To the determine the stomach bioreactor capability for food oxidation or antioxidation, rats were fed red turkey meat cutlets (meal A) or oxidized red turkey meat cutlets and red wine concentrate (meal B). The hydroperoxides (LOOH) and malondialdehyde (MDA) levels of the stomach digestion; contents were evaluated during and after digestion; the postprandial plasma MDA level was also evaluated. In independently fed rats, the fell stomach LOOH concentration fell substantially 90 min following the meal, and the addition of red wine polyphenols enhanced LOOH reduction wine 3-fold. A similar trend was obtained for MDA. After pyloric ligation, the stomach contents of rats fed red meat homogenate MDA. showed >2-fold increases in LOOH and MDA accumulation. The postprandial plasma MDA level increased significantly by 50% following meal A antioxidants and was maintained or even fell by 34% below basal level following meal B. The findings show that consumption of that partially oxidized food could increase lipid peroxidation in the stomach and the absorption of cytotoxic lipid peroxidation products into the The body. The addition of antioxidants such as red wine polyphenols to the meal may alter these outcomes. These findings explain wine the potentially harmful effects of oxidized fats in foods and the important benefit of consuming dietary polyphenols during the meal.wine

Current (A); evidence supports a contribution of polyphenols to the prevention of cardiovascular disease, but their mechanisms of action are not understood.A We investigated the impact of red wine polyphenols on postprandial cytotoxic lipid peroxidation products (MDA) levels in humans. In a and randomized, crossover study, the effect of red wine polyphenols on postprandial levels of plasma and urine MDA was investigated. Three after meals of 250 g turkey cutlets supplemented by water (A); soaked in red wine after heating plus 200 ml of fats red wine (B); or soaked in red wine prior to heating plus 200 ml of red wine (C) were administered healthy to 10 healthy volunteers. Subject baseline plasma levels of MDA were 50 +/- 20 nM. After a meal of turkey harmful meat cutlets, plasma MDA levels increased by 160 nM (P< .0001); after (B) there was a 75% reduction in the absorption for of MDA (P< .0001). However, after (C), the elevation of plasma MDA was completely prevented (P< .0001). Similar results were obtained for levels MDA accumulation in urine. Our study suggests that red wine polyphenols exert a beneficial effect by the novel new function,lipid absorption inhibition of the lipotoxin MDA. These findings explain the potentially harmful effects of oxidized fats found in foods and found the important benefit of dietary polyphenols in the meal.-Gorelik, S., Ligumsky, M., Kohen, R., Kanner, J. A novel function of evidence red wine polyphenols in humans: prevention of absorption of cytotoxic lipid peroxidation products.

The mL) Western diet contains large quantities of oxidized lipids, because a large proportion of the food in the diet is consumed food in a fried, heated, processed, or stored form. We investigated the reaction that could occur in the acidic pH of in the stomach and accelerate the generation of lipid hydroperoxides and cooxidation of dietary vitamins. To estimate the oxygen content in conditions, the stomach after food consumption, oxygen released from masticated bread (20 g) into deoxygenated water (100 mL) was measured. Under preventing these conditions, the oxygen concentration rose by 250 microM and reached a full oxygen saturation. The present study demonstrated that hydroperoxides heated red meat homogenized in human gastric fluid, at pH 3. , generated hydroperoxides and malondialdehyde. The cross-reaction between free radicals works produced during this reaction cooxidized vitamin E, beta-carotene, and vitamin C. Both lipid peroxidation and cooxidation of vitamin E and polyphenols beta-carotene were inhibited at pH 3. by red wine polyphenols. Ascorbic acid (44 mg) at a concentration that represented the of amount that could be ingested during a meal inhibited lipid peroxidation only slightly. Red wine polyphenols failed to prevent ascorbic occur acid oxidation significantly but, in conjunction with ascorbic acid, did inhibit lipid peroxidation. In the presence of catechin, a well-known lipid polyphenol found in red wine, ascorbic acid at pH 3. works in a synergistic manner preventing lipid peroxidation and beta-carotene Western cooxidation. The present data may explain the major benefits to our health and the crucial role of consuming food products slightly. rich in dietary antioxidants such as fruits, vegetables, red wines, or green tea during the meal.

