fluorescent dye fura-2 was applied to measure [Ca²⁺]_i. BAD induced [Ca²⁺]_i rises in a concentration-dependent manner. The response was reduced by removing extracellular Ca²⁺. BAD-evoked Ca²⁺ entry was suppressed by nifedipine, econazole, and SK&F96365. In Ca²⁺-free medium, incubation with the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin abolished BAD-induced [Ca²⁺]_i rise. Inhibition of phospholipase C with U73122 did not alter BAD-induced [Ca²⁺]_i rise. At 10-30μM, BAD inhibited cell viability, which was not reversed by chelating cytosolic Ca²⁺. BAD (20-30μM) also induced apoptosis. Collectively, in OC2 cells, BAD induced a [Ca²⁺]_i rise by evoking phospholipase C-independent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ entry via store-operated Ca²⁺ channels. BAD also caused apoptosis.