Phosphatidylethanolamine experimental conditions

The experimental information about the hydration of the polar head of phospholipids is relatively abundant [25-33] and although it does not lead to a unique scheme and does not fix precisely the preferred sites of hydration, it indicates a number for the bound Avater molecules which altogether is comparable with that suggested by the theoretical studies. Depending upon the experimental conditions and techniques utilized the number of water molecules in the primary hydration shell (most strongly bound) varies at the polar head of phosphatidylcholine (which was more abundantly studied than phosphatidylethanolamine, more difficult to hydrate possibly because of intermolecular interactions) from 2 to 6. A secondary shell of 4-8 molecules of water, less strongly bound than the previous ones, is sometimes distinguished. 

Figure 4.8 Schematic comparison of intrasource separation of lipid categories to the theoretical electrophoretic separation of lipid classes, (a) Schematically shows the selective ionization of different lipid categories under three different experimental conditions with or without adding a small amount of LiOH. (b) Schematically shows the imaginary chromatograms of lipid classes after electrophoretic analyses under corresponding experimental conditions. PC, TAG, FA, PE, and AL stand for phosphatidylcholine, triacylglyceride, nonesterified fatty acid, phosphatidylethanolamine, and anionic lipids, respectively. Christie and Han [lb]. Reproduced with permission of Elsevier.

Fig. 1. The silica high-performance liquid chromatography (HPLC) radiochromatogram for the separation of lipid classes of total lipid extract (2 pL injected from the total of 100 pL methanol solution) from the castor microsomal incubation (60 min) with P" C]-oleic acid. (For HPLC conditions, see Experimental Procedures.) (1) AG (including FA, 2-5 min) (2) the unknown (3) PE (4) PC (5) ricinoleoyl-PC. FA, fatty acid AG, acylglycerol PE, phosphatidylethanolamine PC, phosphatidylcholine.

Prolonged inhalation of dusts by humans (156), rodents (157,158), and other species (159,160) is associated with an increase in the number of type II cells and increased secretion of surfactant. The stimulation of surfactant appears to be directly related to the toxicity of the dust. It may be so florid, as in acute silicosis, that flooding of the alveolar spaces with surfactant lipids and associated proteins may occur, a condition known as alveolar lipoproteinosis (156). In experimental lipoproteinosis in the rat, the major lipid component is disaturated phosphatidylcholine (157), but all lipid fractions are increased. In the sheep model of experimental silicosis, phosphatidylglycerol, phosphatidylethanolamine, and phosphatidylinositol, showed the greatest increases following silica exposure (159). The excess production of surfactant in response to silica dust may be an adaptive response, perhaps to reduce particle cytotoxicity or to compensate for oxidant-induced lipid peroxidation (147,161). 

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