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Selenium is also in volved in thyroid function buy 5mg altace overnight delivery hypertension 5 mg, T cell immunity purchase altace 5mg online heart attack pain, and spermatogenesis [28] trusted altace 10 mg pulse pressure cardiac output, and is a competitive antagonist of potentially carcinogenic heavy metals such as arsenic and cadmium [30] purchase altace 2.5mg without prescription normal pulse pressure 60 year old. Vitamin E is a fat-soluble vitamin known for its antioxidant capacity that is why it is well known as a lipophilic antioxidant that protects membranes from being oxidatively damaged as an electron donor to free radicals [32]. It is well known that all forms of vitamin E are lipid soluble they easily absorbed from the intestinal lumen after dietary intake via micelles created by biliary and pancreatic secretions [34-35]. Vitamin E is then incorporated into chylomicrons and secreted into the circulation where, transported by various lipoproteins, it travels to the liver [36]. Plasma -tocopherol 422 Oxidative Stress and Chronic Degenerative Diseases - A Role for Antioxidants concentrations in humans range from 11 to 37 mol/L, whereas -tocopherol are between 2 and 5 mol/L. The liver plays a central role in regulating -tocopherol levels by directly act ing on the distribution, metabolism, and excretion of this vitamin [37]. This protein facilitates secretion of -toco pherol from the liver into the bloodstream, by acquiring it from endosomes and then deliv ering it to the plasma membrane where it is released and promptly associates with the different nascent lipoproteins [39]. Plasma concentration of vitamin E depends completely on the absorption, tissue delivery, and excretion rate. The estimated -tocopherol half-life in plasma of healthy individuals is ~ 48 to 60 H, which is much longer than the half-life of - tocopherol approximately 15 H. These kinetic data underscore an interesting concept that while -tocopherol levels are maintained, the other forms of vitamin E are removed much more rapidly [40]. The list of clinical disorders expected to be influenced by Se deficiency is rapidly growing with time. Some selected issues regarding the role of Se in health and disease have been briefly out lined as follows: 2. Se and antioxidant activity Selenocysteine is recognized as the 21st amino acid, and it forms a predominant residue of selenoproteins and selenoenzymes in biological tissues. The molecular structure of seleno cystiene is an analogue of cysteine where a sulphur atom is replaced by Se. Even though Se and sulphur share some similar chemical properties, there are also some differences. In the body, both or ganic [selenocysteine(SeCys) and selenomethionine (SeMet)] and inorganic (selenite, selen ate) Se compounds are readily metabolized to various forms of Se metabolites [41]. H Se is further metabolized and in2 volved in the formation of methylselenol and dimethylselenide, which are exhaled or secret ed via the skin. Selenium is also excreted in urine as trimethylselenonium ion and selenosugar compounds [42]. The selenoproteins are classified on the basis of their biologi cal function [25]. The other essen tial antioxidant selenoenzymes are the thioredoxin reductase (TrxR) where they use thioredoxin (Trx) as a substrate to maintain a Trx/TrxR system in a reduced state for remov al of harmful hydrogen peroxide and there are three types of TrxR. Se and depression In [46] selenium s function as an antioxidant, and as a constituent of selenoproteins that are important in redox homeostasis, warrants further investigation as a risk factor for depres sion, and suggest a potentially novel modifiable factor in the primary prevention and man agement of depression. Depression is becoming recognized as an inflammatory disorder, accompanied by an accumulation of highly reactive oxygen species that overwhelm usual defensive physiological processes [47-51]. During times of selenium deficiency, there is preferential storage of selenium in the brain [52]. Selenium has significant modulatory effects on dopamine [53] and dopamine plays a role in the pathophysiology of depression and other psychiatric ill nesses [54]. Diminished levels of selenium in the brain are associated with cognitive decline [55] and Alzheimer s disease [56]. Selenium supplementation has been linked with improve ments in mood [57] and protection against postpartum depression [58]. What is unclear is if low dietary selenium is a risk factor for the development of depression. Alterations in redox biology are established in depression; however, there are no prospec tive epidemiological data on redox-active selenium in depression. It is known that seleni um s function as an antioxidant, and as a constituent of selenoproteins that are important in redox homeostasis, warrants further investigation as a risk factor for depression, and sug gest a potentially novel modifiable factor in the primary prevention and management of de pression. The reasons for the high prevalence and severity of this condition or the increased prevalence