Blood plasma, lipids

Hyperlipemia may manifest itself by an increased concentration of lipids, or certain groups thereof. For example, hypercholesterolemia and hypertriglyceri-demia may be mentioned in this connection. Since practically all the blood plasma lipids make part of lipoproteins, hyperlipemias may be reduced to one of the hyper-lipoproteinemia forms which differ in the varied ratios of plasma lipoproteins of different groups. 

Atherosclerosis is a condition of the organism characterized by elevated levels of atherogenic lipoproteins in blood plasma, lipid deposits (including cholesterol) in the form of esters inside walls of the arterial system, and it is expressed by a gradual difficulty of blood circulation. The most appropriate name for this disease is lipoproteinemia. Clinically, it is manifested in the form of ischemic heart disease, stroke, abnormal cerebral blood flow, and peripheral ischemia. 

S,3R,4E)-form o-erythro-trans-ybrm Present in blood plasma lipids. 

Analysis of Blood Plasma Lipids Using Gas-Liquid Chromatography. Possibility of the Analysis of the Plasma Lipid Profile with the Chrom 41 Insbrument Vnitr. Lek. 22(4) 390-392 (1976) ... 

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. 

Lipoproteins contain lipid Blood plasma lipoproteins ... 

When most lipids circulate in the body, they do so in the form of lipoprotein complexes. Simple, unesterified fatty acids are merely bound to serum albumin and other proteins in blood plasma, but phospholipids, triacylglycerols, cholesterol, and cholesterol esters are all transported in the form of lipoproteins. At various sites in the body, lipoproteins interact with specific receptors and enzymes that transfer or modify their lipid cargoes. It is now customary to classify lipoproteins according to their densities (Table 25.1). The densities are... 

The effect of a statin is usually determined by measuring fasting plasma lipids and lipoproteins after 4-6 weeks of treatment. Liver enzymes and eventually creatine kinase (in case of myositis liver enzymes are usually also elevated) are measured simultaneously to exclude side effects related to liver and muscles. After the treatment goal has been reached, blood sampling is usually performed 1-2 times a year. 

FAT EMULSIONS. When a fat emulsion is administered, the nurse must monitor the patient s ability to eliminate the infused fat from the circulation. The lipidemia must clear between daily infusions. The nurse monitors for lipidemia through assessing the result of the following laboratory exams hemogram, blood coagulation, liver function tests, plasma lipid profile, and platelet count. The nurse reports an increase in any of these laboratory examinations as abnormal. 

Fat absorbed from the diet and lipids synthesized by the liver and adipose tissue must be transported between the various tissues and organs for utilization and storage. Since lipids are insoluble in water, the problem of how to transport them in the aqueous blood plasma is solved by associating nonpolar lipids (triacylglycerol and cholesteryl esters) with amphipathic hpids (phospholipids and cholesterol) and proteins to make water-miscible hpoproteins. 

Since nonpolar lipids are insoluble in water, for transport between the tissues in the aqueous blood plasma they are combined with amphipathic lipids and proteins to make water-miscible lipoproteins. 

Nowadays, consumers would like those antioxidants present in food products not only to stabilise food lipids, but also to be absorbed through the intestinal wall and protect the lipids of blood plasma against oxidation. This effect is relatively evident in the case of tocopherols (which are liposoluble) or ascorbic acid (which is hydrophilic), but much less evidence is available on antioxidants of medium polarity, such as flavonoids, rosemary oleoresins or green or black tea catechins. 

Selley et al. (1992) have recently employed gas chromatography combined with mass spectrometric detection to determine levels of the cytotoxic monounsaturated aldehyde 4-hydroxy-/7 t-2-nonenal in the blood plasma of healthy human subjects, and patients with rheumatoid and osteoarthritis. Intriguingly, this lipid peroxidation end-product is present at a concentration ofc. lx 10 mol/dm in healthy and osteoarthritic human plasma samples (but significantly elevated in those collected from rheumatoid arthritis patients). Although at least some of this could originate from the oxidative degradation of PUFAs invm, there may be a relationship existing between these levels and the frequency of thermally/... 

Burton, G., Joyce, A. and Ingold, K.U. (1983). Is vitamin E the only lipid-soluble, chain-breaking antioxidant in human blood plasma and erythrocyte membranes Arch. Biochem. Biophys. 221, 281-290. 

Frei, B., Stocker, R. and Ames, B.N. (1988). Antioxidant defences and lipid peroxidation in human blood plasma. Proc. Natl Acad. Sci. USA 85, 9748-9752. 

Carotenoids are also present in animals, including humans, where they are selectively absorbed from diet (Furr and Clark 1997). Because of their hydrophobic nature, carotenoids are located either in the lipid bilayer portion of membranes or form complexes with specific proteins, usually associated with membranes. In animals and humans, dietary carotenoids are transported in blood plasma as complexes with lipoproteins (Krinsky et al. 1958, Tso 1981) and accumulate in various organs and tissues (Parker 1989, Kaplan et al. 1990, Tanumihardjo et al. 1990, Schmitz et al. 1991, Khachik et al. 1998, Hata et al. 2000). The highest concentration of carotenoids can be found in the eye retina of primates. In the retina of the human eye, where two dipolar carotenoids, lutein and zeaxan-thin, selectively accumulate from blood plasma, this concentration can reach as high as 0.1-1.0mM (Snodderly et al. 1984, Landrum et al. 1999). It has been shown that in the retina, carotenoids are associated with lipid bilayer membranes (Sommerburg et al. 1999, Rapp et al. 2000) although, some macular carotenoids may be connected to specific membrane-bound proteins (Bernstein et al. 1997, Bhosale et al. 2004). 

