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  1 / 7531 MEDLINE  
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[PMID]:29328669
[Au] Autor:Feng Y; Wang S; Wang H; Peng Y; Zheng J
[Ad] Endereço:Wuya College of Innovation, Shenyang Pharmaceutical University , Shenyang, Liaoning 110016, People's Republic of China.
[Ti] Título:Urinary Methyleugenol-deoxyadenosine Adduct as a Potential Biomarker of Methyleugenol Exposure in Rats.
[So] Source:J Agric Food Chem;66(5):1258-1263, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Methyleugenol (ME), a natural ingredient of several herbs and spices used in the human diet, is hepatocarcinogenic in rodents. Following metabolic activation to the reactive carbocation intermediate, ME can bind covalently to DNA, which is directly associated with its carcinogenicity. In this work, a non-invasive approach to determine ME exposure was established by monitoring the urinary N -(methylisoeugenol-3'-yl)-2'-deoxyadenosine (ME-dA) adduct. The developed method entails liquid-liquid extraction enrichment of urinary ME-dA, incorporation of deuterated ME-dA as an internal standard, and analysis by liquid chromatography coupled tandem mass spectrometry. Male rats (10-12 weeks, 180-200 g) were treated (p.o.) with ME, and ME-dA was excreted in urine in a dose- and time-dependent manner. The non-invasive approach enabled us to successfully determine exposure to ME-containing herbs and spices. These results suggest that ME-dA can potentially serve as an effective biomarker of ME exposure in rats. It is expected that the developed approach of detecting urinary ME-dA will facilitate the investigation of ME carcinogenesis.
[Mh] Termos MeSH primário: Biomarcadores/urina
Carcinógenos
Adutos de DNA/urina
Desoxiadenosinas/urina
Eugenol/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Eugenol/análise
Eugenol/toxicidade
Eugenol/urina
Neoplasias Hepáticas/induzido quimicamente
Masculino
Ratos
Ratos Sprague-Dawley
Especificidade da Espécie
Especiarias/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Carcinogens); 0 (DNA Adducts); 0 (Deoxyadenosines); 29T9VA6R7M (methyleugenol); 3T8H1794QW (Eugenol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b05186


  2 / 7531 MEDLINE  
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[PMID]:28468256
[Au] Autor:Cellai F; Munnia A; Viti J; Doumett S; Ravagli C; Ceni E; Mello T; Polvani S; Giese RW; Baldi G; Galli A; Peluso MEM
[Ad] Endereço:Cancer Risk Factor Branch, Regional Cancer Prevention Laboratory, ISPO-Cancer Research and Prevention Institute, Florence 50139, Italy. f.cellai@ispo.toscana.it.
[Ti] Título:Magnetic Hyperthermia and Oxidative Damage to DNA of Human Hepatocarcinoma Cells.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 29.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Nanotechnology is addressing major urgent needs for cancer treatment. We conducted a study to compare the frequency of 3-(2-deoxy-ß-d-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3 )-one deoxyguanosine (M1dG) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) adducts, biomarkers of oxidative stress and/or lipid peroxidation, on human hepatocarcinoma HepG2 cells exposed to increasing levels of Fe3O4-nanoparticles (NPs) versus untreated cells at different lengths of incubations, and in the presence of increasing exposures to an alternating magnetic field (AMF) of 186 kHz using P-postlabeling. The levels of oxidative damage tended to increase significantly after ≥24 h of incubations compared to controls. The oxidative DNA damage tended to reach a steady-state after treatment with 60 µg/mL of Fe3O4-NPs. Significant dose-response relationships were observed. A greater adduct production was observed after magnetic hyperthermia, with the highest amounts of oxidative lesions after 40 min exposure to AMF. The effects of magnetic hyperthermia were significantly increased with exposure and incubation times. Most important, the levels of oxidative lesions in AMF exposed NP treated cells were up to 20-fold greater relative to those observed in nonexposed NP treated cells. Generation of oxidative lesions may be a mechanism by which magnetic hyperthermia induces cancer cell death.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Dano ao DNA
Hipertermia Induzida/métodos
Neoplasias Hepáticas/terapia
Nanopartículas de Magnetita/uso terapêutico
Estresse Oxidativo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Adutos de DNA/análise
Adutos de DNA/genética
Células Hep G2
Seres Humanos
Peroxidação de Lipídeos
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Adducts); 0 (Magnetite Nanoparticles)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  3 / 7531 MEDLINE  
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[PMID]:29326044
[Au] Autor:Nigam R; Anindya R
[Ad] Endereço:Department of Biotechnology, Indian Institute of Technology Hyderabad, Kandi, Sangareddy, Hyderabad 502285, Telangana, India.
