Juana Benedí
Complutense University of Madrid
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Publication
Featured researches published by Juana Benedí.
Journal of Medicinal Food | 2009
Aránzazu Bocanegra; Sara Bastida; Juana Benedí; Sofía Ródenas; Francisco J. Sánchez-Muniz
While marine algae have traditionally formed part of the Oriental diet, their major use in Western countries has been in the phytocolloid industry. Only a few coastal communities outside Asia have customarily used seaweeds as components of special dishes. Of late, however, seaweeds have gained importance as foodstuffs in Western countries and most recently as components of functional foods because of their high dietary fiber, mineral, vitamin, and phytochemical content, low energy levels, and high concentrations of certain polyunsaturated fatty acids. The present paper reviews the available data for some of the components of the major edible algae and studies several factors that can affect their physiochemical properties (e.g., hydration, water and oil-holding capacity, fermentability, binding capacity, etc.) and, in turn, their nutritional importance. The effects of marine alga consumption on growth and body weight, mineral availability, lipid metabolism, blood pressure, and antioxidant properties are reviewed, together with preliminary data on the effects of some functional foods containing seaweeds on lipid metabolism and gene expression of enzymes engaged in antioxidant protection. This review concludes with some remarks regarding the danger of the improper use of seaweeds in herbal medications. In addition, as the properties of algae are highly dependent on their individual composition, any generalization regarding these properties may be considered misleading and scientifically inappropriate.
Immunology Letters | 2008
Paloma Bermejo; Sagrario Martín-Aragón; Juana Benedí; Cristina Susín; Emanuela Felici; Pedro Gil; José Manuel Ribera; Ángel Mª Villar
Multiple pathogenic factors may contribute to the pathophysiology of Alzheimers disease (AD). Peripheral markers have been used to assess biochemical alterations associated with AD and mild cognitive impairment (MCI) involved in its pathophysiology. The present study was conducted to evaluate inflammatory peripheral markers in elderly patients with MCI, patients with AD and normal elderly subjects. We measured plasma levels of different cytokines (IL-6, TNF-alpha and IFN-alpha) and platelet levels of cyclooxigenase-2 (COX-2) from 34 patients with MCI, 45 patients with AD and 28 age-matched control subjects. MCI and AD patients showed similarities in TNF-alpha and COX-2 levels, and differences in IL-6 and INF-alpha. Whereas augmented IL-6 levels have been found in AD patients, a significant increase in INF-alpha has been detected only in patients with MCI possibly associated with the depression stage frequently found in cognitive impairment. In conclusion, inflammatory response may be an early factor in AD development and these changes in circulating markers are possibly related to the progression of MCI to AD.
Free Radical Research | 2008
Paloma Bermejo; Sagrario Martín-Aragón; Juana Benedí; Cristina Susín; Emanuela Felici; Pedro Gil; José Manuel Ribera; Ángel Mª Villar
There is a great interest in the relationship between Mild Cognitive Impairment (MCI) and the progression to Alzheimers disease (AD). Several studies show the importance of oxidative stress in the pathogenesis of AD. The purpose of this study was the link between oxidative damage, MCI and AD. It analysed protein carbonyls and erythrocyte glutathione system plasma levels of 34 subjects with MCI, 45 subjects with AD and 28 age-matched control subjects. The results showed an increase in protein modification, a decrease in GSH levels and GSH/GSSG ratio in AD and MCI patients compared to age-matched control subjects (p<0.05). The present study shows that some peripheral markers of oxidative stress appear in MCI with a similar pattern to that observed in AD, which suggests that oxidative stress might represent a signal of the AD pathology. AD and MCI are biochemically equivalent. MCI does not necessarily need to progress to AD on a biochemical level.
Life Sciences | 2011
Karim L. Jiménez-Aliaga; Paloma Bermejo-Bescós; Juana Benedí; Sagrario Martín-Aragón
AIMS Quercetin and rutin have been reported to exert numerous pharmacological activities, such as free-radical scavenging, effects on immune and inflammatory cell functions, and could have benefits in Alzheimers disease (AD) by mitigating cellular damage induced by reactive oxygen species (ROS). A key event in AD is the conversion of the β-amyloid (Aβ) peptide into amyloid plaques in the brain. Preventing Aβ aggregation is pursued as a therapeutic strategy for treating AD. In this study, antiamyloidogenic and antioxidant properties of quercetin and rutin were investigated. MAIN METHODS We investigated whether quercetin and rutin affect Aβ25-35 fibrillogenesis, BACE activity and the cellular redox status. KEY FINDINGS Quercetin and rutin inhibited the formation of Aβ fibrils and disaggregated Aβ fibrils. β-secretase enzyme (BACE) activity was significantly inhibited by rutin. To resemble the in vivo Aβ-induced neurotoxicity we used a cell system overexpressing APP Swedish mutation (APPswe), which is associated with early-onset familial AD, and may promote oxidative stress due to the enhanced Aβ production. Quercetin and rutin decreased almost completely ROS generation in H(2)O(2)-treated APPswe cells. Both flavonoids increased intracellular GSH content and the redox status, and for rutin this effect was concentration dependent. Besides, quercetin and rutin diminished the index of lipid peroxidation in comparison with control APPswe cells at all concentrations tested. SIGNIFICANCE Our findings may provide an explanation of the neuroprotective effect of quercetin and rutin, suggesting that they could be dietary phytochemicals able to revert the β-amyloid toxicity in vivo.
