PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27197287-9 2016 Statistically significant SNPs that modified the association of vitamin E assignment and high-grade prostate cancer included SEC14L2, SOD1, and TTPA In the placebo arm, several SNPs, hypothesized to interact with supplement assignment and risk of high-grade prostate cancer, were also directly associated with outcome. Vitamin E 64-73 superoxide dismutase 1 Homo sapiens 134-138 26941058-3 2016 Either curative or prophylactic silibinin and vitamin E groups significantly decreased ASK1 and p38 MAPK levels through increasing the gene expression of Trx1, TrxR1, and PP5 to reduce the oxidative stress as demonstrated by decreasing the levels of NADPH oxidase 4 (NOX4), TBARS and conjugated diene with a concomitant increase in the levels of GSH, CAT, and SOD. Vitamin E 46-55 superoxide dismutase 1 Homo sapiens 360-363 22528588-0 2013 The influence of vitamin E supplementation on erythropoietin responsiveness in chronic hemodialysis patients with low levels of erythrocyte superoxide dismutase. Vitamin E 17-26 superoxide dismutase 1 Homo sapiens 140-160 26805894-13 2016 Concurrently, we also found that a prolonged (48 h) exposure to Vitamin C, Vitamin E and Green tea extract reduced the enzymatic activity of SOD in lung cancer cells. Vitamin E 75-84 superoxide dismutase 1 Homo sapiens 141-144 23688096-2 2014 In addition, the outcome of scaling and root planing (SRP) with and without vitamin E supplementation is evaluated in terms of changes in periodontal parameters and SOD activity in patients with CP. Vitamin E 76-85 superoxide dismutase 1 Homo sapiens 165-168 23324897-6 2013 However, SOD showed a statistically significant increase only after vitamin E intake (23.1%, P<0.05). Vitamin E 68-77 superoxide dismutase 1 Homo sapiens 9-12 24250434-6 2011 Vitamin E supplementation resulted in significant differences in plasma and BAL vitamin E concentrations between the two groups (p-value = 0.01, 0.01), decrease in SOD activities (not differ significantly in plasma (p-value = 0.23)), but with significant differences in BAL (p-value = 0.016) and progressive reduction in Acute Physiology and Chronic Health Evaluation II (APACHE II) (p-value = 0.52) and Sequential Organ Failure Assessment (SOFA) (p-value = 0.008) score in vitamin E group. Vitamin E 0-9 superoxide dismutase 1 Homo sapiens 164-167 16885600-10 2006 Administration of oral vitamin E for one week, along with photoprotection resulted in a significant decrease in MDA levels and activities of all others enzymes except SOD. Vitamin E 23-32 superoxide dismutase 1 Homo sapiens 167-170 19949914-5 2011 Furthermore, CSC exposure caused a reduction of the gene expression of the antioxidant enzymes SOD1, SOD2, GPx, and CAT that was counteracted by Vitamin E (50 muM). Vitamin E 145-154 superoxide dismutase 1 Homo sapiens 95-99 19949914-7 2011 In fact the scavenger vitamin E can block both cell injury and inhibition of SOD1, SOD2, GPx, and CAT induced by CSC exposure. Vitamin E 22-31 superoxide dismutase 1 Homo sapiens 77-81 24250434-7 2011 From the results of this study, it seems that supplementation of vitamin E as a potent antioxidant, along with other supportive measures, can be beneficial in decreasing SOD total activity, ROM production and risk of organ failure in critically ill patients. Vitamin E 65-74 superoxide dismutase 1 Homo sapiens 170-173 18296478-10 2008 The mixture of SPPs, oleic/linoleic acids, and vitamin E was able to partly maintain and recover the fresh enzyme distribution, particularly of SOD. Vitamin E 47-56 superoxide dismutase 1 Homo sapiens 144-147 11828552-1 2002 AIM: To test whether