of asthma over the last 20 years are not well understood. One of a number of environmental factors that have been proposed as a reason for the escalation in asthma prevalence is a decreasing intake of dietary antioxidants [60]. Selenium has been implicated in inflammation by reducing the severity of the inflammatory response through modulation of the pro-inflammatory leu kotrienes, important mediators of acute asthmatic reactions as well as sustaining the inflam matory process causing a late allergic reaction metabolism [62]. Evidence from randomized controlled trials [63] and basic mechanistic work investigating the effect of selenium on markers of inflammation and oxidative stress [62]. Evidences have supported a protective role for selenium in asthma, although other studies have not [64-66]. However, there was a modest association between lower plasma selenium and whole blood glutathione peroxidase activity and higher incidence of persistent wheeze [67]. Selenium in preventing oxidative stress The reactivity of organoselenium compounds [22,68] characterized by high nucleophilicity and antioxidant potential, and provides the basis for their pharmacological activities in mammalian models. Organochalcogens have been widely studied given their antioxidant activity, which confers neuroprotection, antiulcer, and antidiabetic properties. Given the complexity of mammalian models, understanding the cellular and molecular effects of orga nochalcogens has been hampered. In reference [69] the nematode worm Caenorhabditis ele gans is an alternative experimental model that affords easy genetic manipulations, green fluorescent protein tagging, and in vivo live analysis of toxicity. Manganese (Mn)-exposed worms exhibit oxidative-stress-induced neurodegeneration and life-span reduction. These physiological conditions could be food deprivation [70], and iodine and/or selenium (Se) deficiency [71,72] and antithyroid drugs [73] affects bone maturation. Selenium is an important protective ele ment that may be used as a dietary supplement protecting against oxidative stress, cellular damage and bone impairments [74]. Since the beginning of the pandemic in 1981, over 25 million people are estimated to have died from the disease [75]. It is currently a leading cause of death in many parts of the world, and a disease that disproportionately affects the marginalized and socially disadvantaged. There is a historical record showing that organoselenium compounds can be used as antivi ral and antibacterial agents. Selenium in the brain In addition to the well-documented functions of Se as an antioxidant and in the regulation of the thyroid and immune function [80]. Recent advances have indicated a role of Se in the maintenance of brain function [81]. Selenium is widely distributed throughout the body, but is particularly well maintained in the brain, even upon prolonged dietary Se deficiency [82].

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Oxidative stress induces insulin resistance by activating the nuclear factor-kappa B pathway and disrupting normal subcellular distribution of phosphatidylinositol 3- kinase altace 10mg discount prehypertension eyes. Proposed mechanisms for the induction of in sulin resistance by oxidative stress buy generic altace 10mg line blood pressure kits stethoscope. Relation between antioxidant enzyme gene expression and antioxidative defense status of insulin-producing cells cheap altace 5 mg online prehypertension 126. Glucose toxicity in beta-cells: type 2 diabetes discount 10 mg altace otc blood pressure emergency room, good radicals gone bad, and the glutathione connection. Activation of the hexosamine pathway leads to deterioration of pancreatic be ta-cell function through the induction of oxidative stress. Regulation of beta cell glucokinase by S-nitrosy lation and association with nitric oxide synthase. Glucose-induced changes in protein kinase C and ni tric oxide are prevented by vitamin E. Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. Hexosamine pathway is responsible for inhibition by diabetes of phenylephrine-induced inotropy. Vitamins D, C, and E in the prevention of type 2 diabetes mellitus: mod ulation of inflammation and oxidative stress. Biologic activity of carotenoids re lated to distinct membrane physicochemical interactions. Increased risk of non-insulin dependent diabetes mellitus at low plasma vitamin E concentrations: a four year follow up study in men. Low plas ma ascorbate levels in patients with type 2 diabetes mellitus consuming adequate di etary vitamin C. Advances in diabetes for the millennium: vitamins and oxidant stress in diabetes and its complications. Cardio-renal syndrome (or reno-cardiac syndrome, the prefix depending on the primary failing organ) is becoming increasingly recognised [2]. Conventional treatment targeted at either syndrome generally reduces the onset or progression of the other [3]. Pathogenesis of chronic kidney and cardiovascular disease The links It is, in fact, very difficult to separate these chronic diseases, because one is a complication of the other in many