PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27811233-1 2017 As neurons die, cholesterol is released in the central nervous system (CNS); hence, this sterol and its metabolites may represent a biomarker of neurodegeneration, including in amyotrophic lateral sclerosis (ALS), in which altered cholesterol levels have been linked to prognosis. Cholesterol 16-27 superoxide dismutase 1 Homo sapiens 208-211 30063213-8 2018 A significant negative correlation was detected between normalized Cu/Zn superoxide dismutase messenger ribonucleic acid levels and total protein, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total antioxidant status. Cholesterol 153-164 superoxide dismutase 1 Homo sapiens 67-93 32555166-12 2020 Thus, NaB with SOD1 silencing under high cholesterol did not eliminate excessive ROS, and eventually resulted in Abeta accumulation. Cholesterol 41-52 superoxide dismutase 1 Homo sapiens 15-19 32210787-7 2020 The plasma SOD was negatively correlated with the hsCRP, while positively correlated with total cholesterol, HDL-C, and LDL-C in PD patients. Cholesterol 96-107 superoxide dismutase 1 Homo sapiens 11-14 27811233-1 2017 As neurons die, cholesterol is released in the central nervous system (CNS); hence, this sterol and its metabolites may represent a biomarker of neurodegeneration, including in amyotrophic lateral sclerosis (ALS), in which altered cholesterol levels have been linked to prognosis. Cholesterol 231-242 superoxide dismutase 1 Homo sapiens 208-211 27811233-3 2017 In CSF, the concentration of cholesterol was found to be elevated in ALS samples. Cholesterol 29-40 superoxide dismutase 1 Homo sapiens 69-72 27811233-6 2017 We conclude that the acidic branch of bile acid biosynthesis, known to be operative in-part in the brain, is defective in ALS, leading to a failure of the CNS to remove excess cholesterol, which may be toxic to neuronal cells, compounded by a reduction in neuroprotective 3beta,7alpha-dihydroxycholest-5-en-26-oic acid. Cholesterol 176-187 superoxide dismutase 1 Homo sapiens 122-125 24125853-5 2013 SOD activity was positively correlated with both of GSH level and GST activity in seminal plasma, and showed an inverse relationship with both cholesterol efflux and post-thaw abnormal tails of buffalo spermatozoa. Cholesterol 143-154 superoxide dismutase 1 Homo sapiens 0-3 26754536-7 2016 Cholesterol does not change GRX2 expression but it overexpresses SOD1, SOD2, CCS, PRDX1, GSR, GSS, CAT and PNKP. Cholesterol 0-11 superoxide dismutase 1 Homo sapiens 65-69 22403024-6 2012 SOD had a strong interaction with DPPC liposomes containing high concentration of cholesterol. Cholesterol 82-93 superoxide dismutase 1 Homo sapiens 0-3 22671579-8 2012 The results indicated that lipid length and mole percent of cholesterol were important parameters that must be adjusted in order to support a favorable environment for SOD interaction with the lipid. Cholesterol 60-71 superoxide dismutase 1 Homo sapiens 168-171 16876118-4 2006 We found that a negative correlation existed between CuZn-superoxide dismutase and glutathione peroxidase activities in human erythrocytes when the concentrations of both plasma triglycerides and total cholesterol were high. Cholesterol 202-213 superoxide dismutase 1 Homo sapiens 53-78 14699004-9 2004 Reduction of SOD after therapy was negatively correlated with FMD (r=0.38; P=0.01) and positively with total cholesterol (r=-0.56; P<0.001). Cholesterol 109-120 superoxide dismutase 1 Homo sapiens 13-16 16127364-10 2005 If hyperlipidemia and the activity of antioxidative enzymes and TAS were considered without reference to other risk factors of atherosclerosis, it appeared that the decreases in SOD, GPx, and TAS may play a more important role in the development of the atherosclerotic process than isolated increases in free cholesterol or triglyceride levels. Cholesterol 309-320 superoxide dismutase 1 Homo sapiens 178-181 8673732-3 1996 For example, CuZn superoxide dismutase incubated with rat hepatocyte cells in culture inhibits 3-hydroxy-3methylglutaryl CoA reductase, thereby reducing cholesterol synthesis. Cholesterol 153-164 superoxide dismutase 1 Homo sapiens 13-38 12099681-8 2002 Furthermore, the inhibitory effect of Cu,Zn SOD on cholesterol synthesis was completely abolished when the cells were incubated with Cu,Zn SOD in the presence of bisindoilmaleimide (BDM), an inhibitor of protein kinase C (PKC); moreover, we demonstrated that Cu,Zn SOD as well as apo SOD was able to increase PKC activity. Cholesterol 51-62 superoxide dismutase 1 Homo sapiens 44-47 12099681-8 2002 Furthermore, the inhibitory effect of Cu,Zn SOD on cholesterol synthesis was completely abolished when the cells were incubated with Cu,Zn SOD in the presence of bisindoilmaleimide (BDM), an inhibitor of protein kinase C (PKC); moreover, we demonstrated that Cu,Zn SOD as well as apo SOD was able to increase PKC activity. Cholesterol 51-62 superoxide dismutase 1 Homo sapiens 139-142 12099681-8 2002 Furthermore, the inhibitory effect of Cu,Zn