Arylamine N-acetyltransferase 1 in situ N-acetylation on CD3+ peripheral blood mononuclear cells correlate with NATb mRNA and NAT1 haplotype

Human arylamine N -acetyltransferase 1 (NAT1) is responsible for the activation and elimination of xenobiotic compounds and carcinogens. Genetic polymorphisms in NAT1 modify both drug efficacy and toxicity. Previous studies have suggested a role for NAT1 in the development of several diseases. The a...

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Veröffentlicht in:	Archives of toxicology 2018-02, Vol.92 (2), p.661-668
Hauptverfasser:	Salazar-González, Raúl A., Turiján-Espinoza, Eneida, Hein, David W., Niño-Moreno, Perla C., Romano-Moreno, Silvia, Milán-Segovia, Rosa C., Portales-Pérez, Diana P.
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Schlagworte:	Acetylation Acetyltransferase Arylamine N-acetyltransferase Biomedical and Life Sciences Biomedicine Carcinogens CD19 antigen CD3 antigen CD56 antigen Correlation Environmental Health Gene expression Genotypes Haplotypes Leukocytes (mononuclear) Lymphocytes T N-acetyltransferase 1 NAT1 protein Occupational Medicine/Industrial Medicine Peripheral blood mononuclear cells Pharmacology/Toxicology Protein expression Proteins Substrates T cell receptors Toxicity Toxicogenomics Transcription
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creator	Salazar-González, Raúl A. Turiján-Espinoza, Eneida Hein, David W. Niño-Moreno, Perla C. Romano-Moreno, Silvia Milán-Segovia, Rosa C. Portales-Pérez, Diana P.
description	Human arylamine N -acetyltransferase 1 (NAT1) is responsible for the activation and elimination of xenobiotic compounds and carcinogens. Genetic polymorphisms in NAT1 modify both drug efficacy and toxicity. Previous studies have suggested a role for NAT1 in the development of several diseases. The aim of the present study was to evaluate NAT1 protein expression and in situ N -acetylation capacity in peripheral blood mononuclear cells (PBMC), as well as their possible associations with the expression of NAT1 transcript and NAT1 genotype. We report NAT1 protein, mRNA levels, and N -acetylation in situ activity for PBMC obtained from healthy donors. NAT1-specific protein expression was higher in CD3+ cells than other major immune cell subtypes (CD19 or CD56 cells). N -acetylation of pABA varied markedly among the PBMC of participants, but correlated very significantly with levels of NAT1 transcripts. NAT14 subjects showed significantly ( p = 0.017) higher apparent pABA V max of 71.3 ± 3.7 versus the NAT114B subjects apparent V max of 58.5 ± 2.5 nmoles Ac-pABA/24 h/million cells. Levels of pABA N -acetylation activity at each concentration of substrate evaluated also significantly correlated with NAT1 mRNA levels for all samples ( p
doi_str_mv	10.1007/s00204-017-2082-y
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Genetic polymorphisms in NAT1 modify both drug efficacy and toxicity. Previous studies have suggested a role for NAT1 in the development of several diseases. The aim of the present study was to evaluate NAT1 protein expression and in situ N -acetylation capacity in peripheral blood mononuclear cells (PBMC), as well as their possible associations with the expression of NAT1 transcript and NAT1 genotype. We report NAT1 protein, mRNA levels, and N -acetylation in situ activity for PBMC obtained from healthy donors. NAT1-specific protein expression was higher in CD3+ cells than other major immune cell subtypes (CD19 or CD56 cells). N -acetylation of pABA varied markedly among the PBMC of participants, but correlated very significantly with levels of NAT1 transcripts. NAT14 subjects showed significantly ( p = 0.017) higher apparent pABA V max of 71.3 ± 3.7 versus the NAT114B subjects apparent V max of 58.5 ± 2.5 nmoles Ac-pABA/24 h/million cells. Levels of pABA N -acetylation activity at each concentration of substrate evaluated also significantly correlated with NAT1 mRNA levels for all samples ( p < 0.0001). This highly significant correlation was maintained for samples with the NAT14 ( p = 0.002) and NAT114B haplotypes ( p = 0.0106). These results provide the first documentation that NAT1-catalyzed N -acetylation in PBMC is higher in T cell than in other immune cell subtypes and that individual variation in N -acetylation capacity is dependent upon NAT1 mRNA and NAT1 haplotype.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-017-2082-y</identifier><identifier>PMID: 29043425</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acetylation ; Acetyltransferase ; Arylamine N-acetyltransferase ; Biomedical and Life Sciences ; Biomedicine ; Carcinogens ; CD19 antigen ; CD3 antigen ; CD56 antigen ; Correlation ; Environmental Health ; Gene expression ; Genotypes ; Haplotypes ; Leukocytes (mononuclear) ; Lymphocytes T ; N-acetyltransferase 1 ; NAT1 protein ; Occupational Medicine/Industrial Medicine ; Peripheral blood mononuclear cells ; Pharmacology/Toxicology ; Protein expression ; Proteins ; Substrates ; T cell receptors ; Toxicity ; Toxicogenomics ; Transcription</subject><ispartof>Archives of toxicology, 2018-02, Vol.92 (2), p.661-668</ispartof><rights>Springer-Verlag GmbH Germany 2017</rights><rights>Archives of Toxicology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-911f2644a8e851b11dfb4d7c508ec615d2d8473398f0b5ee428bb78c6b1c0bf3</citedby><cites>FETCH-LOGICAL-c372t-911f2644a8e851b11dfb4d7c508ec615d2d8473398f0b5ee428bb78c6b1c0bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-017-2082-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-017-2082-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29043425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Salazar-González, Raúl A.