AJP - Lung Cellular and Molecular Physiology, Vol 268, Issue 4 558-L564, Copyright © 1995 by American Physiological Society
Modulation of Ca2+ influx by a mediator released from human tracheal epithelial cells exposed to ozone in vitro
Q. S. Qu and L. C. Chen
Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987, USA.
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.
