AJP - Lung Cellular and Molecular Physiology, Vol 269, Issue 1 6-10, Copyright © 1995 by American Physiological Society
Genetic control of susceptibility to ozone-induced changes in mouse tracheal electrophysiology
M. Takahashi, S. R. Kleeberger and T. L. Croxton
Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA.
Genetic factors influence the responses of humans and rodents to ozone (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 six additional
inbred strains of mice 6 h after O3 exposures (2 ppm x 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.
