Advance Access publication December 31, 2009 Calcium-Related Processes Involved in the Inhibition of Depolarization- Evoked Calcium Increase by Hydroxylated PBDEs in PC12 Cells

In vitro studies indicated that hydroxylated polybrominated diphenyl ethers (OH-PBDEs) have an increased toxic potential compared to their parent congeners. An example is the OH-PBDE–induced increase of basal intracellular Ca21 concentration ([Ca21]i) by release of Ca 21 from endoplasmic reticulum (ER) and mitochondria and/or influx of extracellular Ca21. ER and mitochondria regulate Ca21 homeostasis in close association with voltage-gated Ca21 channels (VGCCs). Therefore, effects of (OH-)PBDEs on the depolarization-evoked (100mM K1) net increase in [Ca21]i (depolarization-evoked [Ca 21]i) were mea-sured in neuroendocrine pheochromocytoma cells using the Ca21-responsive dye Fura-2. OH-PBDEs dose dependently inhibited depolarization-evoked [Ca21]i. This inhibition was potentiate