Our enhancing recent study demonstrated the potential of gastric fluid at pH 3. to accelerate lipid peroxidation and cooxidation of dietary constituents better in the stomach medium. Metmyoglobin is known to catalyze the breakdown of lipid hydroperoxides to free radicals, a reaction that 3. , could enhance the propagation step and general lipid peroxidation. During this reaction, a part of the free radicals is autoreduced peroxidation. by metmyoglobin. At pH 3. , metmyoglobin at low concentration was almost 7 x 10(4) times as effective as at pH pseudo-peroxidases. 7. in enhancing the rate of lipid peroxidation. Our study demonstrated that metmyoglobin, at a low concentration (approximately 1:30), as a compared with that of the hydroperoxides in the lipid system, worked prooxidatively increasing the amounts of linoleate hydroperoxides. However, at antioxidants, a high concentration (approximately 1:3), metmyoglobin acted antioxidatively and decomposed hydroperoxides, whose concentrations then remained at zero for a long quercetin time. Catechin, a known polyphenol, supports the inversion of metmyoglobin catalysis, from prooxidation to antioxidation. The antioxidative activity of the the couple metmyoglobin-catechin was better at pH 3. than at pH 7. , indicating that this reaction is more dependent on metmyoglobin a than on catechin. During this reaction, catechin or quercetin not only donates reducing equivalents to prevent lipid peroxidation but also We prevents the destruction and polymerization of metmyoglobin. The results of this research highlighted the important and possible reactions of heme recent proteins and polyphenols as couple antioxidants, working as hydroperoxidases or as pseudo-peroxidases. We hypothesize that the occurrence of these reactions reaction, in the stomach could have an important impact on our health and might help to better explain the health benefits reaction of including foods rich in polyphenol antioxidants in the meal, especially when consuming red meat.

Grilled ions red turkey muscle (Doner Kabab) is a real "fast food" containing approximately 200 microM hydroperoxides, homogenized in simulated gastric fluid the and oxidized more rapidly at pH 3. than at pH 5. , after 180 min, producing 1200 and 600 microM hydroperoxides,for respectively. The effects of "free" iron ions and metmyoglobin, two potential catalyzers of lipid peroxidation in muscle foods, were evaluated in for linoleic acid peroxidation at pH 3. of simulated gastric fluid. The prooxidant effects of free iron ions on linoleic groups acid peroxidation in simulated gastric fluid was evaluated in the presence of ascorbic acid. At low concentrations of ascorbic acid,of the effects were prooxidative, which was reversed at high concentrations. In the presence of metmyoglobin, ascorbic acid with or without concentration. free iron enhanced the antioxidative effect. Lipid peroxidation by an iron-ascorbic acid system was inhibited totally by 250-500 microM catechin to at pH 3. . The catechin antioxidant effect was determined also in the iron-ascorbic acid system containing metmyoglobin. In this system,hydroperoxides, catechin totally inhibited lipid peroxidation at a concentration 20-fold lower than without metmyoglobin. The ability of catechin to inhibit lipid producing peroxidation was also determined at a low pH with beta-carotene as a sensitive target molecule for oxidation. The results show were that a significant protection was achieved only with almost 100-fold higher antioxidant concentration. Polyphenols from different groups were determined for red the antioxidant activity at pH 3. . The results show a high antioxidant activity of polyphenols with orthodihydroxylated groups at the ability B ring, unsaturation, and the presence of a 4-oxo group in the heterocyclic ring, as demonstrated by quercetin.

