BASIC FIBROBLAST GROWTH-FACTOR DOES NOT PROTECT AGAINST CLASSICAL RADIATION PNEUMONITIS IN 2 STRAINS OF MICE

Basic fibroblast growth factor recently has been reported to confer si gnificant protection against death from radiation pneumonitis in C3H/H eJ mice. Although the mechanism of this protection remains unknown, on e hypothesis, based on in vitro data, is that basic fibroblast growth factor protects against radiation induced apoptosis in pulmonary endot helial cells. Because of the potential clinical importance of these da ta, we repeated our experiments in two strains of mice with differing sensitivities to radiation pneumonitis. One mouse strain, C3Hf/Kam, or iginated from the same C3H/He strain as the C3H/HeJ mouse used by Fuks et al. in their 1994 study. The other strain, the NCR/Sed-nu/+ strain , is a white mouse heterozygous for the nude trait. In our laboratory, the LD(50) for radiation pneumonitis between 12 and 28 weeks after ir radiation, the standard assay time for this phase of radiation-induced lung damage, is 12.5 Gy in the C3Hf/Kam and 8.5 Gy in the NCR/Sed-nu/ + strain. Contrary to previous results in the literature, we found tha t basic fibroblast growth factor did not protect against radiation pne umonitis in either C3Hf/Kam or NCR/Sed-nu/+ mice. Quantitation of apop tosis after both doses to the lungs of the two strains showed that the incidence of apoptosis was less than 1% in C3Hf/Kam mice and 0.5% in NCR/Sed-nu/+ mice. These apoptotic bodies were scattered throughout th e lung and were not located selectively in endothelial cells of any si ze blood vessels.