Oxidative Stress Markers in Open and Laparoscopic Colectomy for Cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer,Colorectal Neoplasms
PROVIDER: 2074362 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Study of Oxidative stress Markers (F2 Isoprostanes for lipid peroxidation, Carbonyl groups for protein peroxidation, 3 Nitrotyrosine for damage by nitrogens, and 8-Hydroxyguanosine for RNA peroxidation)in patients with colorectal cancer undergo surgical treatment (preoperatively during the intervention and postoperatively) and controls.
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Project description:Objective: To determine the oxidative stress during cycles of chemotherapy in patients after surgery for colorectal cancer, with or without oral zinc supplementation. Subjects: Twenty four adults from both genders participated in this study. All patients underwent stage II, III or IV colorectal cancer surgical resection and were starting chemotherapy in HCFMRP- USP. Patients were randomized into two groups. The first one (QTx-Zn Group, n=10) received 70 mg/d of zinc orally and the second one received placebo (QTx-Placebo Group, n=14) for 16 weeks. The study also included 30 healthy volunteers matched for age, gender and socioeconomic status, who received 70 mg/d of zinc supplement (Control-Zn Group, n=21) or placebo (Control-Placebo Group, n=9) for 16 weeks. Methods: The questionnaires about dietary intake (semiquantitative food frequency and food record), fatigue and quality of life (FACIT-F) and questionnaires that assess the side effects of chemotherapy (CTCAE) were evaluated. Anthropometry and bioelectrical impedance measurements were made. Blood collection was performed before the 1st, 2nd, 3rd and 4th cycles of chemotherapy (median duration of 21 days among cicles). Routine laboratory tests, vitamin E and markers anti and pro-oxidants (MDA, SOD, GPx and isoprostane) ere determined. The control group underwent the same procedures, except for chemotherapy. A longitudinal linear mixed effects model was adjusted for each of the variables of interest. The models were fitted using PROC MIXED of SAS version 9 (SAS, CARY, NC, USA). To analyze the association of categorical variables in the different items of the CTCAE, the investigators used the Fisher exact test. Results: The oral zinc supplementation was sufficient to increase plasma levels of zinc and did not alter food intake, body composition and routine laboratory evaluation of patients undergoing chemotherapy for colorectal cancer. Compared with QTx-Placebo Group, QTx-Zn Group showed lower prevalence of complaint on the salivary gland (17 vs. 75%). Fatigue (43 ± 6 vs. 36 ± 13) and quality of life (126 ± 160 vs. 116 ± 27) has become worst in the period between the 1st and 4th cycles of QTx in QTx-Placebo Group. When compared with QTx-Placebo Group, QTx-Zn Group had higher values of SOD before the 1st (2297 ± 503 vs. 1604 ± 352 USOD/g Hb), 2nd (2037 ± 515 vs. 1712 ± 417 USOD/g Hb) and 4th (2202 ± 323 vs. 1821 ± 360 USOD/g Hb) cycles of QTx. GPx values decreased in QTx-Zn Group before the 3rd cycle of QTx (48.5 ± 7.0 vs. 54.3 ± 2.3 mol NADPH/min/gHb). Conclusions: These data suggest that zinc supplementation reduces complaints related to the change in salivary gland, preserving the quality of life and preventing the worsening of fatigue. The increase in SOD can be attributed to zinc supplementation per se, whereas this mineral is a cofactor that endogenous antioxidant enzyme. The highest activity of SOD increases the production of H2O2, whose detoxification involves the participation of GPx, justifying its reduction. There were no changes in plasma levels of vitamin E, MDA and isoprostane during the study period. Considering the values of MDA and isoprostane, the data indicate that regardless of zinc supplementation, the lipid peroxidation of the cell membrane was unchanged during chemotherapy.
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Project description:Investigating the oxidative stress response: Candida glabrata strains were stressed with hydrogen peroxide and menadione (causing oxygen radicals) to induce the oxidative stress regulon, which is thought to be upregulated during the oxidative burst inside of phagocytic cells.
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Project description:This series represents the rapid response to oxidative stress Keywords: time-course
2005-02-19 | GSE2263 | GEO
Project description:Metabolic network describing oxidative stress response by a mathematical model with a data-driven parameter estimation (from Kuehne2015).
2022-05-26 | MODEL2204220001 | BioModels
Project description:Oxidative stress is a potent inducer of protein ADP-ribosylation. Although the proteins modified under oxidative stress have been identified, it is not clear, whether the number of modified proteins and/or the number ADP-ribosylation sites varies with stress intensity. Here, we investigated both the qualitative and quantitative changes in the HeLa cell ADP-ribosylome induced by mild (4 - 16 uM), moderate (64 - 250 uM), or severe, but non-lethal (1 mM) H2O2 concentrations using shotgun and parallel reaction monitoring mass spectrometry (PRM-MS). After moderate and severe oxidative stress, approximately 50% of proteins not ADP-ribosylated under basal conditions were induced, while ADP-ribosylation of the other 50% already ADP-ribosylated under basal conditions remained constant. In contrast, mild oxidative stress caused a reduction in detectable ADP-ribosylation of many proteins, which were induced under more severe oxidative stress. Overall, the number of ADP-ribosylation sites modified/de-modified did not change significantly under the various degrees of oxidative stress. Moreover, we applied the PRM method to study protein ADP-ribosylation in ovarian cancer cells that display different sensitivities to PARP inhibitors. These studies revealed similar ADP-ribosylation responses following H2O2 treatment, which, however, correlated in extent with ARTD1 abundance in these cells. Overall, our new MS approaches have proven to be highly useful in monitoring cellular protein ADP-ribosylation and have revealed unexpected fluctuations in proteins ADP-ribosylation depending on the degree of oxidative stress.
2016-11-13 | MSV000080334 | MassIVE