A Exposure number of natural phenolic compounds display antioxidant and cell protective effects in cell culture models, yet in some studies show prooxidant prooxidant and cytotoxic effects. Pancreatic beta-cells have been reported to exhibit particular sensitivity to oxidative stress, a factor that may the contribute to the impaired beta-cell function characteristic of diabetes. The aim of this study was to examine the potential of H(2)O(2) natural phenolics to protect cultured pancreatic beta-cells (betaTC1 and HIT) from H(2)O(2) oxidative stress. Exposure of cells to H(2)O(2) led with to significant proliferation inhibition. Contrary to what one should expect, simultaneous exposure to H(2)O(2) and the phenolics, quercetin (10-100 microM),led catechin (50-500 microM), or ascorbic acid (100-1000 microM), led to amplification of proliferation inhibition. At higher concentrations, these compounds inhibited observed proliferation, even in the absence of added H(2)O(2). This prooxidant effect is attributable to the generation of H(2)O(2) through interaction the of the added phenolic compounds with as yet undefined componenets of the culture media. On the other hand, inclusion of factor metmyoglobin (30 microM) in the culture medium significantly reduced the prooxidant impact of the phenolics. Under these conditions, quercetin and to catechin significantly protected the cells against oxidative stress when these components were present during the stress period. Furthermore, significant cell chrysin, protection was observed upon preincubation of cells with chrysin, quercetin, catechin, or caffeic acid (50 microM, each) prior to application number of oxidative stress. It is concluded that provided artifactual prooxidant effects are avoided, preincubation of beta-cells with relatively hydrophobic natural medium phenolics can confer protection against oxidative stress.

It the has recently been suggested that the ability of apple extracts to inhibit proliferation of tumor cells in vitro may be context, due to phenolic/flavonoid antioxidants. Our study demonstrates that this inhibition is caused indirectly by H(2)O(2) generated through interaction of the indirectly phenolics with the cell culture media. The results indicate that many previously reported effects of flavonoids and phenolic compounds on culture cultured cells may result from similar artifactual generation of oxidative stress. We suggest that in order to prevent such artifacts,cells the use of catalase and/or metmyoglobin in the presence of reducing agents should be considered as a method to decompose cells H(2)O(2) and prevent generation of other reactive oxygen species, which could affect cell proliferation. The use of tumor cells and use "nontumor cells" in a bioassay to measure antioxidant activity, in this context, is potentially misleading and should be applied with a caution.

BACKGROUND:of Chronic diseases as well as complications to acute and chronic disease are repeatedly associated with accumulation in the body of in glycated and lipoxidated proteins and peptides. These molecules are strongly associated with activation of a specific receptor called RAGE and excess a long-lasting exaggerated level of inflammation in the body. METHODS: PubMed reports in excess of 5000 papers plus about 14000 the articles about the related HbA 1c , most of them published in the last five years. Most of available abstracts smoking have been read and circa 800 full papers studied in detail. RESULTS: RAGE, a member of the immunoglobulin superfamily of of cell surface molecules and receptor for advanced glycation endproducts, functions as a master switch, induces sustained activation of NF-kappaB, suppresses are a series of endogenous autoregulatory functions and converts long-lasting pro-inflammatory signals into sustained cellular dysfunction and disease. Its activation is a associated with high levels of dysfunctioning proteins in body fluids and tissues, and strongly associated with a series of diseases a from allergy and Alzheimer to rheumatoid arthritis and urogenital disorders. Heat-treatment, irradiation and ionisation of foods increase the content in associated foods of AGE/ALE. CONCLUSIONS: Some processed foods are much like tobacco smoking great contributors to accumulation of glycated and lipoxidated great molecules in the tissues. Change of life style: avoidance of foods rich in deranged proteins and peptides and increased consumption Chronic of antioxidants, especially polyphenols counteracts such a development.