situations. Prevention and treatment of these diseases are major aims in health systems worldwide. However, no matter the cause, the progres sive structural changes that occur in the kidney are characteristically unifying [10]. Alterations in the glomerulus include mesangial cell expansion and contraction of the glomerular tuft, fol lowed by a proliferation of connective tissue which leads to significant damage at this first point of the filtration barrier. Hypertension induces intimal and medial hypertrophy of the intrarenal arteries, leading to hypertensive nephropathy. This is followed by outer cortical glomerulosclerosis with lo cal tubular atrophy and interstitial fibrosis. Compensatory hypertrophy of the inner-cortical glomeruli results, leading to hyperfiltration injury and global glomerulosclerosis. The first two stages have normal, or slightly reduced kidney function but some indication of structural deficit in two samples at least 90 days apart. Stages 3-5 are considered the most concerning, with Stage 3 now being sub-classified into Stages 3a and b because of their diagnostic impor tance. Common themes for causality are oxidative stress and inflammation, be they local or systemic. Left ventricular hypertrophy and myocardial fibrosis also predispose to an increase in electric excitability and ventricular arrhythmias [16]. These ob servations have sparked added interest in the mechanisms of the chronic diseases, and in ways to target these mechanisms with additional therapies, such as antioxidants. Inflammation and chronic kidney and cardiovascular disease The circulating nature of many inflammatory mediators such as cytokines, and inflammato ry or immune cells, indicates that the immune system can act as a mediator of kidney-heart cross-talk and may be involved in the reciprocal dysfunction that is encountered commonly in the cardio-renal syndromes. There are many links with visceral obesity and with increased secretion of inflammatory mediators seen in visceral fat [15]. Proinflam matory cytokines are produced by adipocytes, and also cells in the adipose stroma. The links with oxidative stress as an endogenous driver of the chronic diseases become immedi ately obvious when one admits the close association between oxidative stress and inflamma tion. The characteristics of dyslipidaemia (elevated serum triglycerides, elevated low- density lipoprotein cholesterol, and/or low high-density lipoprotein cholesterol) are also often seen in obese patients and these are all recognized as risk factors for atherosclerosis. An improved understanding of the precise mo lecular mechanisms by which chronic inflammation modifies disease is required before the full implications of its presence, including links with persistent oxidative stress as a cause of chronic disease can be realized. Oxidative stress arises from alterations in the oxidation-reduction balance of cells. The simple oxidant imbalance theory has now grown to incor porate the various crucial pathways and cell metabolism that are also controlled by the in terplay between oxidants and antioxidants [23-27]. The rationale for antioxidant therapies lies in restoring imbalances in the redox environment of cells. Agreement on the role of oxidative stress in the pathogenesis of chronic disease is, however, not complete. Oxidants are involved in highly conserved basic physiological processes and are effectors of their downstream pathways [41, 42]. The specific mechanisms for oxidative stress are difficult to define because of the rapidity of oxidant signalling [31]. For example, protein tyrosine phosphatases are major targets for oxidant signalling since they contain the amino acid residue cysteine that is highly susceptible to oxidative modification [43]. This may indicate the induction of free radicals in response to receptor ac tivation by a cognate ligand in a process that is similar to phosphorylation cascades of intra cellular signalling. However, adequate lev els of both are likely to be vital for normal cell function. There is no evidence to indicate that glutathione synthesis occurs within mitochondria, however the mitochondria have their own distinct pool of glutathione required for the formation of Gpx [50]. Many of these proteins are known to interact with each other, forming re dox networks that have come under investigation for their contribution to dysfunctional oxidant pathways. Mitochondrial-specific isoforms of these proteins also exist and include Grx2, Grx5, Trx2 and Prx3 [52-54], which may be more critical for cell survival compared to their cystolic counterparts [50]. Intracellular synthesis of glutathione from amino acid derivatives (glycine, glutamic acid and cysteine) accounts for the majority of cellular glutathione compared with extracellular glutathione uptake [56]. Oxidative stress and transcriptional control The role of oxidative stress in upstream transcriptional gene regulation is becoming increas ingly recognised. Not only does this provide insight into the physiological role of oxidative stress, but presents regulatory systems that are possibly prone to deregulation.

