PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11958955-7 2002 These results suggest that the aggregation of alpha-synuclein is mediated by the Cu,Zn-SOD/H(2)O(2) system via the generation of hydroxyl radical by the free radical-generating function of the enzyme. Free Radicals 153-165 superoxide dismutase 1 Homo sapiens 87-90 12540279-9 2001 It is a plausible hypothesis that inhibition of SOD may preferentially kill malignant cells through a free radical-mediated mechanism. Free Radicals 102-114 superoxide dismutase 1 Homo sapiens 48-51 11870681-2 2002 Genetic analysis of familial ALS has yielded six loci and one disease gene (SOD1), initially suggesting a role for free radicals in the disease process, although the mechanisms through which the mutant exerts toxicity and results in selective motor neuron death remain uncertain. Free Radicals 115-128 superoxide dismutase 1 Homo sapiens 76-80 11034536-6 2000 Monitoring of SOD and GPX at ten time points: before administration of streptokinase, 1, 3, 6, 12, 18, 24 hours, 2, 3 and 5 days after administration of streptokinase revealed the lowest SOD levels up to one hour before administration of streptokinase, supporting the fact that the maximum production of free radicals is achieved at that time. Free Radicals 304-317 superoxide dismutase 1 Homo sapiens 187-190 17216981-10 2001 Free radicals related markers revealed significant higher level of lipid peroxide, as well as significant lower levels of SOD activity, catalase activity and glutathione S-transferase among exposed workers than among controls (p<0.0001 for all). Free Radicals 0-13 superoxide dismutase 1 Homo sapiens 122-125 11014196-5 2000 Inhibition of SOD causes accumulation of cellular O2- and leads to free-radical-mediated damage to mitochondrial membranes, the release of cytochrome c from mitochondria and apoptosis of the cancer cells. Free Radicals 67-79 superoxide dismutase 1 Homo sapiens 14-17 11225659-17 2000 Although metformin monotherapy ameliorated the imbalance between free radical-induced increase in lipid peroxidation (by reducing the MDA level in both erythrocytes and plasma) and decreased plasma and cellular antioxidant defences (by increasing the erythrocyte activities of Cu, Zn, SOD, catalase and GSH level) and decreased erythrocyte susceptibility to oxidative stress, it had negligible effect to scavenge Fe ion-induced free radical generation in a phospholipid-liposome system. Free Radicals 65-77 superoxide dismutase 1 Homo sapiens 285-288 10459841-4 1999 An imbalance between SOD and GSHPx was said to be crucial in the prevention of toxicity of free radicals (1). Free Radicals 91-104 superoxide dismutase 1 Homo sapiens 21-24 10385054-3 1999 SOD-1 associated FALS mutants may have an altered radiation response due to an enhanced generation of hydroxyl radicals or a compromised ability to neutralize free radicals. Free Radicals 159-172 superoxide dismutase 1 Homo sapiens 0-5 12114769-1 1999 In adrenal glands, oxidative free radicals are synthesized in the course of hormonal production, and enzyme superoxide dismutase (SOD) is considered to scavenge these harmful superoxide radicals and, subsequently, to protect the cells. Free Radicals 29-42 superoxide dismutase 1 Homo sapiens 130-133 9106116-0 1997 Immunocytochemical study of the distribution of the free radical scavenging enzymes Cu/Zn superoxide dismutase (SOD1); MN superoxide dismutase (MN SOD) and catalase in the normal human spinal cord and in motor neuron disease. Free Radicals 52-64 superoxide dismutase 1 Homo sapiens 84-110 9796506-2 1998 Oxygen-derived free radicals are controlled by various cellular defense mechanisms consisting of enzymatic such as superoxide dismutase, catalase, glutathion peroxidase and nonenzymatic scavenger components. Free Radicals 15-28 superoxide dismutase 1 Homo sapiens 115-135 9844955-1 1998 Dysregulation of free radical metabolism as reflected by abnormal erythrocyte activities of three critical enzymes of the antioxidant defense system (AODS), i.e. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), has been reported in schizophrenic patients. Free Radicals 17-29 superoxide dismutase 1 Homo sapiens 162-182 9844955-1 1998 Dysregulation of free radical metabolism as reflected by abnormal erythrocyte activities of three critical enzymes of the antioxidant defense system (AODS), i.e. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), has been reported in schizophrenic patients. Free Radicals 17-29 superoxide dismutase 1 Homo sapiens 184-187 9106116-0 1997 Immunocytochemical study of the distribution of the free radical scavenging enzymes Cu/Zn superoxide dismutase (SOD1); MN superoxide dismutase (MN SOD) and catalase in the normal human spinal cord and in motor neuron disease. Free Radicals 52-64 superoxide dismutase 1 Homo sapiens 112-116 8995206-1 1997 Three enzymes, viz., tartrate-resistant acid phosphatase (TRAP), nitric oxide synthase I (NOS-I), and superoxide dismutase (SOD), involved in the production and metabolism of free radicals or radical equivalents, were demonstrated by immunocytochemistry in the urothelium of the ureters of six patients of various ages. Free Radicals 175-188 superoxide dismutase 1 Homo sapiens 102-122 9092140-1 1997 The recent observation that mutations in cytosolic CuZn-superoxide dismutase (CuZn-SOD) are associated with amyotrophic lateral sclerosis (ALS) suggests that the disease arises from a perturbation of the homeostasis of free radicals resulting in neuronal degeneration by reactive oxygen species. Free Radicals 219-232 superoxide dismutase 1 Homo sapiens 51-76 9092140-1 1997 The recent observation that mutations in cytosolic CuZn-superoxide dismutase (CuZn-SOD) are associated with amyotrophic lateral sclerosis (ALS) suggests that the disease arises from a perturbation of the homeostasis of free radicals resulting in neuronal degeneration by reactive oxygen species. Free Radicals 219-232 superoxide dismutase 1 Homo sapiens 78-86 8995206-1 1997 Three enzymes, viz., tartrate-resistant acid phosphatase (TRAP), nitric oxide synthase I (NOS-I), and superoxide dismutase (SOD), involved in the production and metabolism of free radicals or radical equivalents, were demonstrated by immunocytochemistry in the urothelium of the ureters of six patients of various ages. Free Radicals 175-188 superoxide dismutase 1 Homo sapiens 124-127 8914027-6 1996 Since superoxide dismutase (SOD) attenuated (P < 0.001) LDL-induced MMC apoptosis, it seems to be mediated through the generation of free radicals by mesangial cells (control, 4.3 +/- 1.5%; LDL, 200 micrograms/ml, 19.4 +/- 0.5%; LDL + SOD, 8.1 +/- 1.3% apoptotic cells/field). Free Radicals 136-149 superoxide dismutase 1 Homo sapiens 6-26 8914027-6 1996 Since superoxide dismutase (SOD) attenuated (P < 0.001) LDL-induced MMC apoptosis, it seems to be mediated through the generation of free radicals by mesangial cells (control, 4.3 +/- 1.5%; LDL, 200 micrograms/ml, 19.4 +/- 0.5%; LDL + SOD, 8.1 +/- 1.3% apoptotic cells/field). Free Radicals 136-149 superoxide dismutase 1 Homo sapiens 28-31 8945013-1 1996 The defenses against the production of free radicals and reactive oxygen species (ROS) are to be found in plasma (ascorbate, urate, alpha tocopherol) and in erythrocytes (superoxide dismutase or SOD; catalase or CAT; glutathione peroxidase or GPx). Free Radicals 39-52 superoxide dismutase 1 Homo sapiens 195-198 8906612-3 1996 Mutations of the SOD gene may reduce its superoxide dismutase activity, thereby elevating free radical levels. Free Radicals 90-102 superoxide dismutase 1 Homo sapiens 17-20 8599825-18 1996 These results propose possible role of free radicals with reduced antioxidant activity of SOD and GPx in multiple myeloma. Free Radicals 39-52 superoxide dismutase 1 Homo sapiens 90-93 8840658-1 1996 Free radicals scavengers superoxide dismuatase (SOD) and catalase and lipid peroxidation were studied in 45 patients of aluminium phosphide poisoning irrespective of age and sex admitted to a hospital in north India during the January 1992 to December 1993. Free Radicals 0-13 superoxide dismutase 1 Homo sapiens 48-51 8980931-1 1996 OBJECTIVE: To investigate whether duodenal ulcer (DU) is associated with increased free radical generation at the site of ulceration and to attempt, indirectly, to confirm the hypothesis by determining activity of free radical scavengers such as superoxide dismutase (SOD). Free Radicals 214-226 superoxide dismutase 1 Homo sapiens 246-266 7491999-7 1995 CONCLUSIONS: Reflux esophagitis is mediated by free radicals depleting SOD. Free Radicals 47-60 superoxide dismutase 1 Homo sapiens 71-74 8843965-10 1996 These results propose possible role of free radicals with reduced antioxidant activities of SOD and GPx