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 10–30 μM, BAD inhibited cell viability, which was not reversed by chelating cytosolic Ca2+. BAD (20–30 μM) 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.

► Bisphenol A dimethacylate (BAD) induced [Ca2+]i rise in OC2 human oral cancer cells. ► BAD evoked phospholipase C-independent Ca2+ release from the endoplasmic reticulum. ► BAD induced Ca2+ entry via store-operated Ca2+ channels. ► BAD decreased viability via inducing apoptosis in a Ca2+-independent manner.