Biological effects of oxysterols: current status.
ABSTRACT A review of relevant literature on biological activities of oxysterols (OS) and cholesterol is presented. The data clearly demonstrate manifold biological activities, often detrimental, for OS compared with little or no such activity of a deleterious nature for cholesterol itself. Cholesterol is perhaps the single most important compound in animal tissue and, as such, it is difficult to imagine it as a toxin or hazard. In contrast, OS exhibit cytotoxicity to a wide variety of cells leading to angiotoxic and atherogenic effects; alter vascular permeability to albumin; alter prostaglandin synthesis and stimulate platelet aggregation, an important process facilitating atherosclerosis and thrombosis; alter the functionality of low density lipoprotein (LDL) receptors, possibly stimulating hypercholesterolaemia; modify cholesteryl ester accumulation in various cells, inducing foam cell formation; and enrich the LDL particle in cholesteryl esters, possibly increasing its atherogenicity. Furthermore, OS are mutagenic and carcinogenic, although some have been studied as antitumour agents based on their cytotoxic properties. Moreover, numerous studies have implicated OS in membrane and enzyme alterations that are interrelated with many of the foregoing effects. The authors find that OS deserve much more attention than cholesterol itself in terms of research activity but that unfortunately the reverse is true with regard to funding.
- SourceAvailable from: Magdalena Rudzińska[Show abstract] [Hide abstract]
ABSTRACT: The goal of this study was to monitor changes in the composition of phytosterols and oxyphytosterols in rapeseed oil and French fries during multiple (14 times) deep-frying. Phytosterols (brassicasterol, campesterol, stigmasterol, b-sitosterol and avenasterol), after saponification, were separated by capillary GC. The oxidation products of campesterol, stigmasterol and sitosterol, such as: epimers of 7-hydroxy, 5,6-epoxy, 7-keto and triols, after transesterification and SPE fractionation, were identified by GC/MS and quantified by capillary GC. Results of this research indicate that the content of phytosterols significantly decreased during deep frying of French fries in rapeseed oil (ca. 60%). In addition, the content of oxyphytosterols, particularly triol derivatives, significantly increased. The content of total phytosterols in fresh, good quality rapeseed oil was 5.4 mg/g and decreased after the 14 th frying to 2.0 mg/g. French fries prepared in the first frying oil contained 2.9 mg of phytosterols in 1 g of extracted lipids, but after the 14 th frying they had only 1.1 mg of phytosterols in 1 g of extracted lipids. The level of total oxyphytosterols in fresh good quality rapeseed oil used for frying was 25.1 µg/g. After the 14 th frying it increased to 197.1 µg/g. The content of oxyphytosterols in French fries during frying ranged from 16.8 to 147.6 µg/g of lipids extracted from the products. The dominating oxyphytosterols were epoxy-and 7-hydroxyphytosterols.09/2005; 1455:381-387.
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ABSTRACT: Cells respond to alterations in their membrane structure by activating hydrolytic enzymes. Thus, polyunsaturated fatty acids (PUFAs) are liberated. Free PUFAs react with molecular oxygen to give lipid hydroperoxide molecules (LOOHs). In case of severe cell injury, this physiological reaction switches to the generation of lipid peroxide radicals (LOO.). These radicals can attack nearly all biomolecules such as lipids, carbohydrates, proteins, nucleic acids and enzymes, impairing their biological functions. Identical cell responses are triggered by manipulation of food, for example, heating/grilling and particularly homogenization, representing cell injury. Cholesterol as well as diets rich in saturated fat have been postulated to accelerate the risk of atherosclerosis while food rich in unsaturated fatty acids has been claimed to lower this risk. However, the fact is that LOO. radicals generated from PUFAs can oxidize cholesterol to toxic cholesterol oxides, simulating a reduction in cholesterol level. In this review it is shown how active LOO. radicals interact with biomolecules at a speed transcending usual molecule–molecule reactions by several orders of magnitude. Here, it is explained how functional groups are fundamentally transformed by an attack of LOO. with an obliteration of essential biomolecules leading to pathological conditions. A serious reconsideration of the health and diet guidelines is required.Chemistry - A European Journal 10/2014; · 5.93 Impact Factor
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ABSTRACT: Cholesterol is widely distributed in foods of animal origin, and is susceptible to oxidation to form cholesterol oxidation products (COPs) dur-ing heating and illumination (1-4) . More than 80 Cholesterol oxidation products (COPs) formed in cholesterol-containing foods during heating or illumination have been found to impart a potential hazard to health. Numerous studies have indicated that COPs may have several adverse biological effects, such as muta-genicity, carcinogenicity, angiotoxicity, cytotoxicity, atherogenicity, atherosclerosis, cell mem-brane damage and inhibition of cholesterol biosynthesis. Therefore, the safety of COPs has become a major concern for the public. This paper is an overview of analysis, formation and inhibition of COPs in foods. COPs are routinely extracted by organic solvents, followed by saponification and solid phase extraction for enrichment of COPs, and separation and identifi-cation by thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC) or gas chromatography-mass spectrometry (GC-MS). The identification and quantifi-cation of COPs using the GC-MS technique was found to be rapid and sensitive, however, the formation of artifacts is a major drawback. The HPLC method failed to resolve several geo-metrical isomers, and double bond-free COPs such as isomeric 5,6-epoxides and triol could not be detected with UV. The oxidation of cholesterol can be accelerated by heating, pH, stor-age conditions, the presence of food components and other factors. Several COPs are com-monly present in food systems, including 7α α-OH, 7β β-OH, 5,6α α-EP, 5,6β β-EP, 7-keto, 20α α-OH, 25-OH and triol. Of these COPs, 5,6α α-EP, 5,6β β-EP, 7-keto, 20α α-OH and 25-OH are primary oxidation products, while 7α α-OH, 7β β-OH and triol are secondary products. Some antioxidants have been found to reduce the formation of COPs in an appropriate concentration. Also, ade-quate packaging is necessary to provide a physical barrier for air and light, and thus minimize cholesterol oxidation. Further research is necessary to study how to inhibit COPs formation in foods.