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[PMID]:29478664
[Au] Autor:Xue R; Donovan A; Zhang H; Ma Y; Adams C; Yang J; Hua B; Inniss E; Eichholz T; Shi H
[Ad] Endereço:Department of Chemistry and Environmental Research Center, Missouri University of Science and Technology, Rolla, MO 65409, USA; Center for Single Nanoparticle, Single Cell, and Single Molecule Monitoring (CS(3)M), Missouri University of Science and Technology, Rolla, MO 65409, USA. Electronic addres
[Ti] Título:Simultaneous removal of ammonia and N-nitrosamine precursors from high ammonia water by zeolite and powdered activated carbon.
[So] Source:J Environ Sci (China);64:82-91, 2018 Feb.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:When adding sufficient chlorine to achieve breakpoint chlorination to source water containing high concentration of ammonia during drinking water treatment, high concentrations of disinfection by-products (DBPs) may form. If N-nitrosamine precursors are present, highly toxic N-nitrosamines, primarily N-nitrosodimethylamine (NDMA), may also form. Removing their precursors before disinfection should be a more effective way to minimize these DBPs formation. In this study, zeolites and activated carbon were examined for ammonia and N-nitrosamine precursor removal when incorporated into drinking water treatment processes. The test results indicate that Mordenite zeolite can remove ammonia and five of seven N-nitrosamine precursors efficiently by single step adsorption test. The practical applicability was evaluated by simulation of typical drinking water treatment processes using six-gang stirring system. The Mordenite zeolite was applied at the steps of lime softening, alum coagulation, and alum coagulation with powdered activated carbon (PAC) sorption. While the lime softening process resulted in poor zeolite performance, alum coagulation did not impact ammonia and N-nitrosamine precursor removal. During alum coagulation, more than 67% ammonia and 70%-100% N-nitrosamine precursors were removed by Mordenite zeolite (except 3-(dimethylaminomethyl)indole (DMAI) and 4-dimethylaminoantipyrine (DMAP)). PAC effectively removed DMAI and DMAP when added during alum coagulation. A combination of the zeolite and PAC selected efficiently removed ammonia and all tested seven N-nitrosamine precursors (dimethylamine (DMA), ethylmethylamine (EMA), diethylamine (DEA), dipropylamine (DPA), trimethylamine (TMA), DMAP, and DMAI) during the alum coagulation process.
[Mh] Termos MeSH primário: Amônia/análise
Nitrosaminas/análise
Poluentes Químicos da Água/análise
Purificação da Água/métodos
[Mh] Termos MeSH secundário: Adsorção
Compostos de Alúmen
Amônia/química
Carvão Vegetal/química
Dimetilnitrosamina
Desinfecção
Água Potável
Nitrosaminas/química
Poluentes Químicos da Água/química
Zeolitas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alum Compounds); 0 (Drinking Water); 0 (Nitrosamines); 0 (Water Pollutants, Chemical); 1318-02-1 (Zeolites); 16291-96-6 (Charcoal); 34S289N54E (aluminum sulfate); 7664-41-7 (Ammonia); M43H21IO8R (Dimethylnitrosamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE


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[PMID]:29179064
[Au] Autor:Loukotková L; VonTungeln LS; Vanlandingham M; da Costa GG
[Ad] Endereço:Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States. Electronic address: lucie.loukotkova@fda.hhs.gov.
