Basic fibroblast growth factor recently has been reported to confer significant protection against death from radiation pneumonitis in C3H/HeJ mice. Although the mechanism of this protection remains unknown, one hypothesis, based on in vitro data, is that basic fibroblast growth factor protects against radiation-induced apoptosis in pulmonary endothelial cells. Because of the potential clinical importance of these data, we repeated our experiments in two strains of mice with differeing sensitivities to radiation pneumonitis. One mouse strain, C3Hf/Kam, originated 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 LD50 for radiation pneumonitis between 12 and 28 weeks after irradiation, 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 that basic fibroblast growth factor did not protect against radiation pneumonitis in either C3Hf/Kam or NCR/Sed-nu/+ mice. Quantitation of apoptosis 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 the lung and were not located selectively in endothelial cells of any size blood vessels.


Supported by NIH/NCI Grants CA38106 and CA06294.

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