European Journal of Pharmacology | 2003
M.Francisca Molina-Jimenez; M.Isabel Sanchez-Reus; Juana Benedí
The purpose of this study was to investigate the potential neuroprotective effects of myricetin (flavonoid) and fraxetin (coumarin) on rotenone-induced apoptosis in SH-SY5Y cells, and the possible signal pathway involved in a neuronal cell model of Parkinsons disease. These two compounds were compared to N-acetylcysteine. The viability of cells was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and cytotoxicity was assayed by lactate dehydrogenase (LDH) released into the culture medium. Parameters related to apoptosis, such as caspase-3 activity, the cleavage of poly(ADP-ribose) polymerase and the levels of reactive oxygen species were also determined. Rotenone caused a time- and dose-dependent decrease in cell viability and the degree of LDH release was proportionally to the effects on cell viability. Cells were pretreated with fraxetin, myricetin and N-acetylcysteine at different concentrations for 30 min before exposure to rotenone. Cytotoxicity of rotenone (5 microM) for 16 h was significantly diminished as well as the release of LDH into the medium, by the effect of fraxetin, myricetin and N-acetylcysteine, with fraxetin (100 microM) and N-acetylcysteine (100 microM) being more effective than myricetin (50 microM). Rotenone-induced apoptosis in SH-SY5Y cells was detected by an increase in caspase-3 activity and in the cleavage of poly(ADP-ribose) polymerase. After exposing these cells to rotenone, a significant increase in reactive oxygen species preceded apoptotic events. Fraxetin (100 microM) and N-acetylcysteine (100 microM) not only reduced rotenone-induced reactive oxygen species formation, but also attenuated caspase-3 activity and poly(ADP-ribose) polymerase cleavage at 16 h against rotenone-induced apoptosis. The effect of fraxetin in both experiments was similar to that of N-acetylcysteine. These results demonstrated the protective action of fraxetin and suggest that it can reduce apoptosis, possibly by decreasing free radical generation in SH-SY5Y cells. Myricetin at 100 microM was without any preventive effect.
Journal of Pharmacy and Pharmacology | 1997
Sagrario Martín-Aragón; Juana Benedí; A. Villar
Fraxetin belongs to an extensive group of natural phenolic antioxidants. We have investigated the modifications in endogenous antioxidant capacity; superoxide dismutase (SOD), catalase (CAT), total and selenium‐dependent glutathione peroxidases (GPx) and glutathione reductase (GR) and stress index; glutathione disulphide (GSSG)/reduced glutathione (GSH) ratio and thiobarbituric acid‐reactive substances (TBARs) in liver and brain supernatants of C57BL/6J male 12‐month‐old mice under fraxetin treatment for 30 days.
Neuropharmacology | 2007
María Isabel Sánchez-Reus; M.A. Gómez del Rio; I. Iglesias; M. Elorza; K. Slowing; Juana Benedí
Since oxidative stress is implicated in the pathophysiology of dementia and depression, this study was designed to investigate the pro-oxidant activity of rotenone, the protective role of standardized extract of Hypericum perforatum (SHP), as well as the mRNA levels of antioxidant enzymes, in brain homogenates of rats following exposure to rotenone and SHP extract. Quercetin in liposomes, one active constituent, was tested in the same experimental conditions to serve as a positive control. The animals received pretreatment with SHP (4 mg/kg) or quercetin liposomes (25 and 100 mg/kg) 60 min before of rotenone injection (2 mg/kg). All treatments were given intraperitoneally in a volume of 0.5 ml/kg body weight, for 45 days. Rotenone treatment increased activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of malondialdehyde (MDA). The content of reduced glutathione (GSH) was decreased due to chronic rotenone treatment. Rotenone significantly induced the gene expression of CuZnSOD, MnSOD; CAT and GPx in brain. In contrast, SHP extract exerted an antioxidant action which was related with a decreased of MnSOD activity and mRNA levels of some antioxidant enzymes evaluated. Liposomal quercetin treatment resulted in a significant preservation of the activities of antioxidant enzymes and a decreased in the mRNA levels of these antioxidant enzymes. One possible mechanism of action of SHP extract may be related to quercetin in protecting neurons from oxidative damage. Therefore standardized extract of H. perforatum could be a better alternative for depressed elderly patients with degenerative disorder exhibiting elevated oxidative stress status.