[Ti] Título:A simple and highly sensitive UPLC-ESI-MS/MS method for the simultaneous quantification of nicotine, cotinine, and the tobacco-specific carcinogens N'-nitrosonornicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in serum samples.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1072:229-234, 2018 Jan 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:According to the World Health Organization, the consumption of tobacco products is the single largest cause of preventable deaths in the world, exceeding the total aggregated number of deaths caused by diseases such as AIDS, tuberculosis, and malaria. An important element in the evaluation of the health risks associated with the consumption of tobacco products is the assessment of the internal exposure to the tobacco constituents responsible for their addictive (e.g. nicotine) and carcinogenic (e.g. N-nitrosamines such as NNN and NNK) properties. However, the assessment of the serum levels of these compounds is often challenging from an analytical standpoint, in particular when limited sample volumes are available and low detection limits are required. Currently available analytical methods often rely on complex multi-step sample preparation procedures, which are prone to low analyte recoveries and ex-vivo contamination due to the ubiquitous nature of these compounds as background contaminants. In order to circumvent these problems, we report a facile and highly sensitive method for the simultaneous quantification of nicotine, cotinine, NNN, and NNK in serum samples. The method relies on a simple "one pot" liquid-liquid extraction procedure and isotope dilution ultra-high pressure (UPLC) hydrophilic interaction liquid chromatography (HILIC) coupled with tandem mass spectrometry. The method requires only 10µL of serum and presents a limit of quantification of 0.02nmol (3000pg/mL) nicotine, 0.6pmol (100pg/mL) cotinine, 0.05pmol NNK (10pg/mL), and 0.06pmol NNN (10pg/mL), making it appropriate for pharmacokinetic evaluations.
[Mh] Termos MeSH primário: Carcinógenos/análise
Cotinina/sangue
Nicotina/sangue
Nitrosaminas/sangue
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Cromatografia Líquida de Alta Pressão/métodos
Estabilidade de Medicamentos
Seres Humanos
Limite de Detecção
Modelos Lineares
Reprodutibilidade dos Testes
Espectrometria de Massas por Ionização por Electrospray/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Nitrosamines); 6M3C89ZY6R (Nicotine); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone); K5161X06LL (Cotinine); X656TZ86DX (N'-nitrosonornicotine)
[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:171128
[St] Status:MEDLINE


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[PMID]:28964810
[Au] Autor:Park JE; Jang YL; Jang CY
[Ad] Endereço:Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 04310, Republic of Korea.
[Ti] Título:The tobacco carcinogen NNK disturbs mitotic chromosome alignment by interrupting p53 targeting to the centrosome.
[So] Source:Toxicol Lett;281:110-118, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is the most potent risk factor among tobacco-related carcinogens in lung cancer progression and outcomes. Although genetic mutations and chromosome instability have been detected in NNK-induced lung tumors, the oncogenic mechanisms of NNK are not fully understood. Here, we show that NNK increases chromosomal instability by disrupting spindle microtubule (MT) attachment to the kinetochore (KT) and spindle dynamics. Mechanistically, NNK blocks the targeting of p53 to the centrosome during mitosis, leading to chromosome alignment defects in metaphase. Therefore, lung cancer cells with wild-type p53, such as A594 and H226B, are more resistant to the NNK treatment than p53-mutant lung cancer cells, such as A1299 and H226Br. Although NNK does not affect the levels or transcriptional activity of p53, the reduction of the p53 level at the centrosome exacerbates the NNK-induced chromosome alignment defect in A549 and H226B cells. Therefore, p53 protects against NNK-induced chromosome instability by modulating the function of centrosome-localized p53 and not by modulating transcriptional activity. We conclude that NNK may increase the risk of lung cancer progression and poorer outcomes in patients with p53 mutations by perturbing proper mitotic progression and chromosome integrity.
[Mh] Termos MeSH primário: Carcinógenos/toxicidade
Centrossomo/efeitos dos fármacos
Nitrosaminas/toxicidade
Tabaco/química
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Células A549
Linhagem Celular Tumoral
Centrossomo/metabolismo
Cromossomos Humanos/efeitos dos fármacos
Cromossomos Humanos/genética
Células HeLa
Seres Humanos
Neoplasias Pulmonares/induzido quimicamente
Neoplasias Pulmonares/genética
Mitose/efeitos dos fármacos
Fatores de Risco
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Nitrosamines); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:28806079
[Au] Autor:Puppala M; Narayanapillai SC; Leitzman P; Sun H; Upadhyaya P; O'Sullivan MG; Hecht SS; Xing C
[Ad] Endereço:Department of Medicinal Chemistry, College of Pharmacy, University of Minnesota , Minneapolis, Minnesota 55455, United States.