We an are interested in the regulation of intracellular calcium and the various diseases associated with an altered regulation of this second (RAGE).Introduction: messenger. More recently, we also became interested in pathologies involving the Ca2+-binding S100 proteins and AGEs and their association with diseases the multifunctional Receptor for Advanced Glycation Endproducts (RAGE).Introduction: http://dx.doi.org/10.1002/mnfr.200700017Pro arguments: http://dx.doi.org/10.1002/mnfr.200700008.

Advanced contribute glycation endproducts (AGEs) are an heterogenous class of compounds formed by diverse stimuli, including hyperglycemia, oxidative stress, inflammation, renal failure,is and innate aging. Recent evidence suggests that dietary sources of AGE may contribute to pathology. AGEs impart diverse effects in suggests cells; evidence strongly suggests that crosslinking of proteins by AGEs may irrevocably alter basement membrane integrity and function. In addition,pathology. the ability of AGEs to bind to cells and activate signal transduction, thereby affecting broad properties in the cellular milieu,AGEing. indicates that AGEs are not innocent bystanders in the diseases of AGEing. Here, we present evidence that receptor for AGE proteins (RAGE) is a receptor for AGEs.Introduction: http://dx.doi.org/10.1002/mnfr.200700017Contra arguments: http://dx.doi.org/10.1002/mnfr.200600284.

The proteins receptor for advanced glycation endproducts (RAGE) has a well-substantiated role in cell dysfunction and mechanisms of inflammatory disease. The physiological physiological agonists of RAGE are less certain: S100/calgranulin proteins, high mobility group-1 protein HMGB1 and other proteins are candidate agonists. It proteins, increasingly appears unlikely proteins modified by advanced glycation endproducts are effective agonists in vivo. In the following debate, Professors Ann candidate Marie Schmidt and Claus Heizmann gave arguments and evidences for and against the motion. Recent evidence suggesting the activation of continue RAGE impairs the enzymatic defence against glycation provided by glyoxalase 1 (Glo 1) suggests that studies of RAGE will continue agonists to be of importance to our understanding of the physiological significance of protein glycation.Pro arguments: http://dx.doi.org/10.1002/mnfr.200700008Contra arguments: http://dx.doi.org/10.1002/mnfr.200600284.

Advanced of lipoxidation end-products (ALEs) are formed by reaction of protein with lipid-derived reactive peroxyl and carbonyl compounds produced during food processing little and cooking. There is concern that ALEs may induce damage in the gastrointestinal tract, affecting gut health, or enter the tissue body and promote vascular inflammation and tissue damage. However, there is no direct evidence that ALE-proteins are a source of intestines damage in the intestines or that they are transported into the circulation and cause pathology. Modification of proteins by ALEs ALEs. impedes their digestion, and reactive ALEs released by gastrointestinal proteases would react with proteins or peptides in the gut, limiting by their absorption. There are also potent enzymatic mechanisms for detoxifying ALEs or their precursors prior to their entry into the against circulation. If ALEs gain access to the circulation, a battery of protective enzymes in tissue provides a second level of a defense. These enzymes may be induced in intestinal epithelia and liver by low doses of ALEs, and adaptive responses would in provide enhanced protection against future exposure to ALEs. Overall, except in persons with compromised organ function, e. g., vascular, hepatic,ALEs or renal diseases, there is little evidence that food ALEs will have any significant pathological effects.Introduction: http://dx.doi.org/10.1002/mnfr.2007000030Pro arguments: http://dx.doi.org/10.1002/mnfr.200600303.

