or inhaled antioxidants.
In conclusion, the present study has shown that
pulmonary oxidative stress occurs in a rat model of
Cd-induced emphysema and persistent airway inflammation.
Significant correlations between airway
inflammation, emphysema and pulmonary oxidative
markers as well as between markers of pulmonary
oxidative stress were found. The markers 8-iso-PGF2a
and UA were increased in BALF during the early
response to Cd inhalation, whereas BALF GSH and
BALF AA significantly decreased over time with
repeated exposure. Further studies are indicated to
determine if enhancement of pulmonary antioxidant
defences can attenuate Cd-induced emphysema in
this model.