[Ti] Título:Escherichia coli single-stranded DNA binding protein SSB promotes AlkB-mediated DNA dealkylation repair.
[So] Source:Biochem Biophys Res Commun;496(2):274-279, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Repair of alkylation damage in DNA is essential for maintaining genome integrity. Escherichia coli (E.coli) protein AlkB removes various alkyl DNA adducts including N1-methyladenine (N meA) and N3-methylcytosine (N meC) by oxidative demethylation. Previous studies showed that AlkB preferentially removes N meA and N meC from single-stranded DNA (ssDNA). It can also remove N meA and N meC from double-stranded DNA by base-flipping. Notably, ssDNA produced during DNA replication and recombination, remains bound to E. coli single-stranded DNA binding protein SSB and it is not known whether AlkB can repair methyl adduct present in SSB-coated DNA. Here we have studied AlkB-mediated DNA repair using SSB-bound DNA as substrate. In vitro repair reaction revealed that AlkB could efficiently remove N meC adducts inasmuch as DNA length is shorter than 20 nucleotides. However, when longer N meC-containing oligonuleotides were used as the substrate, efficiency of AlkB catalyzed reaction was abated compared to SSB-bound DNA substrate of identical length. Truncated SSB containing only the DNA binding domain could also support the stimulation of AlkB activity, suggesting the importance of SSB-DNA interaction for AlkB function. Using 70-mer oligonucleotide containing single N meC we demonstrate that SSB-AlkB interaction promotes faster repair of the methyl DNA adducts.
[Mh] Termos MeSH primário: Reparo do DNA
DNA Bacteriano/genética
Proteínas de Ligação a DNA/genética
Proteínas de Escherichia coli/genética
Escherichia coli/genética
Regulação Bacteriana da Expressão Gênica
Oxigenases de Função Mista/genética
[Mh] Termos MeSH secundário: Alquilação
DNA/genética
DNA/metabolismo
Adutos de DNA/química
Adutos de DNA/metabolismo
Dano ao DNA
Metilação de DNA
DNA Bacteriano/metabolismo
DNA de Cadeia Simples/genética
DNA de Cadeia Simples/metabolismo
Proteínas de Ligação a DNA/metabolismo
Escherichia coli/metabolismo
Proteínas de Escherichia coli/metabolismo
Cinética
Oxigenases de Função Mista/metabolismo
Oligonucleotídeos/química
Oligonucleotídeos/metabolismo
Oxirredução
Ligação Proteica
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Adducts); 0 (DNA, Bacterial); 0 (DNA, Single-Stranded); 0 (DNA-Binding Proteins); 0 (Escherichia coli Proteins); 0 (Oligonucleotides); 0 (SSB protein, E coli); 9007-49-2 (DNA); EC 1.- (Mixed Function Oxygenases); EC 1.14.11.- (AlkB protein, E coli)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  4 / 7531 MEDLINE  
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[PMID]:28452951
[Au] Autor:Hang B; Wang P; Zhao Y; Sarker A; Chenna A; Xia Y; Snijders AM; Mao JH
[Ad] Endereço:Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. bo_hang@lbl.gov.
[Ti] Título:Adverse Health Effects of Thirdhand Smoke: From Cell to Animal Models.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by "the four Rs": tobacco chemicals that remain, react, re-emit, and/or are resuspended long after active smoking has ceased. This review summarizes recent research progress in the effects of THS on genotoxicity, metabolism and early life development using cellular and animal models. We first reported that THS generated in laboratory systems caused significant DNA damage in human cell lines. Our finding that THS significantly induces oxidative base lesions has been confirmed in skin wounds of mice models exposed to THS. THS also induced metabolomic changes in human reproductive cell lines. Furthermore, we demonstrated that early exposure to THS not only negatively impacts body weight in both male and female mice, but also induces persistent changes to immunological parameters in peripheral blood in these mice. These results indicate that THS is genotoxic at realistic experimental doses and that there may be a window of susceptibility for some forms of cellular damage induced by THS.