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A role for nuclear transport of truncated huntingtin is further suggested by evidence that preventing nuclear entry of mutated huntingtin protects tranfected primary neurons in culture buy 10mg altace visa hypertension with stage v renal disease, whereas preventing aggregation does not (Saudou et al generic altace 5 mg free shipping fetal arrhythmia 37 weeks. An impor- tant conclusion from these studies is that proteolytic processing of huntingtin appears to be critical for the disease process quality altace 10 mg blood pressure medication images. This is further supported by the results of in vitro studies that show an increased toxicity of smaller compared to larger huntingtin fragments in transfected cells (see below) altace 5 mg discount hypertension life expectancy. Transgenic mice expressing huntingtin 1 171 with 82 glutamine repeats do not show any increase in indices of oxidative stress (Schilling et al. It is possible, however, that the increased resistance to excitotoxicity observed in the R6/1 mice is the result of the development of compensatory mechanisms in vivo. The analysis of excitotoxicity and sensitivity to oxida- tive stress in mice is complicated by the fact that different strains show marked differences in sensitivity (Alexi et al. These changes clearly precede overt neuronal death and perhaps even the onset of neurological symptoms. Importantly, these effects are not the result of the massive loss of striatal or cortical neurons at this age, suggesting a selective neuronal dysfunction (Davies et al. Although this hypothesis has not yet been directly tested at the striato-pallidal synapse, it should be noted that huntingtin is associ- ated with synaptic vesicles and interacts with proteins involved in vesicle trafficking (DiFiglia et al. Normal huntingtin is thought to influence vesicle transport in the secretory and endocytic pathway through association with clathrin-coated vesicles (Velier et al. It is not known whether the polyglutamine expansion in huntingtin alters these functions. However, our recent data suggest that the mutation also causes marked anomalies in the functional properties of striatal and cortical neurons in these mice (Levine et 340 Chesselet and Levine al. In the striatum, this effect was accompanied by a depolarization of the resting membrane and an increase in membrane input resistance. Slices of 6-mo-old mice with 72 repeats showed hyperexcitability and displayed a greater short-term poten- tiation following tetanization. Although paired-pulse facilitation was not affected in 10-mo-old mutant mice, posttetanic potentiation was reduced in these mice. This suggests an impairment of presynaptic release in response to high frequency stimulation. Long-term potentiation was also reduced in one line of knock-in mice (Usdin et al. These cellular deficits could form the basis of the neuronal dysfunction, leading to behav- ioral symptoms at early stages of the disease. It is not possible to evaluate the level of expression of the transgene in these mice for technical reasons. However, other trangenics with a high level of the full-length mutated huntingtin have a milder phenotype. An explanation for this paradox may be provided by in vitro studies that have clearly demonstrated that short huntingtin fragments with expanded polyglutamine repeats are more toxic to neurons than the full-length protein with an identical mutation (Cooper et al. This observation led to the hypothesis that cleavage of huntingtin by proteases is a critical step in the pathophysiology of the disease. Huntingtin can be cleaved by caspase 3, a protease involved in the apoptotic cascade (Wellington et al. Interestingly, the blockade of caspase 1 in transgenic mice delays the onset of motor symptoms, of neurochemical anomalies, and the death of the mice (Ona et al. Noncaspase proteases, however, also seem to be important for the processing of huntingtin. Whether this abnormal processing contributes to the pathophysiology and which proteases are involved, however, remains unknown. Furthermore, few studies have examined the same behavioral, cellular, or molecular effects across several mouse models. Nevertheless, several lines of consistent evidence are emerging from the available comparisons. The mutation seems to induces neuronal dysfunction long before it induces cell death and neuronal dysfunction appears sufficient to induce motor symptoms. Another emerging theme is the importance of protein aggregates, as opposed to nuclear inclusions, at early stages of the disease. Finally, the mouse models are beginning to provide the most sought after infor- mation: a rational approach to the design of new therapies and a way to test them preclinically. In that respect, a critical contribution of the mouse models will be to identify the link between parameters that can be measured in humans (in accessible peripheral tissues or by brain imaging) and the progressive brain pathology. Once validated, these accessible measures will permit great improve- ment in the design of clinical trials, an essential step in bringing the benefit of bench science to the patients. Huntington s Disease Collaborative Research Group (1993) A novel gene contain- ing a trinucleotide repeat that is expanded and unstable in Huntington s disease chromosomes. Expanded glutamine segments in otherwise unrelated pro- teins cause specific neuronal cell loss in each case, suggesting unique pro- tein context-dependent modulation of some intrinsic toxic property of polyglutamine (15 17). One