Toxicological Sciences, Vol 51, 119-125, Copyright © 1999 by Society of Toxicology
RF Robledo, DS Barber and ML Witten
The loss of epithelial barrier integrity in bronchial and bronchiolar
airways may be an initiating factor in the observed onset of toxicant-
induced lung injuries. Acute 1-h inhalation exposures to aerosolized jet
propulsion fuel 8 (JP-8) have been shown to induce cellular and
morphological indications of pulmonary toxicity that was associated with
increased respiratory permeability to 99mTc-DTPA. To address the hypothesis
that JP-8 jet fuel-induced lung injury is initiated through a disruption in
the airway epithelial barrier function, paracellular mannitol flux of
BEAS-2B human bronchial epithelial cells was measured. Incubation of
confluent cell cultures with non-cytotoxic concentrations of JP-8 or
n-tetradecane (C14), a primary constituent of JP-8, for a 1- h exposure
period resulted in dose-dependent increases of paracellular flux. Following
exposures of 0.17, 0.33, 0.50, or 0.67 mg/ml, mannitol flux increased above
vehicle controls by 10, 14, 29, and 52%, respectively, during a 2-h
incubation period immediately after each JP- 8 exposure. C14 caused greater
mannitol flux increases of 37, 42, 63, and 78%, respectively, following
identical exposure conditions. The effect on transepithelial mannitol flux
reached a maximum at 12 h and spontaneously reversed to control values over
a 48-h recovery period, for both JP-8 and C14 exposure. These data indicate
that non-cytotoxic exposures to JP-8 or C14 exert a noxious effect on
bronchial epithelial barrier function that may preclude pathological lung
injury.
ARTICLES
Modulation of bronchial epithelial cell barrier function by in vitro jet propulsion fuel 8 exposure
Department of Pharmacology and Toxicology, The University of Arizona, Tucson 85724-5073, USA.
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