Abstract
The present study aimed to explore the role of endoplasmic reticulum calcium (ER Ca2+) in the apoptosis of human lung type II alveolar epithelial A549 cells induced by paraquat (PQ) in vitro. PQ significantly elevated the intracellular Ca2+ concentration. Treatment with the Ca2+‑ATPase inhibitor thapsigargin significantly increased PQ‑induced cytotoxicity, elevated the intracellular level of Ca2+, and increased the apoptosis rate, the protein expression of glucose‑regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), and the activities of caspase‑7 and caspase‑12 in PQ‑treated cells. By contrast, treatment with heparin, an inositol 1,4,5‑triphosphate receptor inhibitor, remarkably attenuated cytotoxicity and decreased the intracellular level of Ca2+, the apoptosis rate and the expression levels of GRP78, CHOP and Caspases. In conclusion, PQ impaired the regulating function of ER Ca2+ and resulted in an excessive increase of intracellular Ca2+. Therefore, influencing the Ca2+ signaling in the ER influenced the apoptosis of A549 cells via the ER stress pathway.