Hyperoxia, but not thoracic X-irradiation, potentiates bleomycin- and cyclophosphamide-induced lung damage in mice.
The intraperitoneal administration of cyclophosphamide or bleomycin to BALB/c mice resulted in lung cell damage followed by cellular proliferation, which was quantitated by measuring the increase in thymidine incorporation into pulmonary DNA. We have previously shown that administration of the antioxidant butylated hydroxytoluene produces lung damage that can be potentiated by both hyperoxia and thoracic X-irradiation. In the present study we show that hyperoxic exposure also potentiates bleomycin- and cyclophosphamide-induced acute lung damage. However, thoracic X-irradiation does not potentiate bleomycin- and cyclophosphamide-induced lung toxicity.
D000818:Animals; D001761:Bleomycin / Q000633:toxicity*; D003094:Collagen / Q000096:biosynthesis; D003520:Cyclophosphamide / Q000633:toxicity*; D004247:DNA / Q000096:biosynthesis; D006909:Hydroxyproline / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010100:Oxygen / Q000633:toxicity*; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000378:metabolism; D011833:Radiation Injuries, Experimental / Q000209:etiology*; D013909:Thorax / Q000528:radiation effects
D001761:Bleomycin; D003520:Cyclophosphamide; D003094:Collagen; D004247:DNA; D006909:Hydroxyproline; D010100:Oxygen