SOD on cholesterol synthesis was completely abolished when the cells were incubated with Cu,Zn SOD in the presence of bisindoilmaleimide (BDM), an inhibitor of protein kinase C (PKC); moreover, we demonstrated that Cu,Zn SOD as well as apo SOD was able to increase PKC activity. Cholesterol 51-62 superoxide dismutase 1 Homo sapiens 139-142 12099681-8 2002 Furthermore, the inhibitory effect of Cu,Zn SOD on cholesterol synthesis was completely abolished when the cells were incubated with Cu,Zn SOD in the presence of bisindoilmaleimide (BDM), an inhibitor of protein kinase C (PKC); moreover, we demonstrated that Cu,Zn SOD as well as apo SOD was able to increase PKC activity. Cholesterol 51-62 superoxide dismutase 1 Homo sapiens 139-142 12099681-9 2002 Overall, data demonstrate that Cu,Zn SOD affects cholesterol metabolism independently from its dismutase activity and its metal content and that the inhibitory action on cholesterol synthesis is mediated by an activation of protein kinase C. Cholesterol 49-60 superoxide dismutase 1 Homo sapiens 37-40 15473258-2 2004 Substantial evidence has demonstrated that the cytosolic antioxidant enzyme CuZn superoxide dismutase (SOD1) inhibits the HMG-CoA reductase activity in rat hepatocytes and in human fibroblasts by decreasing cholesterol synthesis. Cholesterol 207-218 superoxide dismutase 1 Homo sapiens 76-101 15473258-3 2004 Although these data suggest that SOD1 exerts a physiological role in cholesterol metabolism, it is still unclear whether the decrease of HMG-CoA reductase activity is mediated by transcriptional or by posttranscriptional events. Cholesterol 69-80 superoxide dismutase 1 Homo sapiens 33-37 12099681-0 2002 Effect of Cu,Zn superoxide dismutase on cholesterol metabolism in human hepatocarcinoma (HepG2) cells. Cholesterol 40-51 superoxide dismutase 1 Homo sapiens 10-36 12099681-3 2002 We previously demonstrated that a calf thymus Cu,Zn SOD affects cholesterol metabolism. Cholesterol 64-75 superoxide dismutase 1 Homo sapiens 52-55 12099681-5 2002 The involvement of Cu,Zn SOD in cholesterol metabolism is confirmed further by the presence of this antioxidant enzyme in circulating serum lipoproteins. Cholesterol 32-43 superoxide dismutase 1 Homo sapiens 25-28 23105216-5 1999 Serum superoxide dismutase (SOD) activity was concurrently found to decrease, along with a decrease in high-density lipoprotein (HDL) cholesterol, during the progression of CRF. Cholesterol 134-145 superoxide dismutase 1 Homo sapiens 6-26 23105216-5 1999 Serum superoxide dismutase (SOD) activity was concurrently found to decrease, along with a decrease in high-density lipoprotein (HDL) cholesterol, during the progression of CRF. Cholesterol 134-145 superoxide dismutase 1 Homo sapiens 28-31 9436629-5 1998 Addition of 20 microg/ml superoxide dismutase (SOD) during the CS-modification of HDL caused retrieval of cholesterol efflux activity by 53% and a remarkable decrease in the conjugated dienes level. Cholesterol 106-117 superoxide dismutase 1 Homo sapiens 25-45 9436629-5 1998 Addition of 20 microg/ml superoxide dismutase (SOD) during the CS-modification of HDL caused retrieval of cholesterol efflux activity by 53% and a remarkable decrease in the conjugated dienes level. Cholesterol 106-117 superoxide dismutase 1 Homo sapiens 47-50 7540391-8 1995 A three-fold increase in superoxide (O2-) and a 2.5-fold increase in NO formation followed by an eight-fold increase in peroxynitrite (ONOO-) production by cholesterol-treated microsomes isolated from endothelial cells was observed, one which rose further up to eight-fold in the presence of superoxide dismutase (SOD) (10 U/mL). Cholesterol 156-167 superoxide dismutase 1 Homo sapiens 292-312 7540391-8 1995 A three-fold increase in superoxide (O2-) and a 2.5-fold increase in NO formation followed by an eight-fold increase in peroxynitrite (ONOO-) production by cholesterol-treated microsomes isolated from endothelial cells was observed, one which rose further up to eight-fold in the presence of superoxide dismutase (SOD) (10 U/mL). Cholesterol 156-167 superoxide dismutase 1 Homo sapiens 314-317 33051352-8 2020 Similar to ALS patients, a compensatory down regulation of cholesterol synthesis occurred in the SC of SOD1G93A mice; levels of sterol regulatory element binding protein 2 (SREBP2) - a transcriptional regulator of cholesterol synthesis, progressively declined. Cholesterol 59-70 superoxide dismutase 1 Homo sapiens 103-107 8293516-3 1993 The efficiency of the SOD-entrapment into the positively charged multilamellar vesicles (MLVs), comprising egg yolk phosphatidylcholine and synthetic glucosamine diesters, was enhanced by the addition of cholesterol to the membranes. Cholesterol 204-215 superoxide dismutase 1 Homo sapiens 22-25 32927603-7 2020 The purpose of this review is to analyze in detail the involvement of SOD1 in redox regulation of metabolism, nutrient sensing, cholesterol metabolism and regulation of mitochondrial respiration. Cholesterol 128-139 superoxide dismutase 1 Homo sapiens 70-74