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Low-density lipids

Low-density lipids in the blood cause cholesterol deposits. Their presence and nature, including the position and number of double bonds, can be analyzed by means of ESI-MS techniques <2000JMP224>. Reverse-phase HPLC microsamples containing phospholipids were treated with bis(trimethylsilyl) trifluoroacetamide, then with methoxy-amine, and then exposed for 8 min to ozone gas at room temperature ESI-MS followed and showed the fragments corresponding to ozonides. [Pg.246]

AIR particles are low-density lipid-based particles that are produced by spray drying lipid-albumin-drug solutions. These particles are characterized by their porous surface characteristics and large geometric diameter while having a low aerodynamic diameter [176,177], This technology has been used to produce porous particle powder formulations of L-dopa that have been investigated for the treatment of Parkinson s disease [178],... [Pg.701]

Unwanted deposits of cholesterol occur because cholesterol, being a lipid with no water-soluble end, needs help to be transported around in the bloodstream. The transporters are called low-density lipids. They form little bubbles around the cholesterol, not unlike soap solvates dirt, using their oily hydrocarbon ends to connect with the cholesterol and their organic-acid ends to connect with the watery fluid of blood. The structure of the low-density lipids (abbreviated LDL) helps them deposit their cholesterol load when they reach the cells where it is needed, but, unfortunately, their structure also facilitates the dumping of excess cholesterol on blood vessel walls when the cells have all they need. When we speak of... [Pg.304]

During the course of screening antioxidants from plants, Baek et al. isolated a neolignan from the bark of M. officinalis [37]. A biphenyl compound, 5, 5 -di-2-propenyl-2-hydroxy-3, 2, 3 -trimethoxy-l-l -biphenyl (15), was found to have antioxidant activity similar to commercial synthetic antioxidants 2, 6-di-ter/-butyl-4-methylphenol (BHT) or 3-tert-butyl-4-hydroxyanisole (BHA). Antioxidants are compounds that inactivate free radicals in the body. Free radicals can cause cancer since it can promote the growth of cells by initiating spontaneous mitosis. Furthermore, phenolic antioxidants in wine, especially resveratrol (16), have demonstrated the ability to inhibit human low density lipid (LDL) oxidation in vitro [38]. Frankel mentions other studies suggesting... [Pg.850]

However, under some circumstances, even efficacy can show a nonmonotonic relationship. Suppose that the drug has a beneficial effect on efficacy via one mechanism and a deleterious effect via another. For example, the desirable outcome of a cholesterollowering drug is a reduction in cardiovascular events, but this is mainly achieved through lowering of bad cholesterol, or low-density lipids (LDL) (Law et ah, 2003)... [Pg.332]

Figure 37.4 Lipoproteins. Lipoproteins are macromolecular complexes used by the body to transport lipids in the blood. They are characterised by an outer coat of phospholipids and proteins, which encloses an inner core of hydrophobic TAG and cholesteryl ester. Lipoproteins tire classified according to the way they behave on centrifugation. This in turn corresponds to their relative densities, which depends on the proportion of (high density) protein to (low density) lipid in their structure. For example, high density lipoproteins (HDLs) consist of 50% protein and have the highest density, while chylomicrons (1% protein) tmd very low density lipoproteins (VLDLs) have the lowest density. Figure 37.4 Lipoproteins. Lipoproteins are macromolecular complexes used by the body to transport lipids in the blood. They are characterised by an outer coat of phospholipids and proteins, which encloses an inner core of hydrophobic TAG and cholesteryl ester. Lipoproteins tire classified according to the way they behave on centrifugation. This in turn corresponds to their relative densities, which depends on the proportion of (high density) protein to (low density) lipid in their structure. For example, high density lipoproteins (HDLs) consist of 50% protein and have the highest density, while chylomicrons (1% protein) tmd very low density lipoproteins (VLDLs) have the lowest density.
Cholesterol is biosynthesized in the liver trans ported throughout the body to be used in a va riety of ways and returned to the liver where it serves as the biosynthetic precursor to other steroids But cholesterol is a lipid and isn t soluble in water How can it move through the blood if it doesn t dis solve in if The answer is that it doesn t dissolve but IS instead carried through the blood and tissues as part of a lipoprotein (lipid + protein = lipoprotein) The proteins that carry cholesterol from the liver are called low density lipoproteins or LDLs those that return it to the liver are the high-density lipoproteins or HDLs If too much cholesterol is being transported by LDL or too little by HDL the extra cholesterol builds up on the walls of the arteries caus mg atherosclerosis A thorough physical examination nowadays measures not only total cholesterol con centration but also the distribution between LDL and HDL cholesterol An elevated level of LDL cholesterol IS a risk factor for heart disease LDL cholesterol is bad cholesterol HDLs on the other hand remove excess cholesterol and are protective HDL cholesterol IS good cholesterol... [Pg.1096]