molecular possibility is a glutamine-induced conformational change that alters huntingtin s association with its normal or abnormal protein partners (18,19). Huntingtin-Associated Proteins 349 production, were derived from chemical lesion studies in experimental animals (20 24). Identification of potential huntingtin interactors, however, has not provided direct links to any of these previously proposed models of neurodegeneration (19). This large protein is highly conserved throughout evolution over its entire length, except for the amino-terminal glutamine proline-rich segment (43 47) (Fig. However, the striking identity of the initial 17 amino acids and residues immediately adjacent to the variable segment implies an important biological function for huntingtin s extreme amino-terminus (Fig. Despite its large size, huntingtin shares limited sequence similarity to reported proteins (Fig. These motifs can form a flexible bipartite _-helical structure with intervening loops that may mediate specific protein protein interac- tions, including those involved in nuclear import (48 50). Huntingtin also possesses a putative leucine zipper protein-association domain typically found in proteins that participate in transcription complexes (2,51). Huntingtin is broadly expressed in a variety of peripheral tissues and in the brain, throughout development and in the adult (15,16). In most cells, including neurons, huntingtin is largely a soluble cytoplasmic protein (52 57). However, a portion of the protein decorates microtubules and vesicles (52 57) and is loosely associated with membrane-fractions where it partially colocalizes with markers of endocytic and secretory vesicles (54,55,58). In addition, a small but significant fraction of huntingtin (approx 5%) is found in the nucleus of diverse cell types, suggesting a func- tion in this cellular compartment (59,60). The amino- terminus of huntingtin and its homologs from mouse, rat, and pufferfish (fugu) are aligned to indicate regions of similarity and divergence. Despite striking identity of the flanking residues, the glutamine/proline-rich segment is not conserved through evolution. Huntingtin fragments used as baits in yeast two hybrid screens are depicted as filled bars with the number of independent interactors identified shown below. The asterisk denotes that an interactor was also isolated indepen- dently with a longer bait fragment.

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Phenolic acids may be about one-third of the phenolic compounds in the human s diet [24] buy generic altace 5 mg on-line blood pressure jump. In general best 10mg altace arrhythmia quizzes, the hydroxylated cinnamic acids are more effective than their benzoic acids counterparts [16] generic altace 10mg without a prescription blood pressure chart vaughns 1 pagers com. Despite the antioxidant activity of phenolic compounds and their possible benefits to human health generic 2.5mg altace with visa arteria etmoidal anterior, until the beginning of the last decade, most studies on these substances occurred in relation to their deleterious effects. Although phenolic compounds are traditionally considered antinutrients, and until the moment as non-nutrients because deficiency states are unknown for them, in recent years they have been seen as a group of micro-nutrients in the vegetable kingdom, which are important part of human and animal diet. Researches have also suggested that regular consumption of phenolic compounds directly from plant foods may be more effective in combating oxidative damage in our body than in the form of dietary supplement [26]. This can be explained by the possible synergistic inter actions among food phenolic compounds, increasing the antioxidant capacity of these sub stances.. This way, the content of phenolic compounds and the antioxidant power of a wide variety of plant foods have been investigated. Sources and their antioxidant power Table 1 shows the mean content of total phenolic compounds (mg/ 100 g of sample) of some plant foods. As can be seen in Table 1, phenolic compounds are widely distributed in plant foods. It is known that the abundant phenolic com pounds in red wine are anthocyanin [6, 52]. The green and black teas have been extensively studied, since they may contain up to 30% of their dry weight as phenolic compounds [53]. It has about 7% of the dry weight of the grains [24] and 15% of the dry instant coffee as phenolic compounds [54]. Although in some studies a few statistically significant correlations were found between the levels of total phenolic compounds and antioxidant power of foods, in others the total phe nolics content of samples was highly correlated with the antioxidant capacity. On the other hand, there are still no standard methods and approved for determining the antioxidant power in vitro. The several available tests for this purpose involve different mechanisms of antioxidant defense system, from the chelation of metal ions to the measure of preventing oxidative damage to biomolecules, and offer distinct numerical results that are difficult to compare. In both the methods applied the antioxidant capacity of the fractions of oats was in the following order: pearl ings > flour > trichome = bran. It was concluded through this study that a part of oat antioxi dants, which is rich in phenolic compounds [29], is probably heat-labile because greater antioxidant power was found among the non-steam-treated pearlings. In another study, ten varieties of soft wheat were compared as to their content of total phenolic compounds and