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The in vitro secretion of fibronectin by rat alveolar macrophages recovered following the intratracheal instillation of various mineral dusts was examined using a competitive enzyme-linked immunoassay (CELIA) method. Cells derived with the fibrogenic dusts DQ12 quartz and UICC crocidolite asbestos had elevated rates of fibronectin secretion when compared ith those derived from titanium dioxide or saline. The in vitro culture of alveolar macrophages with dusts did not lead to elevated rates of fibronectin secretion, suggesting that mechanisms other than the direct interaction between dusts and macrophages may be responsible for elevated rates of fibronectin secretion by cells exposed to fibrogenic dusts. This suggests that fibronectin deposition seen in pneumoconiotic lesions in immunohistochemical studies may in part have been derived from macrophages. Thioglycollate-induced activated mouse peritoneal macrophages secreted significantly less fibronectin than resident peritoneal macrophages, a finding contrasting with those of Tsukamoto et al. [7].

Transient cerebral ischemia causes long-lasting inhibition of protein synthesis despite recovery of energy metabolism. We investigated the question if this inhibition is due to the formation of a suppression factor which interferes with the function of the protein synthesizing machinery. For this purpose rats were submitted to 20 minutes four vessel-occlusion followed by recirculation times from 30 minutes to 7 days. Post-mitochondrial supernatant (PMS) from various brain regions was added to a self-contained, cell-free rabbit reticulocyte translational system, and the effect on in vitro protein synthesis was assessed by measuring 14C-leucine incorporation over a duration of 45 minutes. PMS prepared at the end of ischemia from hippocampus, striatum and cerebellum inhibited in vitro protein synthesis by 40%-60% but there was only a minor inhibition by PMS from cerebral cortex. During post-ischemic recirculation cortical PMS transiently induced inhibition of in vitro protein synthesis by 30% but this effect gradually disappeared within one week. The inhibition caused by PMS from hippocampus, striatum and cerebellum was not reversed during recirculation and still amounted to about 40% after 7 days. Inhibition of in vitro protein synthesis could be blocked by heating PMS to 100 degrees C, indicating that the suppressor factor is a protein. The comparison of the in vitro effect of postischemic PMS with previously described in vivo inhibition of protein synthesis demonstrates that the here observed suppressor factor is not able to explain the overall disturbance of protein synthesis in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos-induced cell damage is initiated by a reaction at the plasma membrane. The effect of chrysotile (which is more hemolytic and releases more silicic acid than other types of asbestos) on permeability changes of liposomes has been investigated. The destabilizing effect rises when the amount of chrysotile is increased. Silicon dioxide is one major constituent which could be a hemolytic agent, and a cause of damage. It also caused an increase of permeability of liposomes.

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