Modulation of Ca2+ influx by a mediator released from human tracheal epithelial cells exposed to ozone in vitro

Qu, Q.S.; Chen, L.C.

American Journal of Physiology 268(4 Pt 1): L558-L564

1995


ISSN/ISBN: 0002-9513
PMID: 7733298
Document Number: 449827
Intracellular free Ca-2+ ((Ca-2+)-i) plays a vital role both in maintaining normal cellular function and in cell killing. Few studies have been published regarding its role in ozone (O-3)-induced health effects. This study investigated the effect and mechanism of O-3 exposure on (Ca-2+)-i in human tracheal epithelial (HTE) cells. HTE cells grown on Costar Transwell inserts with a liquid-gas interface were exposed to 0, 0.05, 0.1, 0.2, and 0.4 ppm O-3 at 37 degree C for 1 h. After exposure, (Ca-2+)-i was measured using the fluorescent dye Fluo 3. O-3 at 0.4 ppm produced a significant increase in (Ca-2+)-i, and the increases in (Ca-2+)-i were blocked by verapamil and 8-(diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). These results suggest that the O-3-induced (Ca-2+)-i elevation may involve both Ca-2+ release from internal stores and Ca-2+ influx across the plasma membrane. Furthermore, both buffer and cell lysate of HTE cells exposed to 0.4 ppm O-3 caused a rapid increase in (Ca-2+)-i of THP-1 human phagocytic monocytes, but the buffer and lysate from air exposed cells did not. These results suggest that O-3 exposure causes HTE cells to release a diffusible mediator from the empty Ca-2+-storing organelle and may be responsible for the sustained and persistent (Ca-2+)-i elevation in HTE cells exposed to 0.4 PPM O-3.

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