[Mh] Termos MeSH primário: Poluição por Fumaça de Tabaco
[Mh] Termos MeSH secundário: Poluentes Atmosféricos/toxicidade
Animais
Apoptose/efeitos dos fármacos
Adutos de DNA/química
Adutos de DNA/metabolismo
Dano ao DNA/efeitos dos fármacos
Seres Humanos
Sistema Imunitário/efeitos dos fármacos
Sistema Imunitário/metabolismo
Modelos Animais
Reprodução/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Air Pollutants); 0 (DNA Adducts); 0 (Tobacco Smoke Pollution)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  5 / 7531 MEDLINE  
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[PMID]:29231728
[Au] Autor:Woo H; Lee J; Park D; Jung E
[Ad] Endereço:Biospectrum Life Science Institute , A-1805, U-Tower, 767, Sinsu-ro, Suji-gu, Yongin-si, Gyeonggi-do Republic of Korea.
[Ti] Título:Protective Effect of Mulberry (Morus alba L.) Extract against Benzo[a]pyrene Induced Skin Damage through Inhibition of Aryl Hydrocarbon Receptor Signaling.
[So] Source:J Agric Food Chem;65(50):10925-10932, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benzo[a]pyrene (B[a]P), a type of polycyclic aromatic hydrocarbon, is present in the atmosphere surrounding our environment. Although B[a]P is a procarcinogen, enzymatically metabolized benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) could intercalate into DNA to form bulky BPDE-DNA adducts as an ultimate carcinogenic product in human keratinocytes. The aim of this study was to evaluate the protective effect of mulberry extract, purified from the fruit of Morus Alba L., on B[a]P-induced cytotoxicity in human keratinocytes and its mechanisms of action. In this study, we confirmed that B[a]P induced nuclear translocation and the activation of aryl hydrocarbon receptor (AhR) were decreased by pretreatment of mulberry extract. Mulberry extract could decrease DNA damage through the suppression of B[a]P derived DNA adduct formation and restoration of cell cycle retardation at S phase in a dose-dependent manner. Additionally, cyanidin-3-glucoside (C3G), a major active compound of mulberry extract, showed biological activities to protect the cells from B[a]P exposure, similar to the effectivity of the mulberry extract. These results indicated that the inhibitory effect of C3G against B[a]P inducing skin cancer is attributable to repress the AhR signaling pathway.
[Mh] Termos MeSH primário: Benzo(a)pireno/toxicidade
Morus/química
Extratos Vegetais/farmacologia
Substâncias Protetoras/farmacologia
Receptores de Hidrocarboneto Arílico/metabolismo
Transdução de Sinais/efeitos dos fármacos
Pele/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antocianinas/farmacologia
Adutos de DNA/genética
Adutos de DNA/metabolismo
Dano ao DNA/efeitos dos fármacos
Feminino
Glucosídeos/farmacologia
Seres Humanos
Técnicas In Vitro
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Meia-Idade
Receptores de Hidrocarboneto Arílico/antagonistas & inibidores
Receptores de Hidrocarboneto Arílico/genética
Pele/citologia
Pele/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (DNA Adducts); 0 (Glucosides); 0 (Plant Extracts); 0 (Protective Agents); 0 (Receptors, Aryl Hydrocarbon); 3417WMA06D (Benzo(a)pyrene); 7084-24-4 (cyanidin 3-O-glucoside)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04044


  6 / 7531 MEDLINE  
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[PMID]:29061807
[Au] Autor:Sheikh IA; Beg MA; Yasir M
[Ad] Endereço:King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia iasheikh@kau.edu.sa.
[Ti] Título:Molecular Interactions of Carcinogenic Aromatic Amines, 4-Aminobiphenyl and 4,4'-Diaminobiphenyl, with Lactoperoxidase - Insight to Breast Cancer.
