The action of steroids and triton X-100 upon phospholipid/cholesterol structures.

作者: Gerald Weissmann , Grazia Sessa , Sigmund Weissmann

DOI: 10.1016/0006-2952(66)90198-5

关键词: PhospholipidMembraneTriton X-100Electron microscopeStreptolysinMetaboliteChromatographyLamellar structureChemistryEtiocholanolone

摘要: Abstract Purified lipids (ovolecithin, cholesterol, dicetylphosphate, in 70:10:20 molar ratios) swell spontaneously salt solutions to form spherules which behave as saltcontaining compartments limited by discrete membranes. These structures exhibit permeability characteristics for cations, anions, and water are qualitatively similar those occurring across natural After were permitted the presence of 0.145 M H 2 P0 4 − , CrO 2− glucose, or glycine, any excess marker ions molecules remained uncaptured aqueous phase between lamellae removed dialysis against NaCl/KCl. Subsequently, exposed steroids (5 mM), Triton X-100, streptolysin S, agents that affect membranes lysosomes, mitochondria, erythrocytes. Progesterone, desoxycorticosterone (DOC), diethylstilbestrol, 5 β-H such etiocholanolone, considerably accelerated leakage glycine into surrounding medium, did streptolysin. In contrast, cortisone, cortisol, chloroquine, protect membrane-bounded retarded markers. It was possible contained cortisone preincorporated lipid lamellae. At an optimum preincorporation 1 per cent, (but not its inert metabolite tetrahydrocortisone) proved more resistant induced other steroids. Negatively stained preparations electron microscope showed formed multiple concentric separated approximately 50 A distance. X-100 completely disrupted these structures: only amorphous debris formed. DOC-treated samples emergence new forms: although small, remained, predominant forms a series elongated, tubular, strand-like structures, loops whirls maintained lamellar substructure. studies suggest interact with artificial produce changes their resemble steroidinduced membranes, most likely provoking structural rearrangement layers.

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