[Ti] Título:Pilot in Vivo Structure-Activity Relationship of Dihydromethysticin in Blocking 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O -Methylguanine and Lung Tumor in A/J Mice.
[So] Source:J Med Chem;60(18):7935-7940, 2017 Sep 28.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:(+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-dihydrokavain was completely ineffective. A pilot in vivo structure-activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O -methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications.
[Mh] Termos MeSH primário: Adenoma/prevenção & controle
Anticarcinógenos/uso terapêutico
Guanina/análogos & derivados
Neoplasias Pulmonares/prevenção & controle
Pulmão/efeitos dos fármacos
Pironas/uso terapêutico
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Adenoma/patologia
Animais
Anticarcinógenos/química
Carcinógenos
Feminino
Guanina/antagonistas & inibidores
Guanina/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/induzido quimicamente
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Camundongos
Nitrosaminas
Pironas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7,8-dihydromethysticin); 0 (Anticarcinogenic Agents); 0 (Carcinogens); 0 (Nitrosamines); 0 (Pyrones); 5Z93L87A1R (Guanine); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone); 9B710FV2AE (O-(6)-methylguanine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00921


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[PMID]:28774621
[Au] Autor:Hanigan D; Truong L; Simonich M; Tanguay R; Westerhoff P
[Ad] Endereço:Department of Civil and Environmental Engineering, University of Nevada, Reno, NV 89557-0258, United States; School of Sustainable Engineering and the Built Environment, Arizona State University, Tempe, AZ, 85287-3005, United States. Electronic address: DHanigan@UNR.edu.
[Ti] Título:Zebrafish embryo toxicity of 15 chlorinated, brominated, and iodinated disinfection by-products.
[So] Source:J Environ Sci (China);58:302-310, 2017 Aug.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Disinfection to protect human health occurs at drinking water and wastewater facilities through application of non-selective oxidants including chlorine. Oxidants also transform organic material and form disinfection by-products (DBPs), many of which are halogenated and cyto- and genotoxic. Only a handful of assays have been used to compare DBP toxicity, and researchers are unsure which DBP(s) drive the increased cancer risk associated with drinking chlorinated water. The most extensive data set employs an in vitro model cell, Chinese hamster ovary cells. Traditionally, most DBP research focuses on the threat to human health, but the effects on aquatic species exposed to DBPs in wastewater effluents remain ill defined. We present the developmental toxicity for 15 DBPs and a chlorinated wastewater to a model aquatic vertebrate, zebrafish. Mono-halogenated DBPs followed the in vivo toxicity rank order: acetamides>acetic acids>acetonitriles~nitrosamines, which agrees well with previously published mammalian in vitro data. Di- and tri-halogenated acetonitriles were more toxic than their mono-halogenated analogues, and bromine- and iodine-substituted DBPs tended to be more toxic than chlorinated analogues. No zebrafish development effects were observed after exposure to undiluted or non-concentrated, chlorinated wastewater. We find zebrafish development to be a viable in vivo alternative or confirmatory assay to mammalian in vitro cell assays.
[Mh] Termos MeSH primário: Desinfetantes/toxicidade
Embrião não Mamífero/efeitos dos fármacos
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetulus
Desinfecção/métodos
Água Potável
Nitrosaminas
Águas Residuais
Purificação da Água/métodos
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Disinfectants); 0 (Drinking Water); 0 (Nitrosamines); 0 (Waste Water); 0 (Water Pollutants, Chemical)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


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[PMID]:28735738
[Au] Autor:Horai Y; Ando Y; Kimura S; Arimoto-Kobayashi S
[Ad] Endereço:Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Tsushima, Kita-ku, Okayama 700-8530, Japan.
[Ti] Título:Mutation spectrum resulting in M13mp2 phage DNA exposed to N-nitrosoproline with UVA irradiation.