[So] Source:Anticancer Res;37(11):6245-6249, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Lactoperoxidase (LPO) is an antimicrobial protein present in milk, saliva, gastric secretions, tears and upper respiratory tract secretions. LPO constitutes an important enzyme of the human immune defense system. However, LPO has also been suggested to be involved in breast cancer etiology through production of reactive free radicals and activation of carcinogenic aromatic compounds. Aromatic compounds are generally highly lipophilic and thus accumulate in highly fatty breast tissues. The aromatic compounds 4-aminobiphenyl (ABP) and 4,4'-diaminobiphenyl (BZ) are known to have carcinogenic properties. LPO catalyzes their oxidation and converts them into reactive products which bind to DNA and form adducts. These DNA adducts subsequently lead to breast cancer. MATERIALS AND METHODS: The crystal structure of LPO was obtained from Protein Data Bank. Structures of ABP and BZ were retrieved from PubChem database. Induced Fit Docking was performed using glide module from Schrodinger. RESULTS: The present study reports the structural binding of ABP and BZ with LPO using in silico approaches. The amino acid residues of LPO involved in the binding with the two aromatic ligands were characterized and binding energy values were calculated. CONCLUSION: Both ABP and BZ were placed in the substrate binding site present in the distal heme cavity of LPO with good affinity. The binding mode mimicked that of the natural substrate since these compounds did not disturb the water molecule that plays an important role in the oxidation reaction. Thus, the water molecule is potentially available for facilitating the subsequent activation of the aromatic amines to reactive species which may form DNA adducts leading to breast cancer.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/metabolismo
Neoplasias da Mama/induzido quimicamente
Carcinógenos/metabolismo
Adutos de DNA/metabolismo
Radicais Livres/química
Lactoperoxidase/metabolismo
[Mh] Termos MeSH secundário: Compostos de Aminobifenil/efeitos adversos
Compostos de Aminobifenil/química
Sítios de Ligação
Neoplasias da Mama/enzimologia
Carcinógenos/química
Adutos de DNA/efeitos adversos
Adutos de DNA/química
Feminino
Seres Humanos
Lactoperoxidase/química
Modelos Moleculares
Simulação de Acoplamento Molecular
Estrutura Molecular
Oxirredução
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carcinogens); 0 (DNA Adducts); 0 (Free Radicals); 16054949HJ (4-biphenylamine); EC 1.11.1.- (Lactoperoxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  7 / 7531 MEDLINE  
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[PMID]:28960960
[Au] Autor:Lv S; Zhang Y; Xu B; Xu H; Zhao Y; Chen J; Gao Z; Wu J; Xie J
[Ad] Endereço:State Key Laboratory of Toxicology and Medical Countermeasures and Laboratory of Toxicant Analysis, Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences , 27 Taiping Road, Haidian District, Beijing 100850, China.
[Ti] Título:Synthesis, Characterization, and Identification of New in Vitro Covalent DNA Adducts of Divinyl Sulfone, an Oxidative Metabolite of Sulfur Mustard.
[So] Source:Chem Res Toxicol;30(10):1874-1882, 2017 Oct 16.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Divinyl sulfone (DVS) is an important oxidative metabolic product of sulfur mustard (SM) in vitro and in vivo. Although DVS is not a classical blister agent, its high reactivity and toxicity induced by vinyl groups can also cause blisters like SM upon contact with the skin, eyes, and respiratory organs. The purpose of this paper was to identify whether DVS could covalently bind to DNA bases to form new DNA adducts in cells in vitro. A series of adducts were synthesized and characterized using purine, nucleoside, or DNA, separately, as starting materials. The covalent site, pattern, and relative reactivity of adduct formation were identified and discussed in detail. The results showed that five high abundance site-specific DNA adducts, including two monoadducts and three cross-linked adducts, were obtained when DNA was used as a substrate. When HaCaT cells were exposed to 30 µM of DVS, four new DNA adducts containing monoadducts and cross-linked adducts were found and identified in cells, including N3-A monoadduct, N7-G monoadduct, N7G-N7G bis-adduct, and N3A-N7G cross-linked adduct. Among them, the abundance of N3-A monoadduct was 10 times higher than that of the other three adducts. DNA adduct formation with DVS showed significant differences from that observed with SM. The observation of these new DNA adduct in vitro cells revealed that DNA damage could be also induced by DVS.