</creatorcontrib><creatorcontrib>Turiján-Espinoza, Eneida</creatorcontrib><creatorcontrib>Hein, David W.</creatorcontrib><creatorcontrib>Niño-Moreno, Perla C.</creatorcontrib><creatorcontrib>Romano-Moreno, Silvia</creatorcontrib><creatorcontrib>Milán-Segovia, Rosa C.</creatorcontrib><creatorcontrib>Portales-Pérez, Diana P.</creatorcontrib><title>Arylamine N-acetyltransferase 1 in situ N-acetylation on CD3+ peripheral blood mononuclear cells correlate with NATb mRNA and NAT1 haplotype</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>Arch Toxicol</addtitle><description>Human arylamine N -acetyltransferase 1 (NAT1) is responsible for the activation and elimination of xenobiotic compounds and carcinogens. Genetic polymorphisms in NAT1 modify both drug efficacy and toxicity. Previous studies have suggested a role for NAT1 in the development of several diseases. The aim of the present study was to evaluate NAT1 protein expression and in situ N -acetylation capacity in peripheral blood mononuclear cells (PBMC), as well as their possible associations with the expression of NAT1 transcript and NAT1 genotype. We report NAT1 protein, mRNA levels, and N -acetylation in situ activity for PBMC obtained from healthy donors. NAT1-specific protein expression was higher in CD3+ cells than other major immune cell subtypes (CD19 or CD56 cells). N -acetylation of pABA varied markedly among the PBMC of participants, but correlated very significantly with levels of NAT1 transcripts. NAT14 subjects showed significantly ( p = 0.017) higher apparent pABA V max of 71.3 ± 3.7 versus the NAT114B subjects apparent V max of 58.5 ± 2.5 nmoles Ac-pABA/24 h/million cells. Levels of pABA N -acetylation activity at each concentration of substrate evaluated also significantly correlated with NAT1 mRNA levels for all samples ( p < 0.0001). This highly significant correlation was maintained for samples with the NAT14 ( p = 0.002) and NAT114B haplotypes ( p = 0.0106). These results provide the first documentation that NAT1-catalyzed N -acetylation in PBMC is higher in T cell than in other immune cell subtypes and that individual variation in N -acetylation capacity is dependent upon NAT1 mRNA and NAT1 haplotype.</description><subject>Acetylation</subject><subject>Acetyltransferase</subject><subject>Arylamine N-acetyltransferase</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carcinogens</subject><subject>CD19 antigen</subject><subject>CD3 antigen</subject><subject>CD56 antigen</subject><subject>Correlation</subject><subject>Environmental Health</subject><subject>Gene expression</subject><subject>Genotypes</subject><subject>Haplotypes</subject><subject>Leukocytes (mononuclear)</subject><subject>Lymphocytes T</subject><subject>N-acetyltransferase 1</subject><subject>NAT1 protein</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Peripheral blood mononuclear 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Toxicol</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>92</volume><issue>2</issue><spage>661</spage><epage>668</epage><pages>661-668</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><abstract>Human arylamine N -acetyltransferase 1 (NAT1) is responsible for the activation and elimination of xenobiotic compounds and carcinogens. Genetic polymorphisms in NAT1 modify both drug efficacy and toxicity. Previous studies have suggested a role for NAT1 in the development of several diseases. The aim of the present study was to evaluate NAT1 protein expression and in situ N -acetylation capacity in peripheral blood mononuclear cells (PBMC), as well as their possible associations with the expression of NAT1 transcript and NAT1 genotype. We report NAT1 protein, mRNA levels, and N -acetylation in situ activity for PBMC obtained from healthy donors. NAT1-specific protein expression was higher in CD3+ cells than other major immune cell subtypes (CD19 or CD56 cells). N -acetylation of pABA varied markedly among the PBMC of participants, but correlated very significantly with levels of NAT1 transcripts. NAT14 subjects showed significantly ( p = 0.017) higher apparent pABA V max of 71.3 ± 3.7 versus the NAT114B subjects apparent V max of 58.5 ± 2.5 nmoles Ac-pABA/24 h/million cells. Levels of pABA N -acetylation activity at each concentration of substrate evaluated also significantly correlated with NAT1 mRNA levels for all samples ( p < 0.0001). This highly significant correlation was maintained for samples with the NAT14 ( p = 0.002) and NAT114B haplotypes ( p = 0.0106). These results provide the first documentation that NAT1-catalyzed N -acetylation in PBMC is higher in T cell than in other immune cell subtypes and that individual variation in N -acetylation capacity is dependent upon NAT1 mRNA and NAT1 haplotype.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>29043425</pmid><doi>10.1007/s00204-017-2082-y</doi><tpages>8</tpages></addata></record>
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subjects	Acetylation Acetyltransferase Arylamine N-acetyltransferase Biomedical and Life Sciences Biomedicine Carcinogens CD19 antigen CD3 antigen CD56 antigen Correlation Environmental Health Gene expression Genotypes Haplotypes Leukocytes (mononuclear) Lymphocytes T N-acetyltransferase 1 NAT1 protein Occupational Medicine/Industrial Medicine Peripheral blood mononuclear cells Pharmacology/Toxicology Protein expression Proteins Substrates T cell receptors Toxicity Toxicogenomics Transcription
title	Arylamine N-acetyltransferase 1 in situ N-acetylation on CD3+ peripheral blood mononuclear cells correlate with NATb mRNA and NAT1 haplotype
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