PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21621526-6 2011 Cyp1a1 expression was directly related to the level of NO production and to reduced arsenic cytotoxicity. Arsenic 84-91 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-6 26535918-5 2015 Arsenic inhibited CYP1A1 enzyme activity and reduced the metabolic clearance of FICZ. Arsenic 0-7 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 18-24 26535918-6 2015 Arsenic also led to activated CYP1A1 transcription but only in cells grown in medium containing trace amounts of the endogenous ligand FICZ, pointing to an indirect mechanism of activation. Arsenic 0-7 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 30-36 24161444-9 2014 In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway. Arsenic 86-93 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 150-156 26988683-0 2016 [Relationship of blood aryl hydrocarbon receptor mRNA and cytochrome P450 1A1 mRNA expression with corrected QT interval among residents exposed to arsenic via drinking water]. Arsenic 148-155 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 58-77 26988683-9 2016 CONCLUSIONS: Long-term exposure to arsenic is associated with upregulated blood AhRmRNA and CYP1A1 mRNA expression.Blood CYP1A1 mRNA expression, but not AhRmRNA expression, is associated with prolonged corrected QT interval. Arsenic 35-42 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 92-98 26988683-9 2016 CONCLUSIONS: Long-term exposure to arsenic is associated with upregulated blood AhRmRNA and CYP1A1 mRNA expression.Blood CYP1A1 mRNA expression, but not AhRmRNA expression, is associated with prolonged corrected QT interval. Arsenic 35-42 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 121-127 24161444-0 2014 Methylated pentavalent arsenic metabolites are bifunctional inducers, as they induce cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase through AhR- and Nrf2-dependent mechanisms. Arsenic 23-30 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 85-104 19033395-10 2009 Our findings provided clear evidence that arsenic can enhance CYP1A1 expression and activity via AhR activation, and the arsenic-induced AhR activation is probably triggered by oxidative stress. Arsenic 42-49 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 62-68 19416086-7 2009 In this review, we shed light on the effect of seven heavy metals, namely arsenic, mercury, lead, cadmium, chromium, copper and vanadium, on CYP1A1 and the consequences on drug metabolism. Arsenic 74-81 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 141-147 19033395-0 2009 Involvement of oxidative stress and activation of aryl hydrocarbon receptor in elevation of CYP1A1 expression and activity in lung cells and tissues by arsenic: an in vitro and in vivo study. Arsenic 152-159 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 92-98 19033395-5 2009 However, the effects of arsenic on cytochrome P450 1A1 (CYP1A1) status (expression and activity), which is essential for B[a]P metabolism, either in lung cells or in lung tissues, are never demonstrated. Arsenic 24-31 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 35-54 19033395-5 2009 However, the effects of arsenic on cytochrome P450 1A1 (CYP1A1) status (expression and activity), which is essential for B[a]P metabolism, either in lung cells or in lung tissues, are never demonstrated. Arsenic 24-31 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 56-62 19033395-6 2009 We hypothesized that arsenic would enhance aryl hydrocarbon receptor (AhR) activation leading to CYP1A1 expression and activity in lung cells. Arsenic 21-28 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 97-103 19033395-7 2009 Indeed, our present study successfully demonstrated the elevation of CYP1A1 messenger RNA expression in H1355 cells, a human lung adenocarcinoma cell line, as well as CYP1A1 expression and activity in lung tissues of arsenic-exposed mice. Arsenic 217-224 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 167-173 19033395-8 2009 We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation. Arsenic 159-166 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 47-53 19033395-8 2009 We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation. Arsenic 159-166 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 175-181 19033395-9 2009 Furthermore, we found that arsenic-induced AhR activation and -enhanced CYP1A1 expression can be further increased by a prooxidant, buthionine-(S,R)-sulfoximine, and suppressed by antioxidants, such as N-acetylcysteine and catalase. Arsenic 27-34 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 72-78 16713074-0 2006 Arsenic inhibits induction of cytochrome P450 1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin in human hepatoma cells. Arsenic 0-7 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 30-49 16713074-6 2006 In the present study, we demonstrated that arsenic not only inhibited the TCDD-induced CYP1A1 activation but also interfered with DRE-CALUX bioassay in human hepatoma cells. Arsenic 43-50 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 87-93 11162773-2 2001 The effect of As, Pb, Hg, or Cd (ranked as the most hazardous environmental metals by EPA and ATSDR) on CYP1A1 and 1A2 induction by benzo[a]pyrene (BaP), benzo[b]fluoranthene (BbF), dibenzo[a,h]anthracene (DBahA), benzo[a]anthracene (BaA), and benzo[k]fluoranthene (BkF) has thus been investigated in fresh human hepatocyte cultures. Arsenic 14-16 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 104-110 16099114-9 2005 In this work we demonstrate that genetic biomarkers such as CYP1A1 2A and GSTM1 polymorphisms in addition to DR70 as screening biomarkers might provide relevant information to identify individuals with higher risk for lung cancer, due to arsenic exposure. Arsenic 238-245 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 60-66 16274885-10 2005 Our data clearly show that As(3+)-, Cd(2+)-, and Cr(6+)-induced oxidative stress modulates Cyp1a1 at transcriptional and posttranscriptional levels but induces Nqo1 and Gst ya at the transcriptional level. Arsenic 27-29 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 91-97 16012082-0 2005 CYP1A1 and GSTM1 genetic polymorphisms in lung cancer populations exposed to arsenic in drinking water. Arsenic 77-84 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-6 32417511-2 2020 The transformation follows the route of "dissolution-recrystallization", during which the arsenic pollutant in gypsum is released into the solution, and hence raises the possibility of being distributed into the product of alpha-HH, a potential harm that has always been neglected. Arsenic 90-97 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 223-231 28189647-13 2017 This modulation of CYP1A1 proves that trivalent metabolites of arsenic are highly reactive and could participate in arsenic toxicity. Arsenic 63-70 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 19-25