Cell-cell matrix interactions in induced lung injury: III. Long term effects of X-irradiation on basal laminar proteoglycans.

The lungs of male LAF1 mice were locally irradiated with doses of 5, 9, and 13 Gy. The animals were killed at times corresponding to the appearance of histologically identifiable fibrosis or, for 13 Gy, at the LD50 for these doses and strain of mouse: 63, 36, and 28 weeks postirradiation (PI) respectively. Lungs were excised, incubated in buffer alone, or partially digested with enzymes for determination of relative glycosidase resistance, fixed with ruthenium red/Triton X-100 for demonstration of basal laminar anionic sites, and processed for electron microscopy. Sham-irradiated and untreated control groups (0 Gy, 0 times) were also processed. Tissue was examined ultrastructurally and alterations in both alveolar and capillary basal laminar anionic sites were quantitated. In each of the doses examined the number of anionic sites surpassed normal levels; however, the glycosidase resistance of the regenerated laminae at these late time points was not significantly altered from controls. This contrasts with the marked increase in the glycosidase resistance of laminae regenerating from radiation damage (4-12 weeks PI) reported earlier. The increased numbers of anionic sites were compared to expected values derived from models based on compensatory synthesis and continued accumulation and indicate close correlation with certain aspects of the compensatory synthesis model but not with others. The effects on basal laminar permeability, basal laminar thickening, and fibrotic induction are discussed.