in multiple myeloma. Free Radicals 39-52 superoxide dismutase 1 Homo sapiens 92-95 8738540-5 1996 An inpaired antioxidant enzyme defence system, here represented by SOD and GPx levels, can potentiate injury caused by free radicals in haemodialysis patients. Free Radicals 119-132 superoxide dismutase 1 Homo sapiens 67-70 7554532-5 1995 We propose that the increased GSH-Px and SOD-1 activities could be a protective mechanism for the cells due to the hyperproduction of free radicals in chronic renal failure. Free Radicals 134-147 superoxide dismutase 1 Homo sapiens 41-46 7797532-1 1995 Increased levels of CuZn superoxide dismutase (SOD-1) are cytoprotective in experimental models of neurological disorders associated with free radical toxicity (e.g. stroke, trauma). Free Radicals 138-150 superoxide dismutase 1 Homo sapiens 47-52 8117850-2 1993 We found that PolyHb-SOD-catalase is effective in scavenging oxygen-derived free radicals. Free Radicals 76-89 superoxide dismutase 1 Homo sapiens 21-24 8022792-1 1994 The discovery of missense mutations leading to reduced enzymatic activity in the copper/zinc superoxide dismutase (SOD1) in human familial amyotrophic lateral sclerosis has heightened interest in the role of free radicals in neurodegenerations but left the mechanisms by which they may cause neuronal death unexplained. Free Radicals 208-221 superoxide dismutase 1 Homo sapiens 115-119 7507613-3 1993 The finding of SOD variants in FALS is consistent with the hypothesis that free radicals contribute to the pathogenesis of FALS, and possibly to the pathogenesis of other neurodegenerative disorders such as Parkinson"s disease, in which there is substantial evidence of oxidant stress. Free Radicals 75-88 superoxide dismutase 1 Homo sapiens 15-18 1860379-4 1991 When arterial RBCs were incubated together with various scavengers of free radical (SOD catalase and histidine and mannitol), the production of LPO was less than that of arterial RBC incubation singly (P less than 0.01). Free Radicals 70-82 superoxide dismutase 1 Homo sapiens 84-87 1591881-7 1992 The present study indicates that free radicals and resultantly formed lipid peroxide levels are higher in patients with SLE than those in normal persons, probably contributing to the production of autoantibodies, nephritis, and vasculitis of other organs, and that excessively generated free radicals may play an important role in the pathogenesis of SLE, which is possibly due to diminished SOD activity. Free Radicals 33-46 superoxide dismutase 1 Homo sapiens 392-395 2076828-1 1990 Cu/Zn superoxide dismutase (Cu/Zn SOD), glutathione peroxidase (GPx) and catalase, which are the three main enzymes involved in cellular protection against damage due to oxygen-derived free radicals have been assayed in plasma and erythrocytes obtained from subjects with dementia of the Alzheimer type (DAT) and from controls. Free Radicals 185-198 superoxide dismutase 1 Homo sapiens 0-26 1657737-6 1991 Like superoxide dismutase (SOD) and other oxidatively denatured proteins, glutathione peroxidase inactivated by peroxides or free radicals seems to be degraded preferentially by proteases. Free Radicals 125-138 superoxide dismutase 1 Homo sapiens 5-25 1657737-6 1991 Like superoxide dismutase (SOD) and other oxidatively denatured proteins, glutathione peroxidase inactivated by peroxides or free radicals seems to be degraded preferentially by proteases. Free Radicals 125-138 superoxide dismutase 1 Homo sapiens 27-30 2076828-1 1990 Cu/Zn superoxide dismutase (Cu/Zn SOD), glutathione peroxidase (GPx) and catalase, which are the three main enzymes involved in cellular protection against damage due to oxygen-derived free radicals have been assayed in plasma and erythrocytes obtained from subjects with dementia of the Alzheimer type (DAT) and from controls. Free Radicals 185-198 superoxide dismutase 1 Homo sapiens 28-37 3239107-1 1988 In blood samples of 54 obese persons (13 men, 41 women) some lipid components, malondialdehyde (MDA), and the activities of free radical protecting enzymes superoxide-dismutase (SOD) and glutathione-peroxidase (GSHpx), were determined before and after a seven-day slimming diet of 2.1 MJ/day. Free Radicals 124-136 superoxide dismutase 1 Homo sapiens 156-176 2596324-2 1989 Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Free Radicals 31-43 superoxide dismutase 1 Homo sapiens 