[So] Source:Mutat Res;821:1-4, 2017 Sep.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:N-nitrosoproline (NPRO) is endogenously formed from proline and nitrite. In an effort to delineate the mechanism of NPRO-induced photomutagenicity, we investigated the mutagenic spectrum of NPRO on M13mp2 DNA with UVA irradiation. Following exposure to NPRO and UVA, the mutation frequency increased significantly in an NPRO and UVA dose-dependent manner. The sequence data derived from seventy of the mutants indicated that mutagenesis resulted mainly from an increase in single-base substitutions, the most frequent being GC to CG transversions. Non-clustering of the GC to CG mutations suggests that NPRO+UVA damage to DNA is random. These transversions may be caused by guanine adducts in DNA or in part by oxidatively modified guanine in DNA exposed to NPRO and UVA.
[Mh] Termos MeSH primário: Bacteriófago M13
Dano ao DNA
DNA Viral
Nitrosaminas/toxicidade
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Bacteriófago M13/efeitos dos fármacos
Bacteriófago M13/genética
Bacteriófago M13/efeitos da radiação
DNA Viral/efeitos dos fármacos
DNA Viral/efeitos da radiação
Relação Dose-Resposta a Droga
Relação Dose-Resposta à Radiação
Escherichia coli/efeitos dos fármacos
Escherichia coli/genética
Mutação
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/genética
Estresse Oxidativo/efeitos da radiação
Resposta SOS (Genética)
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Nitrosamines); F8MI03SGY0 (nitrosoproline)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE


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[PMID]:28702879
[Au] Autor:Rana SVS; Verma Y; Singh GD
[Ad] Endereço:Department of Zoology, Toxicology Laboratory, Ch. Charan Singh University, Meerut, UP, 250004, India. sureshvs_rana@yahoo.com.
[Ti] Título:Assessment of genotoxicity amongst smokers, alcoholics, and tobacco chewers of North India using micronucleus assay and urinary 8-hydroxyl-2'-deoxyguanosine, as biomarkers.
[So] Source:Environ Monit Assess;189(8):391, 2017 Aug.
[Is] ISSN:1573-2959
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The main objective of the present study was to screen the genotoxicity caused by individual and combined habits of smoking, tobacco chewing, and alcohol consumption in human population of North India. Study recruited 67 male subjects aged 25 to 65 years. Buccal mucosal cells were subjected to micronucleus (MN) assay, and 8-hydroxyl-2-deoxyguanosine (8-OHdG) was estimated in their urine samples. Number and shape of the MN cells varied in the buccal epithelium of different groups. Maximum number of MN (0.47%) were found in tobacco chewers followed by smokers (0.45%) and alcoholics (0.44%) (P < 0.05). These results reciprocated the concentration of urinary 8-OHdG. Maximum value for 8-OHdG was also recorded in tobacco chewers (21.07 ± 5.51 mg/mg creatinine) followed by smokers (20.25 ± 3.96 mg/mg creatinine) and alcoholics (19.06 ± 3.41 mg/mg creatinine) (P < 0.05). Combined effects of these agents were found to be statistically different from individual effects. Carcinogenic compounds present in cigarette smoke, nitrosamines found in solid tobacco, and acetaldehyde, a metabolic product of alcohol, induce oxidative stress that manifests into genotoxicity. In conclusion, demographical differences occur in the genotoxicity caused by these three habits. MN assay and urinary 8-OHdG are simple, noninvasive, and reliable biomarkers of genotoxicity.
[Mh] Termos MeSH primário: Alcoólicos/estatística & dados numéricos
Dano ao DNA
Desoxiguanosina/análogos & derivados
Exposição Ambiental/estatística & dados numéricos
Poluição por Fumaça de Tabaco/estatística & dados numéricos
Tabaco sem Fumaça
Tabaco
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/urina
Desoxiguanosina/urina
Monitoramento Ambiental
Seres Humanos
Índia
Masculino
Testes para Micronúcleos
Meia-Idade
Nitrosaminas
Estresse Oxidativo
Fumar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Nitrosamines); 0 (Tobacco Smoke Pollution); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); G9481N71RO (Deoxyguanosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1007/s10661-017-6103-3


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[PMID]:28693087
[Au] Autor:Liang QQ; Zheng WW; He GS; Qu WD
[Ad] Endereço:School of Public Health, Fudan University, Key Laboratory of the Public Health and Safety, Ministry of Education, Shanghai 200032, China.
