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.
Background: The influence of a dialysis session using hemodiafiltration with on-line regeneration of the ultrafiltrate (HFR) is compared with that of a conventional hemodialysis session with polysulfone (HD-PS) and with a group of healthy individuals. Methods: Total antioxidant capacity (TAC), antioxidants, i.e., superoxide dismutase (SOD) glutathione peroxidase (GPX), reduced glutathione (GSH) and catalase, and biomarkers of oxidative stress were evaluated in plasma, whole blood and lymphocytes. Results: The study showed decreased plasma TAC, decreased activities of antioxidant enzymes and decreased GSH levels along with increased thiobarbituric-acid-reactive substances and 8–hydroxy-2-deoxyguanosine (8-OHdG) levels in lymphocytes. The antioxidants and biomarkers of lipid and protein damage after dialysis sessions with HFR were similar or better than following HD-PS. Thus, the blood GPX activity was comparable to that of healthy controls and significantly better than following HD-PS. An increase in 8-OHdG levels was observed in the HD-PS group after dialysis but not in the HFR group. Conclusions: These results show that HFR induces less oxidative stress than HD-PS.
The Wine Pomace Products (WPP) prevent the increase of endothelial permeability induced by INF-γ and increase E-cadherin expression in the cell junctions.
High levels of indoleamine 2,3-dioxygenase (IDO) are involved in tumour escape mechanisms. The aim of this study is the evaluation of L-kynurenine of plasma as marker of diagnostic and prognostic in patients with colorectal cancer. The study included 78 patients with colorectal cancer, of whom 15 % were in stage I/II, 30 % in stage III, and 55 % in stage IV, and was compared with a control group of 70 healthy subjects. The receiver operating characteristic (ROC) curve analysis showed an area under the curve of 0.917, with a specificity of 100 % and with a sensitivity to detect cancer of the colon of 85.2 %, taking 1.83 μM as a cut-off point. The overall survival analysis also indicated that patients with low levels of L-kynurenine in plasma increased survival rate after 45 months of follow-up (P = 0.032). These results show that the plasma levels of L-kynurenine could be a good biomarker to differentiate individuals with colorectal cancer from healthy individuals.
Thiosemicarbazones (TSCs), and their copper derivatives, have been extensively studied mainly due to the potential applications as antitumor compounds. A part of the biological activity of the TSC-Cu complexes rests on their reactivity against cell reductants, as glutathione (GSH). The present paper describes the structure of the [Cu(PTSC)(ONO)] compound (1) (HPTSC=pyridine-2-carbaldehyde thiosemicarbazone) and its spectroscopic and magnetic properties. ESI studies performed on the reaction of GSH with 1 and the analogous [{Cu(PTSC*)(ONO)}] derivative (2, HPTSC*=pyridine-2-carbaldehyde 4N-methylthiosemicarbazone) show the absence of peaks related with TSC-Cu-GSH species. However GSH-Cu ones are detected, in good agreement with the release of Cu ions after reduction in the experimental conditions. The reactivity of 1 and 2 with cytochrome c and myoglobin and their activities against HT-29 and SW-480 colon carcinoma cell lines are compared with those shown by the free HPTSC and HPTSC* ligands.
Our aim was to investigate the effect of chemotherapy on plasma total antioxidant capacity and polyphenols in patients with colon cancer. Plasma samples were collected from 70 CRC patients under chemotherapy treatment, and 15 non-treated patients. The control group included 71 healthy individuals. Plasma ABTS and FRAP were measured as biomarkers of antioxidant total capacity and the total phenols as an indicator to determine the polyphenols levels in plasma. Treatment with chemotherapy protocols resulted in a significant decrease of ABTS (-24 %, p < 0.048), FRAP (-15 %, p < 0.046) and polyphenols (-46 %, p < 0.05) compared with the values of those not treated. The total antioxidant capacity was significantly lower (-18 % for ABTS and -12 % for FRAP) in patients with metastasis as compared with patients without metastasis. The plasma total phenols, were also decreased (-16 %, p = 0.005) in metastasis patients. The patients with colorectal cancer have decreased total antioxidant capacity and the values are lower in patients treated with chemotherapy. Furthermore, CEA tumor marker levels are associated with a lower plasma total antioxidant capacity, and therefore with the progress and development of the disease.
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