Most commonly, the lipid metabolism pathology is manifest as hyperlipemia (elevated concentration of lipids in blood) and tissue lipidoses (excessive lipid de-position in tissues). Normally, the lipid contents in the blood plasma are total lipids, 4-8 g/litre triglycerides, 0.5-2.1 mmol/litre total phospholipids, 2.0-3.5 mmol/litre total cholesterol, 4.0-8.0 mmol/litre (esterified cholesterol accounts for 2/3 of total cholesterol). 

Further improvement of the low detection limit was achieved using stripping voltammetry based on facilitated heparin adsorption and desorption [66], Stripping voltammetry yielded a detection limit of 0.13 U mL 1 in sheep blood plasma, which is lower than therapeutic heparin concentrations (>0.2 U mL-1). A linear response function in the range of 0.2-6 U mL 1 was observed. The authors also found that blood polypeptides and lipids with a mass above 25 000 significantly interfered with heparin detection, perhaps by hindrance of a charge transfer reaction at the interface. 

As the superoxide radical is a precursor of the other reactive oxygen species and interacts with blood plasma components under physiological and pathological conditions as well, systems related to its generation are biologically relevant. It should be noted, however, that with respect to the initiation of lipid peroxidation as one of the main causes of oxidative cell damage, its own reactivity is very weak and that only in protonized form is its toxicity comparable to that of lipid peroxyl radicals [18]. 

Figure 7 shows an example of the measurements of the antioxidant capacity of lipid-soluble compounds (ACL). In this figure, recording 1 corresponds to blank, while recordings 2-5 demonstrate the effect of adding lipid extracts from equivalently 20,40, 60, and 80 pL of blood plasma from a healthy volunteer... 

Figure 7 PCL recordings in ACL system. 1, blank 2-5, effects of lipid extracts from, respectively, 20, 40, 60, and 80 i.L of blood plasma from a healthy blood donor. (From Ref. 28.)...

Figure 9 Antiradical capacity in the lipid phase of blood plasma (ACL) determined with the PCL method versus vitamin E (VE) as a sum of a- and y-tocopherols determined with HPLC. (From Ref. 28.)...

Figure 10 Lipid-soluble antioxidants in blood plasma in rabbits fed 4 weeks with probu-col and two newly synthesized compounds. All products were administered in equal amounts. The VE portion is the dark gray portion of the columns. Contr., control group Prob., group fed with probucol S-1 and S-2, groups fed with new antioxidants.

One advance in the area of LLE is the use of solid supports that facilitate the partitioning of the analyte(s) of interest. LLE extraction methods involving nonpolar matrices often suffer from the formation of emulsions, and using the solid support is a possible solution. In one study, polychlorinated biphenyls, dioxins, and furans were extracted from the lipid fraction of human blood plasma [32], using diatomaceous earth as the solid support. Long glass columns (30 cm) were packed with several layers of Chem-Elut (a Varian product) and sodium chloride. The plasma samples were diluted with water and ethanol and passed over the columns. A mixture of isopropanol and hexane (2 3) was passed over the column and the LLE was performed. It can be concluded that the LLE with the solid support is easier to perform and can be applied to other lipid heavy matrices such as milk [32]. 

Lipids are transported in blood plasma bound to proteins, in complexes called lipoproteins... 

Orotic acid in the diet (usually at a concentration of 1 per cent) can induce a deficiency of adenine and pyridine nucleotides in rat liver (but not in mouse or chick liver). The consequence is to inhibit secretion of lipoprotein into the blood, followed by the depression of plasma lipids, then in the accumulation of triglycerides and cholesterol in the liver (fatty liver) [141 — 161], This effect is not prevented by folic acid, vitamin B12, choline, methionine or inositol [141, 144], but can be prevented or rapidly reversed by the addition of a small amount of adenine to the diets [146, 147, 149, 152, 162]. The action of orotic acid can also be inhibited by calcium lactate in combination with lactose [163]. It was originally believed that the adenine deficiency produced by orotic acid was caused by an inhibition of the reaction of PRPP with glutamine in the de novo purine synthesis, since large amounts of PRPP are utilized for the conversion of orotic acid to uridine-5 -phosphate. However, incorporation studies of glycine-1- C in livers of orotic acid-fed rats revealed that the inhibition is caused rather by a depletion of the PRPP available for reaction with glutamine than by an effect on the condensation itself [160]. 

The table also lists important globulins in blood plasma, with their mass and function. The a- and p-globulins are involved in the transport of lipids (lipoproteins see p. 278), hormones, vitamins, and metal ions. In addition, they provide coagulation factors, protease inhibitors, and the proteins of the complement system (see p. 298). Soluble antibodies (immunoglobulins see p. 300) make up the y-globulin fraction. 

Most lipids are barely soluble in water, and many have amphipathic properties. In the blood, free triacylglycerols would coalesce into drops that could cause fat embolisms. By contrast, amphipathic lipids would be deposited in the blood cells membranes and would dissolve them. Special precautions are therefore needed for lipid transport in the blood. While long-chain fatty acids are bound to albumin and short-chain ones are dissolved in the plasma (see p. 276), other lipids are transported in lipoprotein complexes, of which there several types in the blood plasma, with different sizes and composition. 

Prazosin may be particularly useful when patients cannot tolerate other types of antihypertensive agents or when blood pressure is not well controlled by other drugs. Since prazosin does not significantly influence blood uric acid or glucose levels, it can be used in hypertensive patients whose condition is complicated by gout or diabetes meUitus. Prazosin treatment is associated with favorable effects on plasma lipids. Thus, it may be of particular importance in managing patients with hyperlipidemia. 

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