PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29467594-0 2018 Catalase down-regulation in cancer cells exposed to arsenic trioxide is involved in their increased sensitivity to a pro-oxidant treatment. Arsenic Trioxide 52-68 catalase Homo sapiens 0-8 28978146-7 2017 Eriodictyol abrogated As2O3-induced decrease of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activity. Arsenic Trioxide 22-27 catalase Homo sapiens 134-142 28755286-4 2017 The results showed that As2O3 exposure significantly lowered the activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GSH-Px)) and inhibition ability of hydroxyl radicals (OH) and increased the malondialdehyde (MDA) contents. Arsenic Trioxide 24-29 catalase Homo sapiens 100-108 28755286-4 2017 The results showed that As2O3 exposure significantly lowered the activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GSH-Px)) and inhibition ability of hydroxyl radicals (OH) and increased the malondialdehyde (MDA) contents. Arsenic Trioxide 24-29 catalase Homo sapiens 110-113 28978146-7 2017 Eriodictyol abrogated As2O3-induced decrease of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activity. Arsenic Trioxide 22-27 catalase Homo sapiens 144-147 25115845-9 2014 The current study reveals that the functional role of antioxidant enzymes is cellular context and treatment agents dependent; targeting catalase may represent a novel strategy to improve the efficacy of As2O3 in CML treatment. Arsenic Trioxide 203-208 catalase Homo sapiens 136-144 25971879-8 2015 Furthermore, the results demonstrated that MDA content in the gastrointestinal tract was increased, while the activities of CAT, GSH, and GSH-Px and the ability to resist OH was decreased in the As2O3 treatment groups. Arsenic Trioxide 196-201 catalase Homo sapiens 124-127 25115845-0 2014 Targeting catalase but not peroxiredoxins enhances arsenic trioxide-induced apoptosis in K562 cells. Arsenic Trioxide 51-67 catalase Homo sapiens 10-18 25115845-5 2014 We further investigated the possible role of peroxirdoxin 1/2/6 and catalase in determining the cellular sensitivity to As2O3. Arsenic Trioxide 120-125 catalase Homo sapiens 45-76 25115845-7 2014 On the contrary, knockdown of catalase markedly enhanced As2O3-induced apoptosis. Arsenic Trioxide 57-62 catalase Homo sapiens 30-38 18393359-12 2008 Treatment with SOD and catalase significantly reduced the levels of O(2)(*-) levels in ATO-treated cells, but did not inhibit apoptosis along with non-effect on the recovery of GSH depletion. Arsenic Trioxide 87-90 catalase Homo sapiens 23-31 11749846-4 2001 NAC 4 mmol/L, NDMS 200 micromol/L, CAT 80 kU/L, and Quin 2 20 micromol/L could down-regulate apoptosis variously induced by As2O3. Arsenic Trioxide 124-129 catalase Homo sapiens 35-38 11749846-5 2001 NAC and CAT alone could decline telomerase activity in three cell lines and further decline telomerase activities that had been decreased by As2O3, whereas Quin 2 antagonized the decline in K562 and HL-60 cells. Arsenic Trioxide 141-146 catalase Homo sapiens 8-11 11749846-7 2001 NAC, NDMS, CAT, and Quin 2 antagonized in some extent the effect of As2O3 on the three tested cell lines. Arsenic Trioxide 68-73 catalase Homo sapiens 11-14 11778267-8 2000 CONCLUSION: Intracellular GSH level and/or catalase activity are important factors to determine sensitivity of malignant hematopoietic cells to As2O3-induced apoptosis. Arsenic Trioxide 144-149 catalase Homo sapiens 43-51 18511884-7 2008 Treatment with exogenous SOD and catalase reduced the depletion of GSH content in ATO-treated cells. Arsenic Trioxide 82-85 catalase Homo sapiens 33-41 18511884-8 2008 Catalase strongly protected the cells from ATO-induced apoptosis. Arsenic Trioxide 43-46 catalase Homo sapiens 0-8 18511884-9 2008 In addition, treatment with SOD, catalase and NAC slightly inhibited the G1 phase accumulation induced by ATO. Arsenic Trioxide 106-109 catalase Homo sapiens 33-41 21308489-0 2012 Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase. Arsenic Trioxide 0-16 catalase Homo sapiens 97-105 22590507-8 2012 Cell lines transfected with cDNAs for catalase, thioredoxin, or the anti-apoptotic bcl-2 gene were more resistant to arsenic trioxide than mock vector transfected cells. Arsenic Trioxide 117-133 catalase Homo sapiens 38-46 21689642-7 2011 Regarding their sensitivity to anticancer treatments, we observed that cells overexpressing catalase were more sensitive to paclitaxel, etoposide and arsenic trioxide. Arsenic Trioxide 150-166 catalase Homo sapiens 92-100 20403967-11 2010 Increased catalase activity in siXPC cells was suppressed by ATO treatment. Arsenic Trioxide 61-64 catalase Homo sapiens 10-18 18949620-5 2008 Therefore, we explored the relationship between catalase activity and As2O3 sensitivity. Arsenic Trioxide 70-75 catalase Homo sapiens 48-56 18949620-6 2008 In AML and APL cell lines, but not primary patient samples, basal catalase levels matched sensitivity to As2O3. Arsenic Trioxide 105-110 catalase Homo sapiens 66-74 18949620-8 2008 Failure of catalase inhibition to sensitise cells to As2O3 was due to a failure of catalase inhibition to increased levels of reactive oxygen species. Arsenic Trioxide 53-58 catalase Homo sapiens 11-19