Intracellular free Ca2+ ([Ca2+]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 (O3)-induced health effects. This study investigated the effect and mechanism of O3 exposure on [Ca2+]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 O3 at 37 degrees C for 1 h. After exposure, [Ca2+]i was measured using the fluorescent dye Fluo 3. O3 at 0.4 ppm produced a significant increase in [Ca2+]i, and the increases in [Ca2+]i were blocked by verapamil and 8-(diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). These results suggest that the O3-induced [Ca2+]i elevation may involve both Ca2+ release from internal stores and Ca2+ influx across the plasma membrane. Furthermore, both buffer and cell lysate of HTE cells exposed to 0.4 ppm O3 caused a rapid increase in [Ca2+]i of THP-1 human phagocytic monocytes, but the buffer and lysate from air exposed cells did not. These results suggest that O3 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 [Ca2+]i elevation in HTE cells exposed to 0.4 ppm O3.
Implications of the mitochondrial interactome of mammalian thioredoxin 2 for normal cellular function and disease