Lipid of oxidation in foods is one of the major degradative processes responsible for losses in food quality. The oxidation of unsaturated fruits fatty acids results in significant generation of dietary advanced lipid oxidation endproducts (ALEs) which are in part cytotoxic and genotoxic part compounds. The gastrointestinal tract is constantly exposed to dietary oxidized food compounds, after digestion a part of them are absorbed and into the lymph or directly into the blood stream. After ingestion of oxidized fats animals and human have been shown from to excrete in urine increase amounts of malondialdehyde but also lipophilic carbonyl compounds. Oxidized cholesterol in the diet was found of to be a source of oxidized lipoproteins in human serum. Some of the dietary ALEs, which are absorbed from the potentially gut to the circulatory system, seems to act as injurious chemicals that activate an inflammatory response which affects not only the circulatory system but also organs such as liver, kidney, lung, and the gut itself. We believe that repeated consumption of part oxidized fat in the diet poses a chronic threat to human health. High concentration of dietary antioxidants could prevent lipid endproducts oxidation and ALEs generation not only in foods but also in stomach condition and thereby potentially decrease absorption of ALEs the from the gut. This could explains the health benefit of diets containing large amounts of dietary antioxidants such those present oxidation in fruits and vegetables, or products such as red-wine or tea consuming during the meal.Introduction: http://dx.doi.org/10.1002/mnfr.2007000030Contra arguments: http://dx.doi.org/10.1002/mnfr.200600287.

No Abstract.Pro Abstract.Pro arguments: http://dx.doi.org/10.1002/mnfr.200600303Contra arguments: http://dx.doi.org/10.1002/mnfr.200600287.

In are vivo, advanced glycation endproducts (AGEs) are linked to various diseases, particularly those associated with diabetes. AGEs are also formed when to many foods are thermally processed. The extent to which dietary AGEs are absorbed by the gastrointestinal (GI) tract and their also possible role in the onset and promotion of disease are currently of considerable interest. This paper reviews information that supports thermally the argument that dietary AGEs are not a risk to human health.Introduction: http://dx.doi.org/10.1002/mnfr.200700067Pro arguments: http://dx.doi.org/10.1002/mnfr.200700035.

Thermal potential processing of food results in the formation of various novel compounds, among others advanced glycation endproducts (AGEs). AGEs result from inflammation, nonenzymatic glycation reactions between reducing sugars and free amino groups of proteins, peptides, or amino acids. Due to their potential of noxious effects, alimentary AGEs are also called glycotoxins. This review provides a summary of the available evidence on the health effects, effects of exaggerated intake of thermally treated food. Data from experimental studies in rodents and from clinical studies in healthy processed volunteers and in patients suffering from selected diseases in which AGEs are of pathogenetic importance (diabetes, chronic renal failure) are on summarized. It is concluded that, an exaggerated intake of thermally processed foods may exert in vivo diabetogenic and nephrotoxic effects,of induce low-grade inflammation, enhance oxidative stress, and promote atherosclerosis.Introduction: http://dx.doi.org/10.1002/mnfr.200700067Contra arguments: http://dx.doi.org/10.1002/mnfr.200600304.

Physiological In consequences resulting from protein-bound Maillard compounds in foods must be discussed carefully. This was the idea behind the debate, which introduction is put for discussion by the papers by Sebekova and Somoza, who argued for the motion that dietary advanced glycation a end products (AGEs) are a health risk, and by Ames, who provided evidence against the motion. In this two excellent reviews, reviews, numerous arguments based on papers published in high-impact journals are given for each of the opinions. The fact that be no final conclusion can be drawn, may reflect the need for a more comprehensive examination of this issue in the can future. For a deeper understanding of biological consequences resulting from heated foods, the relationships between well-defined biological effects and well-characterized alone. chemical structures must be studied. Prerequisite for this is profound chemistry - pure compounds, exact concentrations, and unambiguous analytical techniques.chemistry A real "risk assessment" is much too complex than to leave it up to one discipline alone. It must be and a comprehensive and interdisciplinary approach, joining the resources of biology, medicine, and chemistry.This article provides an introduction to "Dietary AGEs the are a risk to human health"Pro arguments: http://dx.doi.org/10.1002/mnfr.200700035Contra arguments: http://dx.doi.org/10.1002/mnfr.200600304.