[Mh] Termos MeSH primário: Adutos de DNA/efeitos dos fármacos
Gás de Mostarda/metabolismo
Sulfonas/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Adutos de DNA/química
Dano ao DNA
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Gás de Mostarda/química
Oxirredução/efeitos dos fármacos
Relação Estrutura-Atividade
Sulfonas/análise
Sulfonas/síntese química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Adducts); 0 (Sulfones); 5PFN71LP8M (divinyl sulfone); T8KEC9FH9P (Mustard Gas)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00196


  8 / 7531 MEDLINE  
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[PMID]:28928033
[Au] Autor:Ceppi M; Munnia A; Cellai F; Bruzzone M; Peluso MEM
[Ad] Endereço:Clinical Epidemiology Branch, IRCCS - Ospedale Policlinico San Martino, Largo R. Benzi 10, 16132 Genoa, Italy.
[Ti] Título:Linking the generation of DNA adducts to lung cancer.
[So] Source:Toxicology;390:160-166, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Worldwide, lung cancer is the leading cause of cancer death. DNA adducts are considered a reliable biomarker that reflects carcinogen exposure to tobacco smoke, but the central question is what is the relationship of DNA adducts and cancer? Therefore, we investigated this relationship by a meta-analysis of twenty-two studies with bronchial adducts for a total of 1091 subjects, 887 lung cancer cases and 204 apparently healthy individuals with no evidence of lung cancer. Our study shows that these adducts are significantly associated to increase lung cancer risk. The value of Mean Ratio (MR) of bronchial adducts resulting from the random effects model was 2.64, 95% C.I. 2.00-3.50, in overall lung cancer cases as compared to controls. The significant difference, with lung cancer patients having significant higher levels of bronchial adducts than controls, persisted after stratification for smoking habits. The MR value between lung cancer patients and controls for smokers was 2.03, 95% C.I. 1.42-2.91, for ex-smokers 3.27, 95% C.I. 1.49-7.18, and for non-smokers was 3.81, 95% C.I. 1.85-7.85. Next, we found that the generation of bronchial adducts is significantly related to inhalation exposure to tobacco smoke carcinogens confirming its association with volatile carcinogens. The MR estimate of bronchial adducts resulting from meta-regression was 2.28, 95% Confidence Interval (C.I.) 1.10-4.73, in overall smokers in respect to non-smokers. The present work provides strengthening of the hypothesis that bronchial adducts are not simply relate to exposure, but are a cause of chemical-induced lung cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Adutos de DNA/genética
Neoplasias Pulmonares/genética
Pulmão/química
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Seres Humanos
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/epidemiologia
Prognóstico
Fatores de Proteção
Medição de Risco
Fatores de Risco
Fumar/epidemiologia
Fumar/genética
Abandono do Hábito de Fumar
Prevenção do Hábito de Fumar
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (DNA Adducts)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  9 / 7531 MEDLINE  
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[PMID]:28910999
[Au] Autor:Gouveia MJ; Pakharukova MY; Laha T; Sripa B; Maksimova GA; Rinaldi G; Brindley PJ; Mordvinov VA; Amaro T; Santos LL; Costa JMCD; Vale N
[Ad] Endereço:Center for the Study in Animal Science, ICETA, University of Porto, Rua de D. Manuel II, Apt 55142, 4051-401 Porto, Portugal.
[Ti] Título:Infection with Opisthorchis felineus induces intraepithelial neoplasia of the biliary tract in a rodent model.
[So] Source:Carcinogenesis;38(9):929-937, 2017 Sep 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The liver fluke Opisthorchis felineus is a member of the triad of epidemiologically relevant species of the trematode family Opisthorchiidae, and the causative agent of opisthorchiasis felinea over an extensive range that spans regions of Eurasia. The International Agency for Research on Cancer classifies the infection with the liver flukes Opisthorchis viverrini and Clonorchis sinensis as group 1 agents and a major risk factor for cholangiocarcinoma. However, the carcinogenic potential of the infection with O. felineus is less clear. Here, we present findings that support the inclusion of O. felineus in the Group 1 list of biological carcinogens. Two discrete lines of evidence support the notion that infection with this liver fluke is carcinogenic. First, novel oxysterol-like metabolites detected by liquid chromatography-mass spectroscopy in the egg and adult developmental stages of O. felineus, and in bile, sera, and urine of liver fluke-infected hamsters exhibited marked similarity to oxysterol-like molecules known from O. viverrini. Numerous oxysterols and related DNA-adducts detected in the liver fluke eggs and in bile from infected hamsters suggested that infection-associated oxysterols induced chromosomal lesions in host cells. Second, histological analysis of liver sections from hamsters infected with O. felineus confirmed portal area enlargement, inflammation with severe periductal fibrosis and changes in the epithelium of the biliary tract characterized as biliary intraepithelial neoplasia, BilIN. The consonance of these biochemical and histopathological changes revealed that O. felineus infection in this rodent model induced precancerous lesions conducive to malignancy.
