HYPEROXIA, BUT NOT THORACIC X-IRRADIATION, POTENTIATES BLEOMYCIN-INDUCED AND CYCLOPHOSPHAMIDE-INDUCED LUNG DAMAGE IN MICE

Abstract

I.p. 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. Administration of the antioxidant butylated hydroxytoluene produces lung damage that can be potentiated by both hyperoxia and thoracic X-irradiation. Hyperoxic exposure was also shown to potentiate bleomycin- and cyclophosphamide-induced acute lung damage. Thoracic X-irradiation did not potentiate bleomycin- and cyclophosphamide-induced lung toxicity.