Lung fibrosis induced by diquat after intratracheal administration.
Diquat toxicity to lung was evaluated at various intervals after intratracheal administration to rats. Twelve hours after the injection, both type I and type II pneumocytes developed degenerative changes which were similar in nature to those induced by paraquat. A much larger dose of diquat, however, was needed for the changes compared to paraquat, which is known to be actively taken up by the lung. This morphological evidence suggests that diquat may cause alveolar damage by the same mechanism as paraquat, although it is not actively taken up by the lung. Moreover, initial alveolar damage induced by diquat was followed by lung fibrosis, as with paraquat. Since paraquat is a well known fibrogenic agent, the common property of these two agents in alveolar damage may be a key to interpreting the development of lung fibrosis.
Manabe
J
J
Department of Pathology, University of Tsukuba, Ibaraki, Japan.
Ogata
T
T
D000818:Animals; D004178:Diquat / Q000008:administration & dosage / Q000633:toxicity*; D007442:Intubation, Intratracheal; D008168:Lung / Q000473:pathology; D008297:Male; D010269:Paraquat / Q000633:toxicity; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000473:pathology; D011726:Pyridinium Compounds / Q000633:toxicity*; D051381:Rats; D011916:Rats, Inbred F344
D011726:Pyridinium Compounds; D004178:Diquat; D010269:Paraquat