1. Pulmonary surfactants from ox, rabbit, rat and sheep were isolated and analysed. 2. All preparations had a high anenoic phosphatidylcholine content and would produce stable surface tensions of 0.01 Nm-1 or less. 3. Protein content was 8-18% of the dry weights. A number of proteins were observed; their overall composition were high in hydrophobic amino acid residues. 4. Lipid content varied from 79% (ox) to 90% (rabbit) with phosphatidylcholine representing from 58% (sheep) to 83% (rabbit) of the total lipid. The surfactant preparations were rather similar in lipid composition except that sheep surfactant contained about 10% lysophosphatidylcholine. 5. Hexadecanoic acid was the principal fatty acid. It was particularly high in phosphatidylcholine. 6. Phosphatidylglycerol was a minor constituent of all surfactants but phosphatidyldimethylethanolamine was not detected.
1. Radioactively labelled pulmonary surfactant was prepared in an isolated perfused lung system provided with [14C]hexadecanoate. 2. After intratracheal administration of pulmonary surfactant radioactively labelled components were rapidly distributed into different lung fractions, including macrophages (free cells), but most of the radioactive label was accumulated by the lung tissue. 3. Alveolar macrophages, maintained in a variety of culture media in the presence and absence of mineral particles, incorporated a low percentage (11%) of radioactively labelled components when incubated with the surfactant, although evolution of labelled CO2 (6% of the original total activity) suggested that some breakdown of the components had taken place. 4. In similar cultures little intracellular accumulation or extracellular release of non-esterified fatty acids was demonstrated, indicating minimal catabolism of the high-molecular-weight lipid components of surfactant (particularly phosphatidylcholine). 5. However, experiments in vitro designed to simulate the lysosomal degradation of endocytosed surfactant indicated that the macrophage had enzymes capable of releasing non-esterified fatty acids, particularly hexadecanoate, from the lipoprotein complex. 6. It is argued that lung cells, other than alveolar macrophages, may also have a role in surfactant turnover.
The interaction between chrysotile and three lysosomal enzymes (acid phosphatase, acid RNase and acid protease) in isolated lysosomal enzyme-rich preparations (LEP), from sheep alveolar macrophages maintained in the presence and absence of serum components or pulmonary surfactant at pH 5.0 and pH 7.0 for up to 22 days, is investigated. It is concluded that chrysotile does not inhibit or enhance lysosomal enzyme activity at either pH but may preferentially absorb specific enzymes and that the binding reaction between any given enzyme and mineral can be dependent on the presence of other organic compounds. The release of three hydrolytic enzymes (f-galactosidase, acid RNase and protease) from cultured rabbit alveolar macrophages, in the presence of different concentrations of bovine serum (5-20%) and in the presence and absence of chrysotile for 72 hr, was also studied. Chrysotile enhances early differential release of each hydrolytic enzyme, but after 72 hr both control and chrysotile-treated cultures (maintained in 10-20% serum) have very similar intraand extracellular levels of hydrolytic activity. The apparent differential release of lysosomal enzymes by untreated macrophages, which is dependent on serum concentration and time in vitro, is discussed.
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