145-165 2521568-1 1989 Activity of the free radical scavenging enzyme, superoxide dismutase (SOD-1), was determined in fibroblast cell lines derived from familial Alzheimer"s patients, trisomy 21 patients and normal controls. Free Radicals 16-28 superoxide dismutase 1 Homo sapiens 70-75 3239107-1 1988 In blood samples of 54 obese persons (13 men, 41 women) some lipid components, malondialdehyde (MDA), and the activities of free radical protecting enzymes superoxide-dismutase (SOD) and glutathione-peroxidase (GSHpx), were determined before and after a seven-day slimming diet of 2.1 MJ/day. Free Radicals 124-136 superoxide dismutase 1 Homo sapiens 178-181 3229124-12 1988 We conclude that traditional culture conditions support generation of free radicals in tissue culture media that suppress both growth and superoxide dismutase activity. Free Radicals 70-83 superoxide dismutase 1 Homo sapiens 138-158 3490244-0 1986 Clinical efficacy of a new antiinflammatory drug with free radicals scavenging properties: superoxide dismutase (SOD) and catalase of human origin. Free Radicals 54-67 superoxide dismutase 1 Homo sapiens 91-111 3490244-0 1986 Clinical efficacy of a new antiinflammatory drug with free radicals scavenging properties: superoxide dismutase (SOD) and catalase of human origin. Free Radicals 54-67 superoxide dismutase 1 Homo sapiens 113-116 422668-1 1979 It has been postulated that superoxide dismutase (SOD) protects cells from free radical-induced damage. Free Radicals 75-87 superoxide dismutase 1 Homo sapiens 28-48 6621591-5 1983 It has been suggested [9] that the failure of some laboratories to detect increases in sister-chromatid exchanges after treatment with the tumor promoter phorbol-myristate-acetate (PMA) may be due to high concentrations of the free-radical-scavenging enzyme superoxide dismutase (SOD) in the sera used and that heat inactivation of the sera may be responsible for these differences. Free Radicals 227-239 superoxide dismutase 1 Homo sapiens 258-278 6621591-5 1983 It has been suggested [9] that the failure of some laboratories to detect increases in sister-chromatid exchanges after treatment with the tumor promoter phorbol-myristate-acetate (PMA) may be due to high concentrations of the free-radical-scavenging enzyme superoxide dismutase (SOD) in the sera used and that heat inactivation of the sera may be responsible for these differences. Free Radicals 227-239 superoxide dismutase 1 Homo sapiens 280-283 6171347-8 1981 Thus, these results indicate that SOD is able to bind to PM-2 DNA and inhibit BLM-induced degradation independently of its free radical-scavenging activity. Free Radicals 123-135 superoxide dismutase 1 Homo sapiens 34-37 422668-1 1979 It has been postulated that superoxide dismutase (SOD) protects cells from free radical-induced damage. Free Radicals 75-87 superoxide dismutase 1 Homo sapiens 50-53 27889384-2 2017 Superoxide dismutase 1 (SOD1) is an antioxidant responsible for reducing free radicals. Free Radicals 73-86 superoxide dismutase 1 Homo sapiens 0-22 32234491-5 2020 The liver serum biomarkers such as ALT and AST, elated levels of free radicals inducing oxidative stress characterized by a surge in Nrf-2, FOXO-1 and HO-1 genes and diminution of anti-oxidant activity characterized by a decline in SOD, GPx, and CAT genes. Free Radicals 65-78 superoxide dismutase 1 Homo sapiens 232-235 32091028-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 4-31 32091028-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 33-37 32091028-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 122-126 32091028-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 157-161 31695223-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 4-31 31695223-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 33-37 31695223-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 122-126 31695223-1 2019 The superoxide dismutase type 1 (SOD1) gene is the first responsible gene mapped in amyotrophic lateral sclerosis type 1 (ALS1), and it codes for the enzyme SOD1, the function of which is to protect against damage mediated by free radicals deriving from oxygen. Free Radicals 226-239 superoxide dismutase 1 Homo sapiens 157-161 30400150-1 2018 Superoxide dismutase (SOD) is the only known enzyme to directly scavenge a free radical. Free Radicals 75-87 superoxide dismutase 1 Homo sapiens 0-20 30400150-1 