Potentiation of Cd-induced pulmonary injury in alpha 1-antitrypsin suppressed rats.
The interrelationship of alpha 1-antitrypsin (alpha 1-AT) or serum trypsin inhibitor capacity (TIC) level and cadmium exposure in the induction of pulmonary lesions was investigated. Sprague-Dawley rats were exposed to CdCl2, galactosamine, or galactosamine + CdCl2 for 24 hr. Biochemical study indicated a 20% reduction of serum TIC in animals exposed to galactosamine. A marked, 50%, reduction of serum TIC was induced in animals exposed to galactosamine + CdCl2. Histopathological study revealed no major morphological lesions in lungs of animals exposed to either CdCl2 or galactosamine. However, extensive lesions, including polymorphonuclear leukocyte (PMN) infiltration, distortion and distention of the alveolar spaces, and massive hemorrhages were observed in the lungs of animals exposed to galactosamine + CdCl2. It is believed that cadmium can induce rapid lesions in the pulmonary tissues when the alpha 1-AT is significantly suppressed. The present investigation has provided direct evidence on the importance and interrelationship of cadmium and alpha 1-AT in pulmonary lesion development.
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D005688:Galactosamine / Q000494:pharmacology; D008168:Lung / Q000473:pathology; D008171:Lung Diseases / Q000097:blood / Q000139:chemically induced / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D000515:alpha 1-Antitrypsin / Q000097:blood*
D000515:alpha 1-Antitrypsin; D002104:Cadmium; D005688:Galactosamine