EFFECTS OF REACTIVE OXYGEN SPECIES ON INTRACELLULAR CALCIUM IN BOVINE TRACHEAL EPITHELIUM: Modulation by Nitric Oxide

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Abstract
We studied the effects of reactive oxygen species (ROS) on intracellular Ca 2+ concentration (\[Ca2+]i) and their possible modulation by nitric oxide (NO) in fura-2-loaded cultured bovine tracheal epithelium. Hypoxanthine (HX) and xanthine oxidase (XO), which generate superoxide anion (O2-) and hydrogen peroxide (H2O2), dose dependently increased \[Ca2+]i. The increase in \[Ca2+]i was reduced in the presence of superoxide dismutase (SOD, 200 U/mL) and catalase (200 U/mL) by 29% and 43%, respectively. The iron chelator o-phenanthroline and the hydroxyl radical (OH) scavenger dimethylthiourea (DMTU) more potently inhibited the response of \[Ca2+]i. H2O2- derived OH generated by the Fenton reaction caused a marked \[Ca2+]i elevation, but exogenous H2O2 did not. Sodium nitroprusside (100 muM), an NO donor, potentiated HX-XO induced \[Ca2+]i rise by 50%, an effect that was abolished in the presence of SOD or DMTU. These results suggest that OH formed by interaction of O2- and H2O2 in the presence of iron may play a major role in the HX-XO induced disruption of airway epithelial Ca 2+ homeostasis, and that NO potentiates ROS-induced \[Ca2+]i response, presumably by reacting with O2- and producing OH.

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