[Mh] Termos MeSH primário: Neoplasias dos Ductos Biliares/parasitologia
Ductos Biliares Intra-Hepáticos/parasitologia
Carcinogênese
Colangiocarcinoma/parasitologia
Opistorquíase/complicações
Opisthorchis/patogenicidade
[Mh] Termos MeSH secundário: Animais
Neoplasias dos Ductos Biliares/sangue
Neoplasias dos Ductos Biliares/patologia
Neoplasias dos Ductos Biliares/urina
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/urina
Biópsia
Colangiocarcinoma/sangue
Colangiocarcinoma/patologia
Colangiocarcinoma/urina
Cromatografia Líquida de Alta Pressão
Cricetinae
Adutos de DNA/sangue
Adutos de DNA/urina
Seres Humanos
Masculino
Neoplasias Experimentais/sangue
Neoplasias Experimentais/parasitologia
Neoplasias Experimentais/urina
Opistorquíase/patologia
Oxisteróis/sangue
Oxisteróis/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (DNA Adducts); 0 (Oxysterols)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx042


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[PMID]:28867292
[Au] Autor:Myler LR; Gallardo IF; Soniat MM; Deshpande RA; Gonzalez XB; Kim Y; Paull TT; Finkelstein IJ
[Ad] Endereço:Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA; Howard Hughes Medical Institute, The University of Texas at Austin, Austin, TX 78712, USA; Center for Systems and Synthetic Biology, The University of Texas at Austin, Austin, TX 78712, USA.
[Ti] Título:Single-Molecule Imaging Reveals How Mre11-Rad50-Nbs1 Initiates DNA Break Repair.
[So] Source:Mol Cell;67(5):891-898.e4, 2017 Sep 07.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA double-strand break (DSB) repair is essential for maintaining our genomes. Mre11-Rad50-Nbs1 (MRN) and Ku70-Ku80 (Ku) direct distinct DSB repair pathways, but the interplay between these complexes at a DSB remains unclear. Here, we use high-throughput single-molecule microscopy to show that MRN searches for free DNA ends by one-dimensional facilitated diffusion, even on nucleosome-coated DNA. Rad50 binds homoduplex DNA and promotes facilitated diffusion, whereas Mre11 is required for DNA end recognition and nuclease activities. MRN gains access to occluded DNA ends by removing Ku or other DNA adducts via an Mre11-dependent nucleolytic reaction. Next, MRN loads exonuclease 1 (Exo1) onto the free DNA ends to initiate DNA resection. In the presence of replication protein A (RPA), MRN acts as a processivity factor for Exo1, retaining the exonuclease on DNA for long-range resection. Our results provide a mechanism for how MRN promotes homologous recombination on nucleosome-coated DNA.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Quebras de DNA de Cadeia Dupla
Enzimas Reparadoras do DNA/metabolismo
Proteínas de Ligação a DNA/metabolismo
Proteínas Nucleares/metabolismo
Nucleossomos/enzimologia
Reparo de DNA por Recombinação
Imagem Individual de Molécula
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/genética
Adutos de DNA/genética
Adutos de DNA/metabolismo
Enzimas Reparadoras do DNA/genética
Proteínas de Ligação a DNA/genética
Difusão
Exodesoxirribonucleases/genética
Exodesoxirribonucleases/metabolismo
Seres Humanos
Autoantígeno Ku/genética
Autoantígeno Ku/metabolismo
Proteína Homóloga a MRE11
Microscopia de Fluorescência
Proteínas Nucleares/genética
Nucleossomos/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (DNA Adducts); 0 (DNA-Binding Proteins); 0 (MRE11A protein, human); 0 (NBN protein, human); 0 (Nuclear Proteins); 0 (Nucleosomes); 0 (Rad50 protein, human); EC 3.1.- (EXO1 protein, human); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.- (MRE11 Homologue Protein); EC 3.6.4.12 (XRCC5 protein, human); EC 3.6.4.12 (Xrcc6 protein, human); EC 4.2.99.- (Ku Autoantigen); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE



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