2018 Superoxide dismutase (SOD) is the only known enzyme to directly scavenge a free radical. Free Radicals 75-87 superoxide dismutase 1 Homo sapiens 22-25 29405030-3 2017 Altered oxidative stress biomarker profile has been repeatedly reported in ALS patients, which may suggest that abnormal free radical production is relevant in the ALS pathogenesis. Free Radicals 121-133 superoxide dismutase 1 Homo sapiens 75-78 29405030-3 2017 Altered oxidative stress biomarker profile has been repeatedly reported in ALS patients, which may suggest that abnormal free radical production is relevant in the ALS pathogenesis. Free Radicals 121-133 superoxide dismutase 1 Homo sapiens 164-167 27889384-2 2017 Superoxide dismutase 1 (SOD1) is an antioxidant responsible for reducing free radicals. Free Radicals 73-86 superoxide dismutase 1 Homo sapiens 24-28 19771301-2 2008 A disturbance in the antioxidant defense system, including antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSHPx), due to free radical-induced oxidative injury has also been implicated in various neuropsychiatric disorders. Free Radicals 149-161 superoxide dismutase 1 Homo sapiens 79-99 28299326-1 2017 Although, as an antioxidant enzyme, human Cu,Zn superoxide dismutase 1 (hSOD1) can mitigate damage to cell components caused by free radicals generated by aerobic metabolism, large-scale manufacturing and clinical use of hSOD1 are still limited by the challenge of rapid and inexpensive production of high-quality eukaryotic hSOD1 in recombinant forms. Free Radicals 128-141 superoxide dismutase 1 Homo sapiens 72-77 28299326-1 2017 Although, as an antioxidant enzyme, human Cu,Zn superoxide dismutase 1 (hSOD1) can mitigate damage to cell components caused by free radicals generated by aerobic metabolism, large-scale manufacturing and clinical use of hSOD1 are still limited by the challenge of rapid and inexpensive production of high-quality eukaryotic hSOD1 in recombinant forms. Free Radicals 128-141 superoxide dismutase 1 Homo sapiens 221-226 28299326-1 2017 Although, as an antioxidant enzyme, human Cu,Zn superoxide dismutase 1 (hSOD1) can mitigate damage to cell components caused by free radicals generated by aerobic metabolism, large-scale manufacturing and clinical use of hSOD1 are still limited by the challenge of rapid and inexpensive production of high-quality eukaryotic hSOD1 in recombinant forms. Free Radicals 128-141 superoxide dismutase 1 Homo sapiens 221-226 29350504-1 2017 Background/Aim: Superoxide dismutase (SOD) is the critical enzyme in the detoxification of superoxide radicals because those are the first species produced in the majority of biological free radical producing reactions. Free Radicals 186-198 superoxide dismutase 1 Homo sapiens 16-36 29350504-1 2017 Background/Aim: Superoxide dismutase (SOD) is the critical enzyme in the detoxification of superoxide radicals because those are the first species produced in the majority of biological free radical producing reactions. Free Radicals 186-198 superoxide dismutase 1 Homo sapiens 38-41 28702226-4 2015 Superoxide Dismutase (SOD) is one of the most effective antioxidant enzyme defense systems against free radicals. Free Radicals 99-112 superoxide dismutase 1 Homo sapiens 0-20 28702226-4 2015 Superoxide Dismutase (SOD) is one of the most effective antioxidant enzyme defense systems against free radicals. Free Radicals 99-112 superoxide dismutase 1 Homo sapiens 22-25 24070210-2 2013 Human body has evolved an effective defense system including superoxide dismutase (SOD) and catalase against the toxicity of these free radicals. Free Radicals 131-144 superoxide dismutase 1 Homo sapiens 61-81 24070210-2 2013 Human body has evolved an effective defense system including superoxide dismutase (SOD) and catalase against the toxicity of these free radicals. Free Radicals 131-144 superoxide dismutase 1 Homo sapiens 83-86 21221594-15 2012 We think that the decrement in SOD levels may be related with the utilized antioxidants due to the increased free radicals and the compensatory increment in the other steps of the antioxidant system. Free Radicals 109-122 superoxide dismutase 1 Homo sapiens 31-34 21896300-1 2012 Excessive free radical production or oxidative stress may be involved in the pathophysiology of schizophrenia as evidenced by increased superoxide dismutase (SOD) activities, a critical enzyme