| 11781140 |
Gonzalez A, Schmid A, Salido GM, Camello PJ, Pariente JA: XOD-catalyzed ROS generation mobilizes calcium from intracellular stores in mouse pancreatic acinar cells. Cell Signal. 2002 Feb;14(2):153-9.
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 microM). Neither 2-aminoethoxy-diphenylborate (2-APB) (70 microM) nor ryanodine (50 microM) suppressed ROS-evoked Ca (2+) release. ROS still released Ca (2+) when the endoplasmic reticulum Ca (2+)-ATPase was blocked with thapsigargin (1 microM), or when rotenone (10 microM) 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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