Am. J. Respir. Cell Mol. Biol., Vol 17, No. 5, Nov 1997, 552-560.
Site- and cell-specific alteration of lung copper/zinc and manganese superoxide dismutases by chronic ozone exposure
BL Weller, JD Crapo, J Slot, G Posthuma, CG Plopper and KE Pinkerton
Department of Anatomy, California Regional Primate Research Center, School of Veterinary Medicine, University of California at Davis, 95616, USA.
The antioxidant enzymes copper/zinc (Cu-Zn) and manganese (Mn) superoxide
dismutase (SOD) have been implicated in protection of the lungs from
oxidant damage. Mn SOD in particular may be related to acquired tolerance
in cells following chronic ozone exposure. In order to study these
protective and adaptive phenomena in oxidant injury, the cellular location
and relative abundance of Mn SOD and Cu-Zn SOD were examined in the lungs
of Fischer 344 rats following exposure to 0.0 and 1.0 ppm ozone for up to 3
mo using immunolabeling and morphometric techniques. Cu-Zn SOD labeling was
found to be markedly reduced following ozone exposure in epithelial cells
within airways and parenchyma. In contrast, a significant increase was
noted in Mn SOD labeling in the centriacinar regions of exposed lungs for
both alveolar macrophages and epithelial type II cells. Mn SOD labeling per
epithelial type II cell was significantly increased in alveoli 0-400 microm
beyond the bronchiole-alveolar duct junction (BADJ), while type II cell Mn
SOD labeling was similar to control values with greater distance down the
alveolar duct. No induction of Mn SOD was noted in type I epithelial cells,
fibroblasts, or Clara cells. Thus, alterations in Cu-Zn and Mn SOD are both
site and cell specific in the lungs. The differential increase in Mn SOD in
type II cells of the proximal alveolar duct may reflect the ability of
these cells to acquire tolerance and to resist further injury to repeated
ozone exposure.