Gerontology | 1998
Sagrario Martín-Aragón; Juana Benedí; A. Villar
The attempt to retard senescence by environmental manipulation includes the use of nutrients or drugs that decrease the oxidative damage to tissues associated with aging. The effects of esculetin treatment (25 mg/kg, orally for 30 days), a phenolic antioxidant compound, on the glutathione system and lipid peroxidation were examined in liver supernatants from male C57BL/6J mice. The effects of esculetin were compared to treatment with 3,5-di-terc-butyl-4-hydroxytoluene (BHT), a well-known synthetic phenolic antioxidant. Reduced glutathione (GSH) concentration in liver supernatants was only increased significantly in esculetin-treated mice compared to control animals, whereas the concentration of oxidized glutathione (GSSG) was significantly decreased by BHT treatment compared to the control group. The GSSG/GSH ratio was significantly lower in esculetin and BHT groups than in the control group. The decrease in this ratio was greater in BHT-treated mice than in esculetin-treated mice. Increases in glutathione reductase (GR) activity were observed with both treatments, although BHT resulted in a superior induction of this activity compared to esculetin. The extent of decline in the GSSG/GSH ratio was correlated with the increase in GR activity. The formation of thiobarbituric acid-reactive substances (TBARs), an index of stress, was lower following treatment with esculetin and BHT compared to control mice (although not significant). This index was very similar for both treatments. Based on the level of TBARs obtained in this study, the accumulation of lipid peroxides declines when the GSH levels are enhanced or GSSG levels are decreased. Finally, we found similar antioxidant effects in vivo with esculetin and BHT treatments and a decrease in the oxidative damage evaluated. The enhancement of glutathione status following esculetin treatment could be a possible defense strategy for the organism under ‘stress conditions’ and may be related to the delay of age-dependent degenerative disorders.
Journal of The American College of Nutrition | 2007
Amaia Canales; Juana Benedí; Meritxell Nus; Josana Librelotto; José M. Sánchez-Montero; Francisco J. Sánchez-Muniz
Background: A number of recent studies indicate that antioxidants reduce the oxidative stress associated with the development of coronary heart diseases (CHD). Objective: (i) To investigate whether the erythrocyte catalase (CAT), superoxide dismutase (SOD), total glutathione, reduced glutathione (GSH), oxidized glutathione (GSSG), and lipid peroxidation (LPO), and serum uric acid and paraoxonase-1 (PON1) are modified at increased CHD-risk individuals consuming walnut-enriched meat (WM), (ii) to evaluate whether these changes were influenced by basal serum cholesterol, body mass index or smoking habit. Design: The study was a non blinded, cross-over, placebo-controlled trial in which 22 volunteers (60% overweight and 40% obese) with increased CHD-risk were randomly assigned to receive WM or control meat (CM) during two different periods of 5 weeks. Results: A significant interaction time*treatment (p < 0.05) was observed in all enzymes and substrates tested except HDL-C, uric acid and LPO. The treatment significantly increased CAT activity, total glutathione and GSSG (p < 0.05). Significant gender*time*treatment interaction (p = 0.043) for total glutathione was found increasing at the end of the WM period in male but not changing in female. Total glutathione and GSH/GSSG ratio (p < 0.05) were lower in smokers. Hypercholesterolemics presented higher uric acid (p < 0.05) but no enzyme activities or substrate concentrations were different from those of normocholesterolemics. Conclusions: The WM tested appears to be a functional food as it improved the antioxidant status of increased CHD-risk volunteers. Despite its high energy content, it also appears adequate for overweight and obese people because did not exert negative effect upon body weight.
Phytotherapy Research | 1998
Sagrario Martín-Aragón; Belén Basabe; Juana Benedí; A. Villar
Vaccinium myrtillus L. is a well‐known bilberry shrub belonging to the Ericaceae family. It has been reported to have multiple pharmacological activities from its anthocyanosidic fraction: ophthalmic, vasoprotective, antiinflammatory, wound‐healing, antiulcer and antiatherosclerosis. It is to be expected that several activities might be related to a possible antioxidant action from anthocyanosides. An anthocyanoside complex extract from Vaccinium myrtillus was tested for its ability to inhibit lipid peroxidation and to scavenge hydroxyl and superoxide radicals. An antiperoxidative action of this V. myrtillus extract was assayed by the Fe3+‐ADP/NADPH method in rat liver microsomes. Interaction of this anthocyanoside extract with hydroxyl radicals was evaluated in the Fe3+‐EDTA‐H2O2 deoxyribose system. The superoxide scavenging action of this plant extract was established according to the reaction of phenazine methasulphate in the presence of NADH and molecular oxygen. The anthocyanoside complex extract was able to inhibit lipid peroxidation (IC50 = 50.28 μg/mL) and to scavenge superoxide anion (IC50 < 25 μg/mL). The ability to remove hydroxyl radical exerted by this extract was detectable from 50 μg/mL of extract in the reaction mixture.