Vitamin a deficiency enhances ozone-induced lung injury.
Paquette, Nicole C., Liu-Yi Zhang, William A. Ellis, Alan L. Scott,
and Steven R. Kleeberger.
Departments of Environmental Health Sciences and Molecular
Microbiology and Immunology, The Johns Hopkins University School of
Hygiene and Public Health, Baltimore, Maryland 21205
APStracts 2:0192L, 1995.
The present study determined the effects of vitamin A (vA) deficiency
on the responses to ozone (O3) challenges in two inbred strains of
mice that are differentially susceptible to O3-induced lung
inflammation. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3)
dams at two week gestation were fed test diets containing either 0 or
10 [mu]g retinol/g diet. In mice that were maintained on vA
sufficient (vA+) diet, lung and liver tissue concentrations of vA and
retinyl palmitate (R-P) were significantly (P < 0.05) lower in
the B6 strain compared to C3 as measured by HPLC techniques. vA and
R-P levels were significantly (P < 0.05) reduced in lung and
liver tissues of eight week old B6 and C3 mice that were maintained
on a vitamin A deficient (vA-) diet. vA+ and vA- mice of both strains
were exposed to air or 0.3 ppm O3/72 h and lung injury was assessed
by differential cell count and total protein concentration in
bronchoalveolar lavage (BAL) returns. Ozone exposure caused
significantly (p < 0.05) greater increases in inflammatory cells
and total protein in BAL returns of vA+ B6 mice than vA+ C3 mice. vA
deficiency significantly (p < 0.05) enhanced O3-induced
increases in polymorphonuclear leukocytes (PMNs) in C3 mice and
epithelial cell loss in both strains. Compared to vA+ mice, lung
permeability was also significantly (p < 0.05) enhanced in vA-
mice of both strains exposed to O3. Vitamin A replacement partially
reversed the O3-induced lung injury which was enhanced by vA- diet.
Results indicate that vA may have an important role in the
pathogenesis of O3-induced lung injury in differentially susceptible
inbred strains of mice.
Received 24 March 1995; accepted in final form 9 October 1995.
APS Manuscript Number L94-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95