Cholesterol-Induced Variations in the Domain Structure Fluctuations and Microdynamics of Lipid Membranes.
Summary of "Cholesterol-Induced Variations in the Domain Structure Fluctuations and Microdynamics of Lipid Membranes."
Broadband ultrasonic attenuation spectra (100 kHzto 2 GHz) of aqueous solutions of vesicles from 1,2-dimyristoyl-l-3-phosphatidylcholine, with different amounts of cholesterol admixed, have been measured at temperatures between 20 and 28 °C. The spectra have been evaluated in terms of suitable relaxation functions. They are discussed in view of the effect of cholesterol on the membrane behavior around the gel-fluid phase transition temperature T(m). In addition to a frequency-independent asymptotic high-frequency term, all spectra reveal a critical term and a Debye-type relaxation term with relaxation time around 0.5 ns. The former is evaluated in the light of the Bhattacharjee-Ferrell dynamic scaling theory. It is assigned to the critical domain structure fluctuations of the membranes. Critical slowing of fluctuations is demonstrated. Also shown are relations of the critical amplitudes to thermodynamic parameters. The Debye term reflects the rotational isomerization of the phospholipid alkyl chains. The relaxation time of isomerization reveals a significant steplike change at T(m). At moderate cholesterol content an additional Debye relaxation term exists. It is assigned to the axial diffusion of the membrane molecules. Because it likewise shows effects of slowing near T(m), the diffusion appears to be coupled to the domain structure fluctuations. A further relaxation term at small cholesterol concentration is assumed to be due to small-range shape fluctuations of vesicles near the phase transition temperature.
Drittes Physikalisches Institut, Georg-August-Universität Göttingen , Friedrich-Hund-Platz 1, 37077 Göttingen, Germany.
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Name: The journal of physical chemistry. B
Medical and Biotech [MESH] Definitions
A spectroscopic technique which uses the Mossbauer effect (inelastic scattering of gamma radiation resulting from interaction with heavy nuclei) to monitor the small variations in the interaction between an atomic nucleus and its environment. Such variations may be induced by changes in temperature, pressure, chemical state, molecular conformation, molecular interaction, or physical site. It is particularly useful for studies of structure-activity relationship in metalloproteins, mobility of heavy metals, and the state of whole tissue and cell membranes.
An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes. The large lipoproteins (CHYLOMICRONS; VLDL) are to transport triglycerides, and the small lipoproteins (LDL; HDL) are to transport cholesterol.
High-density Lipoproteins, Pre-beta
A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.
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