PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27713515-9 2016 However, there were nominally statistically significant interactions for SNPs in acrylamide-metabolizing enzymes: CYP2E1 (rs915906 and rs2480258) and the deletions of GSTM1 and GSTT1. Acrylamide 81-91 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 114-120 29748789-0 2018 The polymorphism rs2480258 within CYP2E1 is associated with different rates of acrylamide metabolism in vivo in humans. Acrylamide 79-89 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 34-40 29748789-2 2018 CYP2E1 is the most important enzyme in the metabolism of acrylamide (AA) by operating its oxidation into glycidamide (GA). Acrylamide 57-67 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6 27713515-10 2016 Although in need of confirmation, the interactions between acrylamide intake and CYP2E1 SNPs contribute to the evidence for a causal relationship between acrylamide and endometrial cancer risk. Acrylamide 59-69 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 81-87 27713515-10 2016 Although in need of confirmation, the interactions between acrylamide intake and CYP2E1 SNPs contribute to the evidence for a causal relationship between acrylamide and endometrial cancer risk. Acrylamide 154-164 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 81-87 27497234-5 2016 In comparison with human CYP2E1, camel CYP2E1 more efficiently binds to small toxins as aniline, benzene, catechol, amides, butadiene, toluene and acrylamide. Acrylamide 147-157 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 25-31 24508477-6 2014 Only in HepG2 cells, low concentration of acrylamide was able to induce CYP2E1 expression significantly. Acrylamide 42-52 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 72-78 25989052-6 2015 Chronic low dose acrylamide exposure in mice relevant to human exposure levels results in significantly increased levels of DNA damage in terms of glycidamide adducts in spermatocytes, the specific germ cell stage where Cyp2e1 is expressed. Acrylamide 17-27 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 220-226 24508477-7 2014 Knockdown of CYP2E1 restrained acrylamide to increase viability of HepG2 cells. Acrylamide 31-41 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 13-19 18418580-0 2008 Human CYP2E1 mediates the formation of glycidamide from acrylamide. Acrylamide 56-66 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 6-12 22392284-2 2012 Acrylamide is metabolized into glycidamide by CYP2E1. Acrylamide 0-10 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 46-52 22392284-7 2012 Similarly, CYP2E1-associated aniline 4-hydroxylase (ANH) activity, protein levels, and mRNA levels increased 2.1- and 2.6-fold, 2.4- and 3.2-fold, and 1.4- and 1.9-fold following 1.25 and 2.5 mM acrylamide treatments, respectively. Acrylamide 195-205 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 11-17 21402133-0 2011 Association of CYP2E1, GST and mEH genetic polymorphisms with urinary acrylamide metabolites in workers exposed to acrylamide. Acrylamide 115-125 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 15-21 20034532-6 2010 The observed trend is likely due to a competitive effect between ethanol and acrylamide as both are substrates for cytochrome P450 2E1. Acrylamide 77-87 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 115-134 19190172-0 2009 In vivo role of cytochrome P450 2E1 and glutathione-S-transferase activity for acrylamide toxicokinetics in humans. Acrylamide 79-89 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 16-35 19190172-9 2009 The changes in acrylamide toxicokinetics upon CYP2E1 blockade provide evidence that CYP2E1 is a major but not the only enzyme mediating acrylamide epoxidation in vivo to glycidamide in humans. Acrylamide 15-25 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 46-52 19190172-9 2009 The changes in acrylamide toxicokinetics upon CYP2E1 blockade provide evidence that CYP2E1 is a major but not the only enzyme mediating acrylamide epoxidation in vivo to glycidamide in humans. Acrylamide 15-25 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 84-90 19190172-9 2009 The changes in acrylamide toxicokinetics upon CYP2E1 blockade provide evidence that CYP2E1 is a major but not the only enzyme mediating acrylamide epoxidation in vivo to glycidamide in humans. Acrylamide 136-146 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 84-90 18049993-3 2007 Acrylamide is neurotoxic and is metabolized by cytochrome P-450 (CYP) 2E1 to a mutagenic epoxide, glycidamide. Acrylamide 0-10 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 47-73 17660004-0 2008 Ethanol enhanced the genotoxicity of acrylamide in human, metabolically competent HepG2 cells by CYP2E1 induction and glutathione depletion. Acrylamide 37-47 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 97-103 18049993-9 2007 Early life immaturities tended to exert a greater effect on acrylamide than glycidamide dosimetry because immaturities in CYP2E1 and glutathione counteract one another for glycidamide AUC, but both lead to greater acrylamide dose. Acrylamide 60-70 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 122-128 17267090-2 2007 As the intestinal mechanisms of acrylamide absorption are poorly investigated we studied the transport of acrylamide in differentiated Caco-2 cells and its effects on biotransformation enzymes (CYP2E1 and glutathione S-transferase) and glutathione levels. Acrylamide 106-116 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 194-200 15982677-17 2005 CYP2E1 polymorphisms and variability in CYP2E1 activity associated with, for example, diabetes, obesity, starvation, and alcohol consumption, may result in altered metabolic efficiencies leading to differential susceptibilities to acrylamide toxicities in humans. Acrylamide 231-241 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6 15982677-17 2005 CYP2E1 polymorphisms and variability in CYP2E1 activity associated with, for example, diabetes, obesity, starvation, and alcohol consumption, may result in altered metabolic efficiencies leading to differential susceptibilities to acrylamide toxicities in humans. Acrylamide 231-241 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 40-46 33399867-14 2020 Cyp2e1, which catalyses the bioactivation of acrylamide to glycidamide, was not induced after acrylamide treatment. Acrylamide 45-55 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6 15355880-12 2005 Thus, CYP2E1 polymorphisms in human populations, resulting in variable enzyme metabolic activities, may produce differential susceptibilities to acrylamide toxicities. Acrylamide 145-155 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 6-12 35250264-11 2022 Theoretically, acrylamide and glycidamide concentration should correlate to each other; however in reality, there are other factors (such as CYP2E1 polymorphism, dietary intake, etc) that can cause variation in their respective concentration. Acrylamide 15-25 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 141-147 35250264-2 2022 Acrylamide is metabolized by the CYP2E1 enzyme in the body to form glycidamides, an epoxide that is reactive to DNA and can form carcinogenic adducts. Acrylamide 0-10 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 33-39