[Ti] Título:[Quantitative structure-activity relationship prediction of carcinogenicity of N-nitroso compounds based on category approach and read-across].
[So] Source:Zhonghua Yu Fang Yi Xue Za Zhi;51(7):621-627, 2017 Jul 06.
[Is] ISSN:0253-9624
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:New quantitative structure-activity relationship (QSAR) method was used to predict N-nitroso compounds (NOCs) carcinogenicity. This could provide evidences for health risk assessment of the chemicals. Total 74 chemical substances of NOCs were included as target chemicals for this validation study by using QSAR Toolbox based on category approach and read-across. The included 74 NOCs were categorized and subcategorized respectively using "Organic functional groups, Norbert Haider " profiler and "DNA binding by OASIS V.1.1" profiler. Carcinogenicity of rat were used as target of prediction, the carcinogenicity of analogues in chemical categories were cross-read to obtain the carcinogenic predictive results of the target chemicals. Results 74 NOCs included 26 nonclic N-nitrosamines, 24 cyclic N-nitrosamines and 24 N-nitrosamides The sensitivity, specificity and concordance of the category approach and read-across for predicting carcinogenicity of 74 NOCs were 75% (48/64), 70%(7/10) and 74% (55/74) respectively. The concordance for noncyclic N-nitrosamines, cyclic N-nitrosamines and N-nitrosamides were 88% (23/26), 71% (17/24) and 63% (15/24) respectively. QSAR based on category approach and read-across is good for prediction of NOCs carcinogenicity, and can be used for high-throughput qualitative prediction of NOCs carcinogenicity.
[Mh] Termos MeSH primário: Carcinógenos/toxicidade
Compostos Nitrosos/toxicidade
Relação Quantitativa Estrutura-Atividade
[Mh] Termos MeSH secundário: Animais
Testes de Carcinogenicidade
Nitrosaminas
Ratos
Medição de Risco
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Nitrosamines); 0 (Nitroso Compounds); 0 (nitrosamides)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-9624.2017.07.009


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[PMID]:28653505
[Au] Autor:Fujimoto J; Nunomura-Nakamura S; Liu Y; Lang W; McDowell T; Jakubek Y; Ezzeddine D; Kapere Ochieng J; Petersen J; Davies G; Fukuoka J; Wistuba II; Ehli E; Fowler J; Scheet P; Kadara H
[Ad] Endereço:Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX.
[Ti] Título:Development of Kras mutant lung adenocarcinoma in mice with knockout of the airway lineage-specific gene Gprc5a.
[So] Source:Int J Cancer;141(8):1589-1599, 2017 Oct 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the urgency for prevention and treatment of lung adenocarcinoma (LUAD), we still do not know drivers in pathogenesis of the disease. Earlier work revealed that mice with knockout of the G-protein coupled receptor Gprc5a develop late onset lung tumors including LUADs. Here, we sought to further probe the impact of Gprc5a expression on LUAD pathogenesis. We first surveyed GPRC5A expression in human tissues and found that GPRC5A was markedly elevated in human normal lung relative to other normal tissues and was consistently downregulated in LUADs. In sharp contrast to wild-type littermates, Gprc5a mice treated chronically with the nicotine-specific carcinogen NNK developed LUADs by 6 months following NNK exposure. Immunofluorescence analysis revealed that the LUADs exhibited abundant expression of surfactant protein C and lacked the clara cell marker Ccsp, suggesting that these LUADs originated from alveolar type II cells. Next, we sought to survey genome-wide alterations in the pathogenesis of Gprc5a LUADs. Using whole exome sequencing, we found that carcinogen-induced LUADs exhibited markedly higher somatic mutation burdens relative to spontaneous tumors. All LUADs were found to harbor somatic mutations in the Kras oncogene (p. G12D or p. Q61R). In contrast to spontaneous lesions, carcinogen-induced Gprc5a LUADs exhibited mutations (variants and copy number gains) in additional drivers (Atm, Kmt2d, Nf1, Trp53, Met, Ezh2). Our study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a loss and tobacco carcinogen exposure and that may constitute targets for prevention and early treatment of this disease.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Neoplasias Pulmonares/genética
