High-density lipoproteins formation

Systemic treatment of 13-cis retinoic acid frequently leads to cheilitis and eye irritations (e.g., unspecific cornea inflammation). Also other symptoms such as headache, pruritus, alopecia, pains of joints and bone, and exostosis formation have been reported. Notably, an increase of very low density lipoproteins and triglycerides accompanied by a decrease of the high density lipoproteins has been reported in 10-20% of treated patients. Transiently, liver function markers can increase during oral retinoid therapy. Etretinate causes the side effects of 13-cis retinoid acid at lower doses. In addition to this, generalized edema and centrilobulary toxic liver cell necrosis have been observed. 

In adult brain most cholesterol synthesis occurs in astrocytes. Apoprotein E (apoE) is the major apolipopro-tein of the CNS and it is secreted by astrocytes. In astrocyte cultures apoE appears in the media as cholesterol-rich particles of a size similar to peripheral HDL (5-12 nm) (Fig. 2-7). The ATP-dependent transporter ABCA1, expressed by both astrocytes and neurons, promotes the formation of the apoE-stabilized high-density lipoprotein (HDL)-sized particles from astrocytic cholesterol. 

One role of high density lipoprotein (HDL) is to collect unesterified cholesterol from cells, including endothelial cells of the artery walls, and return it to the liver where it can not only inhibit cholesterol synthesis but also provide the precursor for bile acid formation. The process is known as reverse cholesterol transfer and its overall effect is to lower the amount of cholesterol in cells and in the blood. Even an excessive intracellular level of cholesterol can be lowered by this reverse transfer process (Figure 22.10). Unfortunately, the level of HDL in the subendothelial space of the arteries is very low, so that this safety valve is not available and all the cholesterol in this space is taken up by the macrophage to form cholesteryl ester. This is then locked within the macrophage (i.e. not available to HDL) and causes damage and then death of the cells, as described above. 

Hartree-Fock calculations, peracid alkene epoxidation, 48-50 Hazardous materials commercial codes, 621 emergency response, 746-7 environmental hazards, 747, 751-3 labels, 751-3 NIOSH Pocket Guide, 749 occupational hazards, 747-9 safety issues, 744-9 HDL see High-density lipoprotein Heat of formation see Enthalpy of formation HEHP (1-hydroxyethyl hydroperoxide), 605, 638... 

Estrogens lower serum cholesterol levels by stimulating the formation of high-density lipoproteins and reducing low-density lipoproteins. Reductions in serum albumin and antithrombin III synthesis can occur in the presence of elevated female sex steroids. 

Miccoli R, Zhu Y, Daum U, Wessling J, Huang Y, Navalesi R, Assmann G, Eckardstein A von (1997) A natural apolipoprotein A-I variant, apoA-I (L141R)Pisa, interferes with the formation of alpha-high density lipoproteins (HDL) but not with the formation of pre beta 1-HDL and influences efflux of cholesterol into plasma. J Lipid Res 38 1242-1253... 

The fourth major lipoprotein type, high-density lipoprotein (HDL), originates in the liver and small intestine as small, protein-rich particles that contain relatively little cholesterol and no cholesteryl esters (Fig. 21-40). HDLs contain apoA-I, apoC-I, apoC-II, and other apolipoproteins (Table 21-3), as well as the enzyme lecithin-cholesterol acyl transferase (LCAT), which catalyzes the formation of cholesteryl esters from lecithin (phosphatidylcholine) and cholesterol (Fig. 21-41). LCAT on the surface of nascent (newly forming) HDL particles converts the cholesterol and phosphatidylcholine of chylomicron and VLDL remnants to cholesteryl esters, which begin to form a core, transforming the disk-shaped nascent HDL to a mature, spherical HDL particle. This cholesterol-rich lipoprotein then returns to the liver, where the cholesterol is unloaded some of this cholesterol is converted to bile salts. 

The plasma lipoproteins are spherical macromolecular complexes of lipids and specific proteins (apolipoproteins or apoproteins). The lipoprotein particles include chylomicrons, very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). They differ in lipid and protein composition, size, and density (Figure 18.13). Lipoproteins function both to keep their component lipids soluble as they transport them in the plasma, and also to provide an efficient mechanism for transporting their lipid contents to (and from) the tissues. In humans, the transport system is less perfect than in other animals and, as a result, humans experience a yradual deposition of lipid—especially cholesterol—in tissues. This is a potentially life-threat-en ng occurrence when the lipid deposition contributes to plaque formation, causing the narrowing of blood vessels (atherosclerosis). 

While the primary role of LDL appears to be the transport of esterified cholesterol to tissues, the high density lipoproteins (HDL) carry excess cholesterol away from most tissues to the liver 205 207 The apoA-I present in the HDL particle not only binds lipid but activates LCAT, which catalyzes formation of cholesteryl esters which migrate into the interior of the HDL and are carried to the liver. 

Microbial formation of plant isoquinolines became an attractive issue over recent years [116]. Magnoflorine was of particular interest thanks to its pharmacological activities. On one hand, it was found that this aporphine alkaloid protects human high density lipoprotein (HDL) against lipid peroxidation but it also exhibits anti-HIV activity [117-119]. New production strategies for this alkaloid will be vital in the future. 

GJ Hopkins, LBF Chang, PJ Barter. Role of lipid transfers in the formation of a subpopulation of small high density lipoproteins. J Lipid Res 26 218-229, 1985. 

H26. Hoffman, J. S., and Benditt, E. P., Changes in high density lipoprotein content following endotoxin administration in the mouse Formation of serum amyloid protein-rich subfractions. /. Bud. Chem. 257, 10510-10517 (1982). 

Lipoproteins transport hydrophobic fats in plasma (Fig. 13-2). The major lipoproteins (Chap. 6) circulating in the blood are chylomicrons, VLDLs (very low density lipoproteins), LDLs (low-density lipoproteins), and HDLs (high-density lipoproteins). IDLs (intermediate density lipoproteins) are derived from VLDLs in the formation of LDLs. Fatty acids are important cellular... 

Figure 1. Proposed yet speculative mechanism by which high-density lipoprotein (HDL) increases in response to exercise via increased lipoprotein lipase (LPL) activity. During lipolysis. components of Tg-rich lipoproteins are transferred to and incorporated into HDL, leading to the formation of HDL.. Very low density lipoprotein (VLDL), chylomicron (chylo).

High serum levels of cholesterol cause disease and death by contributing to the formation of atherosclerotic plaques in arteries throughout the body. This excess cholesterol is present in the form of the low density lipoprotein particle, so-called "bad cholesterol. "The ratio of cholesterol in the form of high density lipoprotein, sometimes referred to as "good cholesterol," to that in the form of LDL can be used to evaluate susceptibility to the development of heart disease. For a healthy person, the LDL/HDL ratio is 3.5. 

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