the activities of erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) can be affected by oral iron (OI) treatment, parenteral iron (PI) treatment, and parenteral iron treatment with vitamin E supplementation (PIE) in iron deficiency anemia. Vitamin E 226-235 superoxide dismutase 1 Homo sapiens 73-76 16823356-6 2006 The P/A ratio (TBARS/SOD+CAT+GPx) was significantly lower in vitamin E in comparison with placebo, but after 30 min and 24 h restitution it returned to pre-exercise level. Vitamin E 61-70 superoxide dismutase 1 Homo sapiens 21-24 14709952-0 2004 The effect of vitamin E treatment on tardive dyskinesia and blood superoxide dismutase: a double-blind placebo-controlled trial. Vitamin E 14-23 superoxide dismutase 1 Homo sapiens 66-86 14709952-3 2004 The present study was designed to replicate this finding in a group of Chinese patients with TD, and to examine the effect of vitamin E treatment on blood superoxide dismutase (SOD), a critical enzyme in the detoxification of free radicals. Vitamin E 126-135 superoxide dismutase 1 Homo sapiens 155-175 14709952-3 2004 The present study was designed to replicate this finding in a group of Chinese patients with TD, and to examine the effect of vitamin E treatment on blood superoxide dismutase (SOD), a critical enzyme in the detoxification of free radicals. Vitamin E 126-135 superoxide dismutase 1 Homo sapiens 177-180 14709952-9 2004 Blood SOD levels were significantly increased after treatment with vitamin E (P = 0.001), but no change with placebo treatment (P < 0.05). Vitamin E 67-76 superoxide dismutase 1 Homo sapiens 6-9 14709952-11 2004 Moreover, the efficacy of vitamin E may be due to its ability to increase SOD level, which may reduce oxidative injure in tardive dyskinesia. Vitamin E 26-35 superoxide dismutase 1 Homo sapiens 74-77 16155359-0 2005 Comparison of effect of vitamin E-coated dialyzer and oral vitamin E on hemodialysis-induced Cu/Zn-superoxide dismutase. Vitamin E 24-33 superoxide dismutase 1 Homo sapiens 93-119 16155359-0 2005 Comparison of effect of vitamin E-coated dialyzer and oral vitamin E on hemodialysis-induced Cu/Zn-superoxide dismutase. Vitamin E 59-68 superoxide dismutase 1 Homo sapiens 93-119 15956459-7 2005 Indeed, adding 7.5 microM vitamin E (a natural antioxidant) also restored the concentrations of ADD1 and fatty acid synthase mRNA, which were decreased by DHA treatment; however, the DHA or the antioxidant treatment did not change the expression of antioxidation genes (superoxide dismutase 1 and glutathione peroxidase 1) in porcine stromal vascular cells. Vitamin E 26-35 superoxide dismutase 1 Homo sapiens 270-292 11163531-7 2001 Pretreatment of HCAECs with trolox and vitamin E decreased superoxide anion generation (p <.05 vs. epinephrine alone) and blocked the subsequent upregulation of SOD mRNA and protein. Vitamin E 39-48 superoxide dismutase 1 Homo sapiens 164-167 8755101-3 1996 Vitamin E protects phospholipids from oxidation, regulates AOS condition, SOD-activity and promotes in such way the tissue functional disturbances correction of the animals tested. Vitamin E 0-9 superoxide dismutase 1 Homo sapiens 74-77 7779577-5 1995 The semen plasma superoxide dismutase (SOD) and GSSG tended to increase with the time of vitamin E administration, but the increment did not reach a significant level by the seventh week. Vitamin E 89-98 superoxide dismutase 1 Homo sapiens 17-37 7779577-5 1995 The semen plasma superoxide dismutase (SOD) and GSSG tended to increase with the time of vitamin E administration, but the increment did not reach a significant level by the seventh week. Vitamin E 89-98 superoxide dismutase 1 Homo sapiens 39-42