The study of the antioxidant capacity of foodstuffs requires the use of diverse determination methods to gain a wider picture of their multiple effects. The aim of this work was to evaluate the "antioxidant profile" of red wines applying TAC (total antioxidant capacity) methods: 2,2'-azinobis(3-ethyl-benzthiazoline-6-sulfonic acid) (ABTS), 2,2-diphenyl-1-picrylhydrazyl, N,N-dimethyl-p-phenylenediamine dihydrochloride, oxygen radical absorbance capacity, ferric reducing/antioxidant power, hydroxyl and superoxide radical scavenger activities, and biomarkers of oxidative stress methods such as lipid peroxidation inhibition and inhibition of damage to DNA. Furthermore, levels of total polyphenols (TPP) of wines were also evaluated. Three bottles of 107 different Spanish red wines (total samples 321), made from different grape varieties, aging processes, and vintages, were analyzed. The validation of TAC methods, the first step in this work, provided a good linearity, proportionality, and low detection limits. Among these methods, the ABTS was the most satisfactory for its rapidity, cost, and precision. All wines showed an important capacity to scavenge hydroxyl radicals and were capable of blocking superoxide radicals but with 10 times lower intensity. Wines also showed important protective action on biomarkers of oxidative stress; they were much more active to inhibit lipid peroxidation than DNA oxidation. Few statistically significant correlations among levels of TPP and antioxidant properties of wines were detected. Furthermore, values of these correlations were very low.
Evaluation of the total antioxidant capacity of solid matrices without extraction steps is a very interesting 10 alternative for food researchers and also for food industries. These methodologies have been denominated by QUENCHER from 11 quick, easy, new, cheap, and reproducible assays. To demonstrate and highlight the validity of QUENCHER (Q) methods, values 12 of Q-method validation were showed for the first time, and they were tested with products of well-known different chemical The most commonly applied in vitro TAC methodologies 42 are based on diverse strategies to evaluate (1) the reducing 43 ability of antioxidants, such as the Folin−Ciocalteu (FC) and 44 ferric reducing/antioxidant power (FRAP) assays; (2) the 45 scavenging of stable free radicals by antioxidants, including the 46 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) 47 and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays; and (3) 48 the scavenging of short-lived radicals by competition 49 mechanisms, such as peroxyl radicals in the oxygen radical
BackgroundTreatment with selective vitamin D receptor activators such as paricalcitol have been shown to exert an anti-inflammatory effect in patients on hemodialysis, in addition to their action on mineral metabolism and independently of parathyroid hormone (PTH) levels. The objective of this study was to evaluate the additional antioxidant capacity of paricalcitol in a clinical setting.MethodsThe study included 19 patients with renal disease on hemodialysis, of whom peripheral blood was obtained for analysis at baseline and three months after starting intravenous paricalcitol treatment. The following oxidizing and inflammatory markers were quantified: malondialdehyde (MDA), nitrites and carbonyl groups, indoleamine 2,3-dioxygenase (IDO), tumor necrosis factor alfa (TNF-α), interleukin-6 (IL-6), interleukin-18 (IL-18) and C-reactive protein (CRP). Of the antioxidants and anti-inflammatory markers, superoxide dismutase (SOD), catalase, reduced glutathione (GSH), thioredoxin, and interleukin-10 (IL-10) levels were obtained.ResultsBaseline levels of oxidation markers MDA, nitric oxide and protein carbonyl groups significantly decreased after three months on paricalcitol treatment, while levels of GSH, thioredoxin, catalase and SOD activity significantly increased. After paricalcitol treatment, levels of the inflammatory markers CRP, TNF-α, IL-6 and IL-18 were significantly reduced in serum and the level of anti-inflammatory cytokine IL-10 was increased.ConclusionsIn renal patients undergoing hemodialysis, paricalcitol treatment significantly reduces oxidative stress and inflammation, two well known factors leading to cardiovascular damage.
Deletions of loci on chromosomes 5q, 17p, 18q, and 22q, together with the incidence of p53 mutations and amplification of the double minute-2 gene were investigated in the sporadic colorectal tumors of 44 patients from a Spanish community. Chromosome deletions were analyzed by means of loss of heterozygosity analysis using a restriction fragment length polymorphism assay. Allelic losses were also detected by polymerase chain reaction (PCR)-single-stranded conformation polymorphism (SSCP) analysis of a polymorphic site in intron 2 of the p53 gene. The percentages of genetic deletions on the screened chromosomes were 39.3% (5q), 58.3% (17p), 40.9% (18q), and 40% (22q). Mutations in p53 exons 2-9 were examined by PCR-SSCP analysis and direct sequencing of the mutated region. Twenty of 44 tumor samples (45.45%) showed mutations at various exons except for exons 2, 3, and 9, the most frequent changes being G-->T transversion and C-->T transition. Because oxygen-free radicals play a role in the carcinogenesis process, we evaluated the oxidative status of the colorectal tumors. Antioxidant activities, lipid peroxidation, and DNA-damaged product concentrations in colon tumors and normal mucosa were compared. In tumor tissues, superoxide dismutase and catalase decreased fourfold and twofold, respectively, whereas glutathione peroxidase and reduced glutathione increased threefold. Malondialdehyde and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were twofold higher in colorectal tumors than in normal mucosa. Seven of 10 DNA tumor samples (70%) showing higher values of 8-OHdG also had genetic alterations at different chromosomal loci. In these samples, the p53 gene was deleted or mutated in 71.4% of cases. We concluded that the observed changes in the oxidative metabolism of the tumor cells and the consecutive increase in DNA damage may potentiate the genomic instability of different chromosomal regions, leading to further cell malignancy and tumor expansion.
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