antioxidant capacity [30]. On the other hand, searching the antioxidant capacity of vegetables in the genus Brassica and the best solvent (ethanol, acetone and methanol) for the extraction of their phenolic compounds [56], the results showed that the solvent used significantly affects the phenolics content and the properties of the studied extract. Methanolic extract showed the largest con tent of total phenolics of broccoli, Brussels sprouts, and white cabbage. In this study, the an tioxidant power of the samples was confirmed by different reactive oxygen species and showed to be concentration-dependent. Kale extracts have also been evaluated as to their content of total phenolic compounds and antioxidant capacity [33]. Herbs and spices are of particular interest, since they have been proved to have high content of phenolic compounds and high antioxidant capacity. A positive linear relationship was found between the content of total phenolic compounds and the antioxidant power of samples. This study concluded that basils have valuable antioxidant properties for culinary and possible medical application. The results obtained showed that hydrolyzed and non hydrolyzed extracts of black pepper contained significantly more phenolic compounds when compared with those of white pepper. A dose-dependent effect was observed for all extracts concerning the power of removing free radical and reactive oxygen species, the black pepper extracts being the most effective. This study concluded that the pepper, especially black, which is an important com ponent in the diet of many sub-Saharan and Eastern countries due to its nutritional impor tance, can be considered an antioxidant and radical scavenging. However, evaluating the content of phenolic compounds and antioxidant capacity of 14 herbs and spices [37], al though a significant correlation has been obtained between the phenolics content and anti oxidant capacity of samples, it was found that the trend of the antioxidant capacity was different according to the method applied. This study concluded that the antioxidant power of plant samples should be interpreted with caution when measured by different methods. In spite of that fact, regardless of the method used, the samples were rich in antioxidants. In addition to the studies already mentioned, the antioxidant capacity of 36 plant extracts was evaluated by the -carotene and linoleic acid model system [31] and the content of total phenolic compounds of the extracts was determined. The antioxidant capacity calculated as percentage of oxida tion inhibition ranged from a maximum of 92% in turmeric extracts to a minimum of 12. The antioxidant power of the samples significantly and positively correlated with their content of total phenolic compounds, allowing the conclusion that the plant foods with high content of phenolic com pounds can be sources of dietary antioxidants. The results showed that the antioxidants composition and concentra tion varied significantly among the different vegetables. The coriander, Chinese kale, water spinach and red chili showed high content of total phenolics and high antioxidant power. Due to the growing recognition of their nutritional and therapeutic value, many fruits have also been investigated as to their content of phenolic compounds and antioxidant capacity. By evaluating the antioxidant capacity and total phenolics content, in addition to flavanol and monomeric anthocyanins, it was found from the flesh and peel of 11 apple cultivars [57] that the concentrations of the parameters investigated differed significantly among the culti vars and were higher in the peel in comparison to the flesh. The content of total phenolics and antioxidant capacity were significantly correlated in both flesh and peel. It was conclud ed that the contribution of phenolics to the antioxidant power in apple peel suggests that peel removal may induce a significant loss of antioxidants. It is also known that one of the most important sources of antioxidants among fruits is small red fruits. However, significant differences were found in the total phenolics content among the differ ent cultivars and growing seasons. Despite this, the studied cultivars showed high antioxi dant power, which was highly correlated with the samples phenolic compounds. However, the cultivars analyzed showed high antioxidant capacity, which was correlated with the phenolic compounds found in them. In this study significant increases were also found in the content of total phenolic compounds and antioxidant power during the ripen ing of fruits. Additionally, different solvents were applied for comparing the antioxidant ca pacity and the yield of total phenolic compounds present in the extracts of sour and sweet cherries [40]. It was found that the solubility of phenolic compounds was more effective in extracts of sweet cherries with use of methanol at 50% and in extracts of sour cherries with the use of acetone at 50%. Extracts from lyophilized sour cherries (methanolic and acetone water-mixtures) presented in average twice as high phenolic compounds than ethanolic ex tracts. It was concluded in this work that the strong antioxidant power of extracts of sour cherries is due to the substantial amount of total phe nolic compounds present in them and that the fresh sour cherry can be considered as a good dietary source of phenolic compounds. The total phenolics content, total monomeric antho cyanins and antioxidant capacities of 14 wild red raspberry accessions were also examined [59].

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