Abstract
In fura-2 loaded isolated mouse pancreatic acinar cells, xanthine oxidase (XOD)-catalyzed reactive oxygen species (ROS) generation caused an increase in the cytosolic Ca 2+ concentration ([Ca 2+] i) by release of Ca 2+ from intracellular stores. The ROS-induced Ca 2+ signals showed large variability in shape and time-course and resembled in part Ca 2+ signals in response to physiological secretagogues. ROS-induced Ca 2+ mobilization started at the luminal cell pole and spread towards the basolateral side in a wave manner. ROS-evoked Ca 2+ responses were not inhibited by the phospholipase C (PLC) inhibitor U73122 (10 μM). Neither 2-aminoethoxy-diphenylborate (2-APB) (70 μM) nor ryanodine (50 μM) suppressed ROS-evoked Ca 2+ release. ROS still released Ca 2+ when the endoplasmic reticulum Ca 2+-ATPase was blocked with thapsigargin (1 μM), or when rotenone (10 μM) was added to release Ca 2+ from mitochondria. Our results suggest that pancreatic acinar cells ROS do not unspecifically affect Ca 2+ homeostasis. ROS primarily affect Ca 2+ stores located in the luminal cell pole, which is also the trigger zone for agonist-induced Ca 2+ signals. Release of Ca 2+ induces Ca 2+ waves carried by Ca 2+-induced Ca 2+ release and produces thereby global Ca 2+ signals. Under oxidative stress conditions, the increase in [Ca 2+] i could be one mechanism contributing to an overstimulation of the cell which could result in cell dysfunction and cell damage.
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