Genetic control of susceptibility to ozone-induced changes in mouse
tracheal electrophysiology.
Takahashi, Masahiko, Steven R. Kleeberger, and Thomas L. Croxton.
Departments of Environmental Health Sciences and Anesthesiology
& Critical Care Medicine, The Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205
APStracts 2:0035L, 1995.
Genetic factors influence the responses of men and rodents to O3
inhalation. We previously demonstrated differential O3-induced
decreases of tracheal potential (VT) in C57BL/6J (B6) and C3H/HeJ
(C3) strain mice. To characterize the genetic basis of this strain
-specific response we measured VT in progeny of B6 and C3 strain mice
and in 6 additional inbred strains of mice 6 h after O3 exposures (2
ppm _ 3 h). First filial generation (F1) mice and second generation
backcrosses with the resistant parent were uniformly resistant. The
distribution of VT in second generation backcrosses with the
susceptible parent resembled that of a population composed of
resistant and susceptible mice in a 1:1 ratio. These data suggested
simple autosomal recessive inheritance of susceptibility. However,
overlapping distributions prevented statistical confirmation of that
hypothesis. Strain screening revealed a susceptible phenotype in
129/J, A/J, B6, C3HeB/FeJ, and SJL/J and a resistant phenotype in
AKR/J, C3, and CBA/J inbred mouse strains. Because this pattern of
susceptibility to changes in VT differs from that of susceptibility
to lung inflammation, the genetic factors that determine these two
responses to acute O3 are not identical.
Received 21 November 1994; accepted in final form 20 February
1995.
APS Manuscript Number L335-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.