in the detoxification of superoxide radicals. Free Radicals 10-22 superoxide dismutase 1 Homo sapiens 136-156 21896300-1 2012 Excessive free radical production or oxidative stress may be involved in the pathophysiology of schizophrenia as evidenced by increased superoxide dismutase (SOD) activities, a critical enzyme in the detoxification of superoxide radicals. Free Radicals 10-22 superoxide dismutase 1 Homo sapiens 158-161 21383993-5 2011 Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). Free Radicals 63-76 superoxide dismutase 1 Homo sapiens 0-20 21383993-5 2011 Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). Free Radicals 63-76 superoxide dismutase 1 Homo sapiens 22-25 20595380-7 2010 Here, we identify COMMD1 as a novel protein regulating SOD1 activation and associate COMMD1 function with the production of free radicals. Free Radicals 124-137 superoxide dismutase 1 Homo sapiens 55-59 21387752-16 2010 CONCLUSIONS: Clinical changes occurring during CVD were linearly dependant on SOD activity and concentration of Zn and Cu ions, which suggested the participation of free radicals in CVD Free Radicals 165-178 superoxide dismutase 1 Homo sapiens 78-81 24046909-4 2013 The decreased levels of SOD, glutathione and total antioxidant status in leprosy patients may indicate a degradation of these antioxidant enzymes by free radicals during detoxification processes. Free Radicals 149-162 superoxide dismutase 1 Homo sapiens 24-27 19771301-2 2008 A disturbance in the antioxidant defense system, including antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSHPx), due to free radical-induced oxidative injury has also been implicated in various neuropsychiatric disorders. Free Radicals 149-161 superoxide dismutase 1 Homo sapiens 101-104 17884519-5 2007 CONCLUSION: The reduction of SOD activity observed may result from insufficient scavenging capacity of free radicals. Free Radicals 103-116 superoxide dismutase 1 Homo sapiens 29-32 12531810-1 2003 2-Methoxyestradiol (2-ME), a new anticancer agent currently in clinical trials, has been demonstrated to inhibit superoxide dismutase (SOD) and to induce apoptosis in leukemia cells through a free radical-mediated mechanism. Free Radicals 192-204 superoxide dismutase 1 Homo sapiens 113-133 12940695-2 2003 BACKGROUND: Superoxide dismutase, glutathione peroxidase and catalase are the three main enzymes that control the biological effects of the reactive oxygen species (free radicals). Free Radicals 165-178 superoxide dismutase 1 Homo sapiens 12-32 17394531-9 2007 These data suggest that mitochondrial-produced O(2) (*) radicals play a critical role in mutant SOD1-mediated neuronal toxicity and implicate mitochondrial-produced free radicals as potential therapeutic targets in ALS. Free Radicals 165-178 superoxide dismutase 1 Homo sapiens 96-100 16820996-1 2006 Superoxide dismutase (SOD) is reported to be the major enzymatic defence against free radicals and common oxidants. Free Radicals 81-94 superoxide dismutase 1 Homo sapiens 0-20 16820996-1 2006 Superoxide dismutase (SOD) is reported to be the major enzymatic defence against free radicals and common oxidants. Free Radicals 81-94 superoxide dismutase 1 Homo sapiens 22-25 14529456-4 2003 Recent developments in genetic engineering as well as chemical modeling, have allowed for the production of novel free radical scavengers including mutated forms of superoxide dismutase (SOD) and low molecular weight SOD mimics with extended circulating half-lives and/or significant membrane permeability"s. Free Radicals 114-126 superoxide dismutase 1 Homo sapiens 165-185 14529456-4 2003 Recent developments in genetic engineering as well as chemical modeling, have allowed for the production of novel free radical scavengers including mutated forms of superoxide dismutase (SOD) and low molecular weight SOD mimics with extended circulating half-lives and/or significant membrane permeability"s. Free Radicals 114-126 superoxide dismutase 1 Homo sapiens 187-190 14529456-4 2003 Recent developments in genetic engineering as well as chemical modeling, have allowed for the production of novel free radical scavengers including mutated forms of superoxide dismutase (SOD) and low molecular weight SOD mimics with extended circulating half-lives and/or significant membrane permeability"s. Free Radicals 114-126 superoxide dismutase 1 Homo sapiens 217-220