Proteínas Proto-Oncogênicas p21(ras)/genética
Receptores Acoplados a Proteínas-G/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/induzido quimicamente
Adenocarcinoma/enzimologia
Adenocarcinoma/metabolismo
Animais
Carcinógenos/toxicidade
Linhagem da Célula
Genes Supressores de Tumor
Seres Humanos
Neoplasias Pulmonares/induzido quimicamente
Neoplasias Pulmonares/enzimologia
Neoplasias Pulmonares/metabolismo
Camundongos
Camundongos Knockout
Mutação
Nitrosaminas/toxicidade
Proteínas Proto-Oncogênicas p21(ras)/metabolismo
Receptores Acoplados a Proteínas-G/biossíntese
Receptores Acoplados a Proteínas-G/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (GPRC5A protein, human); 0 (GPRC5A protein, mouse); 0 (KRAS protein, human); 0 (Nitrosamines); 0 (Receptors, G-Protein-Coupled); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30851


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[PMID]:28651431
[Au] Autor:Lipowicz PJ; Seeman JI
[Ad] Endereço:Research, Development & Regulatory Affairs, Altria Client Services LLC , 601 East Jackson Street, Richmond, Virginia 23219, United States.
[Ti] Título:A Model To Estimate the Sources of Tobacco-Specific Nitrosamines in Cigarette Smoke.
[So] Source:Chem Res Toxicol;30(8):1556-1561, 2017 Aug 21.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tobacco-specific nitrosamines (TSNAs) are one of the most extensively and continually studied classes of compounds found in tobacco and cigarette smoke.1-5 The TSNAs N-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) have been characterized by the US Food and Drug Administration (FDA) as harmful and potentially harmful constituents in tobacco products,6 and cigarette manufacturers report their levels in cigarette tobacco filler and cigarette smoke to the FDA. NNN and NNK are classified by IARC as carcinogenic to humans.7 TSNAs transfer from tobacco to smoke by evaporation driven by heat and the flow of gases down the cigarette rod. Other TSNA sources in smoke include pyrorelease, where room temperature-unextractable TSNAs are released by smoking, and pyrosynthesis, where TSNAs are formed by reactions during smoking. We propose the first model that quantifies these three sources of TSNA in smoke. In our model, evaporative transfer efficiency of a TSNA is equated to the evaporative transfer efficiency of nicotine. Smoke TSNA measured in excess of what is transferred by evaporation is termed "pyrogeneration," which is the net sum of pyrorelease and pyrosynthesis minus pyrodegredation. This model requires no internal standard, is applicable to commercial cigarettes "as is," and uses existing analytical methods. This model was applied to archived Philip Morris USA data. For commercial blended cigarettes, NNN pyrogeneration appears to be unimportant, but NNK pyrogeneration contributes roughly 30-70% of NNK in smoke with the greater contribution at lower tobacco NNK levels. This means there is an opportunity to significantly reduce smoke NNK by up to 70% if pyrogeneration can be decreased or eliminated, perhaps by finding a way to grow and cure tobacco with reduced matrix-bound NNK. For burley research cigarettes, pyrogeneration may account for 90% or more of both NNN and NNK in smoke.
[Mh] Termos MeSH primário: Modelos Químicos
Nitrosaminas/química
Fumar
Tabaco/química
[Mh] Termos MeSH secundário: Carcinogênese
Gases/química
Seres Humanos
Nicotina/química
Nitrosaminas/análise
Temperatura Ambiente
Tabaco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gases); 0 (Nitrosamines); 6M3C89ZY6R (Nicotine); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone); X656TZ86DX (N'-nitrosonornicotine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00046



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