LIPOPROTEINS. Blood plasma lipoproteins are prominent examples of the class of proteins conjugated with lipid. The plasma lipoproteins function primarily in the transport of lipids to sites of active membrane synthesis. Serum levels of low density lipoproteins (LDLs) are often used as a clinical index of susceptibility to vascular disease. [Pg.126]

Cells in the atheroma derived from both macrophages and smooth muscle cells that have accumulated modified low-density lipoproteins. Their cytoplasm laden with lipid causes the foamy appearance on microscopy... [Pg.508]

Figure 15-6. Transport and fate of major lipid substrates and metabolites. (FFA, free fatty acids LPL, lipoprotein lipase MG, monoacylglycerol TG, triacylglycerol VLDL, very low density lipoprotein.)... Figure 15-6. Transport and fate of major lipid substrates and metabolites. (FFA, free fatty acids LPL, lipoprotein lipase MG, monoacylglycerol TG, triacylglycerol VLDL, very low density lipoprotein.)...
Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP. Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP.
Four major groups of lipoproteins are recognized Chylomicrons transport lipids resulting from digestion and absorption. Very low density lipoproteins (VLDL) transport triacylglycerol from the liver. Low-density lipoproteins (LDL) deliver cholesterol to the tissues, and high-density lipoproteins (HDL) remove cholesterol from the tissues in the process known as reverse cholesterol transport. [Pg.217]

Figure 26-5. Factors affecting cholesterol balance at the cellular level. Reverse cholesterol transport may be initiated by pre 3 HDL binding to the ABC-1 transporter protein via apo A-l. Cholesterol is then moved out of the cell via the transporter, lipidating the HDL, and the larger particles then dissociate from the ABC-1 molecule. (C, cholesterol CE, cholesteryl ester PL, phospholipid ACAT, acyl-CoA cholesterol acyltransferase LCAT, lecithinicholesterol acyltransferase A-l, apolipoprotein A-l LDL, low-density lipoprotein VLDL, very low density lipoprotein.) LDL and HDL are not shown to scale. Figure 26-5. Factors affecting cholesterol balance at the cellular level. Reverse cholesterol transport may be initiated by pre 3 HDL binding to the ABC-1 transporter protein via apo A-l. Cholesterol is then moved out of the cell via the transporter, lipidating the HDL, and the larger particles then dissociate from the ABC-1 molecule. (C, cholesterol CE, cholesteryl ester PL, phospholipid ACAT, acyl-CoA cholesterol acyltransferase LCAT, lecithinicholesterol acyltransferase A-l, apolipoprotein A-l LDL, low-density lipoprotein VLDL, very low density lipoprotein.) LDL and HDL are not shown to scale.
In the last few decades, several epidemiological studies have shown that a dietary intake of foods rich in natural antioxidants correlates with reduced risk of coronary heart disease particularly, a negative association between consumption of polyphenol-rich foods and cardiovascular diseases has been demonstrated. This association has been partially explained on the basis of the fact that polyphenols interrupt lipid peroxidation induced by reactive oxygen species (ROS). A large body of studies has shown that oxidative modification of the low-density fraction of lipoprotein (LDL) is implicated... [Pg.5]

As has already been stated, the carotenoids are lipophilic and are therefore absorbed and transported in association with the lipoprotein particles. In theory, this fortuitous juxtaposition of lipid and carotenoid should confer protection on the lipid through the antioxidant properties of the carotenoid. No doubt some antioxidant protection is afforded by the presence of the carotenoids derived from the diet. However, with one or two exceptions, human supplementation studies have not supported a role for higher dose carotenoid supplements in reducing the susceptibility of the low-density lipoproteins to oxidation, either ex vivo or in vivo (Wright et al, 2002 Hininger et al, 2001 Iwamoto et al, 2000). [Pg.112]

BAUM J A, TENG H, ERDMAN J W Jr, WEIGEL R M, KLEIN B P, PERSKY V W, FREELS S, SURYA P, BAKHIT R M, RAMOS E, SHAY N F and POTTER s M (1998) Long-term intake of soy protein improves blood lipid profiles and increases mononuclear cell low-density-lipoprotein receptor messenger RNA in hypercolesterolemic postmenopausal women. Am J Clin Nutr. 68 (3) 545-51. [Pg.212]


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